The ER–Golgi intermediate compartment is a key membrane source for the LC3 lipidation step of autophagosome biogenesis
Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membran...
Saved in:
| Published in | eLife Vol. 2; p. e00947 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
eLife Sciences Publications Ltd
06.08.2013
eLife Sciences Publications, Ltd |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting early autophagosome formation. In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo. We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum–Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo. Moreover, we find that the ERGIC acts by recruiting the early autophagosome marker ATG14, a critical step for the generation of preautophagosomal membranes.
Cells continually adapt their behavior to accommodate changes in their environment. For example, when nutrients are abundant, cells can grow or proliferate; in times of scarcity, however, they must conserve resources for essential tasks. In particular, during periods of starvation, cells can cannibalize themselves in a process called autophagy, which literally means ‘self-eating’. Structures called autophagosomes engulf bits of cytoplasm and carry the contents to the digestive compartment of the cell, the lysosome, to be broken down into their constituent parts. This can include the degradation of proteins into amino acids, which can then be recycled into other proteins needed by the cell.
In cells, proteins are shipped to their destinations—which can be the plasma membrane or a specific organelle within the cell—via a delivery system known as the secretory pathway. This pathway begins in the endoplasmic reticulum (ER), where many of these proteins are made. From the ER, the proteins move to a compartment called the Golgi apparatus, which then sends them to their destinations, or to the lysosome to be broken down. Between the ER and Golgi they pass through a structure called the ER–Golgi intermediate compartment (ERGIC).
Although the signaling pathways that initiate autophagy are known, less is understood about the actual formation of the autophagosomes. Now, Ge et al. have developed an in vitro system to study their formation, and gone on to identify a membrane that is both necessary and sufficient to create these structures.
Previous studies have implicated a variety of membranes—including the plasma membrane and the membranes belonging to the ER, the Golgi apparatus, the lysosome and various other organelles—in the formation of autophagosomes. To identify which of these membranes might be involved, Ge et al. focused on a protein called LC3 that is a key marker for the formation of the autophagosome. This protein is recruited to the growing autophagosome by a lipid, so discovering which membranes can add a lipid to LC3 should shed light on the assembly process.
By separating the full range of organelles in a cell lysate into fractions (a process called fractionation), Ge et al. found that the ERGIC was the most active membrane to attach lipid to LC3. Additionally, the lipid was only added when signaling pathways that stimulate autophagy—such as the PI3K pathway—were activated. Together, these results provide insight into the mechanism of autophagosome formation, and the structures in the cell that participate in this process. |
|---|---|
| AbstractList | Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting early autophagosome formation. In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo. We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum–Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo. Moreover, we find that the ERGIC acts by recruiting the early autophagosome marker ATG14, a critical step for the generation of preautophagosomal membranes.DOI: http://dx.doi.org/10.7554/eLife.00947.001 Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting early autophagosome formation. In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo. We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum–Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo. Moreover, we find that the ERGIC acts by recruiting the early autophagosome marker ATG14, a critical step for the generation of preautophagosomal membranes. Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting early autophagosome formation. In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo. We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum–Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo. Moreover, we find that the ERGIC acts by recruiting the early autophagosome marker ATG14, a critical step for the generation of preautophagosomal membranes. DOI: http://dx.doi.org/10.7554/eLife.00947.001 Cells continually adapt their behavior to accommodate changes in their environment. For example, when nutrients are abundant, cells can grow or proliferate; in times of scarcity, however, they must conserve resources for essential tasks. In particular, during periods of starvation, cells can cannibalize themselves in a process called autophagy, which literally means ‘self-eating’. Structures called autophagosomes engulf bits of cytoplasm and carry the contents to the digestive compartment of the cell, the lysosome, to be broken down into their constituent parts. This can include the degradation of proteins into amino acids, which can then be recycled into other proteins needed by the cell. In cells, proteins are shipped to their destinations—which can be the plasma membrane or a specific organelle within the cell—via a delivery system known as the secretory pathway. This pathway begins in the endoplasmic reticulum (ER), where many of these proteins are made. From the ER, the proteins move to a compartment called the Golgi apparatus, which then sends them to their destinations, or to the lysosome to be broken down. Between the ER and Golgi they pass through a structure called the ER–Golgi intermediate compartment (ERGIC). Although the signaling pathways that initiate autophagy are known, less is understood about the actual formation of the autophagosomes. Now, Ge et al. have developed an in vitro system to study their formation, and gone on to identify a membrane that is both necessary and sufficient to create these structures. Previous studies have implicated a variety of membranes—including the plasma membrane and the membranes belonging to the ER, the Golgi apparatus, the lysosome and various other organelles—in the formation of autophagosomes. To identify which of these membranes might be involved, Ge et al. focused on a protein called LC3 that is a key marker for the formation of the autophagosome. This protein is recruited to the growing autophagosome by a lipid, so discovering which membranes can add a lipid to LC3 should shed light on the assembly process. By separating the full range of organelles in a cell lysate into fractions (a process called fractionation), Ge et al. found that the ERGIC was the most active membrane to attach lipid to LC3. Additionally, the lipid was only added when signaling pathways that stimulate autophagy—such as the PI3K pathway—were activated. Together, these results provide insight into the mechanism of autophagosome formation, and the structures in the cell that participate in this process. DOI: http://dx.doi.org/10.7554/eLife.00947.002 Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting early autophagosome formation. In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo. We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum–Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo. Moreover, we find that the ERGIC acts by recruiting the early autophagosome marker ATG14, a critical step for the generation of preautophagosomal membranes. Cells continually adapt their behavior to accommodate changes in their environment. For example, when nutrients are abundant, cells can grow or proliferate; in times of scarcity, however, they must conserve resources for essential tasks. In particular, during periods of starvation, cells can cannibalize themselves in a process called autophagy, which literally means ‘self-eating’. Structures called autophagosomes engulf bits of cytoplasm and carry the contents to the digestive compartment of the cell, the lysosome, to be broken down into their constituent parts. This can include the degradation of proteins into amino acids, which can then be recycled into other proteins needed by the cell. In cells, proteins are shipped to their destinations—which can be the plasma membrane or a specific organelle within the cell—via a delivery system known as the secretory pathway. This pathway begins in the endoplasmic reticulum (ER), where many of these proteins are made. From the ER, the proteins move to a compartment called the Golgi apparatus, which then sends them to their destinations, or to the lysosome to be broken down. Between the ER and Golgi they pass through a structure called the ER–Golgi intermediate compartment (ERGIC). Although the signaling pathways that initiate autophagy are known, less is understood about the actual formation of the autophagosomes. Now, Ge et al. have developed an in vitro system to study their formation, and gone on to identify a membrane that is both necessary and sufficient to create these structures. Previous studies have implicated a variety of membranes—including the plasma membrane and the membranes belonging to the ER, the Golgi apparatus, the lysosome and various other organelles—in the formation of autophagosomes. To identify which of these membranes might be involved, Ge et al. focused on a protein called LC3 that is a key marker for the formation of the autophagosome. This protein is recruited to the growing autophagosome by a lipid, so discovering which membranes can add a lipid to LC3 should shed light on the assembly process. By separating the full range of organelles in a cell lysate into fractions (a process called fractionation), Ge et al. found that the ERGIC was the most active membrane to attach lipid to LC3. Additionally, the lipid was only added when signaling pathways that stimulate autophagy—such as the PI3K pathway—were activated. Together, these results provide insight into the mechanism of autophagosome formation, and the structures in the cell that participate in this process. Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting early autophagosome formation. In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo. We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum-Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo. Moreover, we find that the ERGIC acts by recruiting the early autophagosome marker ATG14, a critical step for the generation of preautophagosomal membranes. DOI:http://dx.doi.org/10.7554/eLife.00947.001. Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting early autophagosome formation. In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo. We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum-Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo. Moreover, we find that the ERGIC acts by recruiting the early autophagosome marker ATG14, a critical step for the generation of preautophagosomal membranes. DOI:http://dx.doi.org/10.7554/eLife.00947.001.Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate the formation of autophagosomes remains elusive. Here, we establish a cell-free assay based on LC3 lipidation to define the organelle membrane supporting early autophagosome formation. In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo. We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum-Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo. Moreover, we find that the ERGIC acts by recruiting the early autophagosome marker ATG14, a critical step for the generation of preautophagosomal membranes. DOI:http://dx.doi.org/10.7554/eLife.00947.001. |
| Author | Melville, David Ge, Liang Schekman, Randy Zhang, Min |
| Author_xml | – sequence: 1 givenname: Liang surname: Ge fullname: Ge, Liang organization: Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, United States – sequence: 2 givenname: David surname: Melville fullname: Melville, David organization: Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, United States – sequence: 3 givenname: Min surname: Zhang fullname: Zhang, Min organization: Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, United States – sequence: 4 givenname: Randy surname: Schekman fullname: Schekman, Randy organization: Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, United States |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23930225$$D View this record in MEDLINE/PubMed |
| BookMark | eNptkt9qFDEUxgep2Fp75b0EvBFka_5OkhuhLLUWFgSp4F3IZM7sZp2ZjElG7J3v4Bv6JKa7tbTF3ORw8svHOd85z6uDMYxQVS8JPpVC8Hew8h2cYqy5fFIdUSzwAiv-9eBefFidpLTF5UiuFNHPqkPKNMOUiqPq59UG0PnnP79-X4R-7ZEfM8QBWm8zIBeGycY8wJiRT8iib3CNBhiaaEdAKczRAepCRLmIrJYM9X7yrc0-jChlmFDokJ1zmDZ2HVIYADU-rGGE5NOL6mln-wQnt_dx9eXD-dXy42L16eJyebZaOMFJXjSkZrTFXWsplk61tusY1URaRUFTJkhDuGwwo7IlvG4k2BI4axvaNK2ilB1Xl3vdNtitmaIfbLw2wXqzS4S4NqVF73owQkqFGdFKMMeFoLprOGaaKOWwJKIrWu_3WtPcFI9c8SXa_oHow5fRb8w6_DBMslpwXgTe3ArE8H2GlM3gk4O-L36GORnCiWa8gKqgrx-h2-L3WKwyRNd1rWuib7p7db-iu1L-DbgAb_eAiyGlCN0dQrC52SCz2yCz26BCk0e083k3z9KO7__75y98VsqH |
| CitedBy_id | crossref_primary_10_1016_j_biochi_2022_10_004 crossref_primary_10_7554_eLife_58504 crossref_primary_10_1038_s41594_024_01300_y crossref_primary_10_1038_s41556_018_0092_5 crossref_primary_10_1002_iub_2611 crossref_primary_10_1016_j_jgg_2022_07_001 crossref_primary_10_1038_ncomms11808 crossref_primary_10_1093_jb_mvad099 crossref_primary_10_1080_21541248_2016_1220779 crossref_primary_10_1038_cr_2013_159 crossref_primary_10_1016_j_jsb_2016_04_005 crossref_primary_10_1073_pnas_2021293118 crossref_primary_10_1111_febs_13661 crossref_primary_10_1016_j_bbamem_2021_183731 crossref_primary_10_1016_j_bbamem_2024_184308 crossref_primary_10_1016_j_cub_2018_06_035 crossref_primary_10_1038_ncb3579 crossref_primary_10_3390_ijms21103689 crossref_primary_10_12677_ACM_2019_93027 crossref_primary_10_18632_oncotarget_18221 crossref_primary_10_15252_embj_2021110057 crossref_primary_10_1016_j_celrep_2024_114619 crossref_primary_10_1091_mbc_E18_11_0743 crossref_primary_10_1080_15548627_2015_1017178 crossref_primary_10_1073_pnas_1523145113 crossref_primary_10_1091_mbc_e16_11_0762 crossref_primary_10_1093_jnen_nlab029 crossref_primary_10_1038_nri_2016_100 crossref_primary_10_3389_fimmu_2024_1352479 crossref_primary_10_1002_1873_3468_14983 crossref_primary_10_3390_ijms252011160 crossref_primary_10_3390_cells5020024 crossref_primary_10_1016_j_bbalip_2021_158956 crossref_primary_10_1016_j_neuron_2017_01_022 crossref_primary_10_1016_j_ymeth_2014_12_008 crossref_primary_10_1080_15548627_2024_2367907 crossref_primary_10_1038_ncomms9045 crossref_primary_10_1016_j_molcel_2019_12_028 crossref_primary_10_1038_s41423_019_0240_2 crossref_primary_10_1091_mbc_e17_01_0022 crossref_primary_10_1038_s41467_022_31181_y crossref_primary_10_7554_eLife_45777 crossref_primary_10_1002_ptr_7551 crossref_primary_10_1111_boc_201400065 crossref_primary_10_1083_jcb_201705047 crossref_primary_10_3389_fimmu_2020_578038 crossref_primary_10_1080_15548627_2020_1796321 crossref_primary_10_1083_jcb_202203083 crossref_primary_10_1038_cr_2016_146 crossref_primary_10_7554_eLife_42253 crossref_primary_10_15252_embj_201695081 crossref_primary_10_1073_pnas_1814552115 crossref_primary_10_15252_embj_201592695 crossref_primary_10_1038_s41422_023_00782_7 crossref_primary_10_1080_15548627_2019_1596478 crossref_primary_10_1016_j_jbior_2018_02_003 crossref_primary_10_1038_s41598_018_21106_5 crossref_primary_10_1002_advs_202405127 crossref_primary_10_15252_embj_201797006 crossref_primary_10_1016_j_tibs_2021_01_006 crossref_primary_10_1073_pnas_1316356110 crossref_primary_10_7554_eLife_21690 crossref_primary_10_1016_j_yexcr_2023_113635 crossref_primary_10_1146_annurev_cellbio_100818_125418 crossref_primary_10_1002_bies_202400038 crossref_primary_10_1016_j_jmb_2017_01_002 crossref_primary_10_1016_j_devcel_2017_03_015 crossref_primary_10_1371_journal_ppat_1006609 crossref_primary_10_1016_j_jmb_2019_09_005 crossref_primary_10_1016_j_bbagrm_2023_194936 crossref_primary_10_1016_j_celrep_2016_01_047 crossref_primary_10_1016_j_mib_2016_11_004 crossref_primary_10_1038_s42003_024_07191_5 crossref_primary_10_3390_cells12040621 crossref_primary_10_1146_annurev_neuro_071013_014149 crossref_primary_10_3390_cells7120278 crossref_primary_10_1016_j_virs_2024_01_001 crossref_primary_10_1038_s41467_025_57408_2 crossref_primary_10_1016_j_jmb_2024_168472 crossref_primary_10_3389_fphys_2016_00470 crossref_primary_10_1007_s10534_014_9773_0 crossref_primary_10_1042_BST20220713 crossref_primary_10_1080_15548627_2020_1732713 crossref_primary_10_1146_annurev_biochem_061516_044820 crossref_primary_10_1038_cr_2017_4 crossref_primary_10_1080_15548627_2018_1505153 crossref_primary_10_1111_bph_13052 crossref_primary_10_1016_j_antiviral_2024_105955 crossref_primary_10_1016_j_bbalip_2016_01_006 crossref_primary_10_3389_fimmu_2018_01024 crossref_primary_10_1016_j_bbamcr_2019_118627 crossref_primary_10_1016_j_cub_2017_10_054 crossref_primary_10_1083_jcb_202404047 crossref_primary_10_1084_jem_20150956 crossref_primary_10_1016_j_xgen_2024_100510 crossref_primary_10_1128_IAI_00110_15 crossref_primary_10_3389_fmicb_2021_661446 crossref_primary_10_1038_s41586_019_1006_9 crossref_primary_10_1007_s00418_018_1717_2 crossref_primary_10_1038_s41467_018_06275_1 crossref_primary_10_3390_ijms232113643 crossref_primary_10_1016_j_ceb_2018_04_003 crossref_primary_10_1242_jcs_141036 crossref_primary_10_1038_srep06952 crossref_primary_10_1038_s41467_024_52818_0 crossref_primary_10_1016_j_tibs_2020_12_010 crossref_primary_10_15252_embj_2022112387 crossref_primary_10_1080_15548627_2023_2254191 crossref_primary_10_3390_ijms19123783 crossref_primary_10_1016_j_cell_2021_10_017 crossref_primary_10_1042_BST20200130 crossref_primary_10_1186_s40880_017_0219_2 crossref_primary_10_1089_dna_2017_4115 crossref_primary_10_1093_cvr_cvab158 crossref_primary_10_1007_s10495_015_1108_2 crossref_primary_10_3389_fpls_2020_00477 crossref_primary_10_1016_j_cub_2022_04_071 crossref_primary_10_1093_brain_awu278 crossref_primary_10_1016_j_tcb_2022_08_006 crossref_primary_10_1016_j_devcel_2017_11_024 crossref_primary_10_1007_s12032_024_02539_7 crossref_primary_10_1016_j_ceb_2014_02_005 crossref_primary_10_3390_biomedicines10051027 crossref_primary_10_1080_15548627_2021_1994297 crossref_primary_10_3389_fpls_2016_01655 crossref_primary_10_1038_s41421_020_0161_3 crossref_primary_10_1016_j_febslet_2015_05_008 crossref_primary_10_1016_j_fsi_2018_06_044 crossref_primary_10_15252_embj_2019103563 crossref_primary_10_1016_j_molcel_2016_04_020 crossref_primary_10_1038_s41422_021_00563_0 crossref_primary_10_15252_embr_201744837 crossref_primary_10_1038_s41422_025_01085_9 crossref_primary_10_1038_s41467_020_18153_w crossref_primary_10_1080_15548627_2021_1896157 crossref_primary_10_1083_jcb_202211039 crossref_primary_10_1016_j_jmb_2016_10_029 crossref_primary_10_1016_j_redox_2015_01_003 crossref_primary_10_1080_15548627_2020_1779468 crossref_primary_10_3390_cells9051184 crossref_primary_10_1038_s41556_024_01445_4 crossref_primary_10_1042_BST20140247 crossref_primary_10_1051_medsci_20173303004 crossref_primary_10_15252_embj_2022112845 crossref_primary_10_1016_j_tplants_2018_05_002 crossref_primary_10_15252_embr_201439076 crossref_primary_10_7554_eLife_85837 crossref_primary_10_1038_s41590_020_0730_5 crossref_primary_10_1016_j_cell_2019_12_005 crossref_primary_10_1083_jcb_201810099 crossref_primary_10_1038_cddis_2016_230 crossref_primary_10_1038_s41594_021_00614_5 crossref_primary_10_1016_j_tibs_2016_08_001 crossref_primary_10_1016_j_molimm_2018_06_265 crossref_primary_10_1073_pnas_1811874115 crossref_primary_10_1016_j_mcn_2022_103754 crossref_primary_10_1083_jcb_202404152 crossref_primary_10_1016_j_yexcr_2017_02_017 crossref_primary_10_1002_cpcb_33 crossref_primary_10_1038_cddis_2017_370 crossref_primary_10_1007_s00418_019_01829_w crossref_primary_10_1038_s41421_021_00268_z crossref_primary_10_1002_bies_201800004 crossref_primary_10_1016_j_plantsci_2019_01_017 crossref_primary_10_1016_j_sbi_2016_09_010 crossref_primary_10_3390_ijms222413232 crossref_primary_10_1002_jcp_31512 crossref_primary_10_1051_medsci_2024013 crossref_primary_10_3390_ijms222112087 crossref_primary_10_1371_journal_ppat_1004747 crossref_primary_10_1038_s41467_023_36553_6 crossref_primary_10_1016_j_devcel_2017_02_016 crossref_primary_10_1038_s41477_021_00997_9 crossref_primary_10_1016_j_molcel_2023_04_026 crossref_primary_10_1083_jcb_201408075 crossref_primary_10_1016_j_yexcr_2015_02_003 crossref_primary_10_3389_fimmu_2017_00165 crossref_primary_10_1016_j_cell_2020_03_031 crossref_primary_10_3390_cells11192996 crossref_primary_10_1007_s00726_014_1765_4 crossref_primary_10_1093_burnst_tkz001 crossref_primary_10_1016_j_chom_2015_07_001 crossref_primary_10_1016_j_lfs_2017_08_029 crossref_primary_10_3389_fcell_2020_564975 crossref_primary_10_1007_s12035_016_0140_8 crossref_primary_10_1007_s00018_015_2034_8 crossref_primary_10_1093_hmg_ddv126 crossref_primary_10_1080_15548627_2018_1493315 crossref_primary_10_1042_BST20140183 crossref_primary_10_1016_j_devcel_2023_03_014 crossref_primary_10_1016_j_semcancer_2021_09_003 crossref_primary_10_1101_cshperspect_a041258 crossref_primary_10_1080_15548627_2019_1628539 crossref_primary_10_1083_jcb_201812135 crossref_primary_10_1242_bio_058736 crossref_primary_10_1371_journal_pbio_2007044 crossref_primary_10_1016_j_scib_2025_03_045 crossref_primary_10_1016_j_ejphar_2020_173660 crossref_primary_10_1128_jvi_01476_22 crossref_primary_10_4161_auto_27242 crossref_primary_10_1080_15548627_2020_1838117 crossref_primary_10_1080_21505594_2020_1726594 crossref_primary_10_1080_15548627_2021_1943177 crossref_primary_10_1016_j_pbi_2019_05_009 crossref_primary_10_1186_s40478_016_0324_5 crossref_primary_10_1007_s00418_018_1689_2 crossref_primary_10_1016_j_celrep_2016_04_062 crossref_primary_10_1016_j_tibs_2021_03_006 crossref_primary_10_1016_j_yjmcc_2015_12_005 crossref_primary_10_1038_s41418_017_0017_z crossref_primary_10_1360_nso_20220018 crossref_primary_10_1016_j_mad_2016_01_003 crossref_primary_10_1073_pnas_2002110117 crossref_primary_10_1080_15548627_2017_1378838 crossref_primary_10_1128_JVI_02399_20 crossref_primary_10_1128_mBio_02021_17 crossref_primary_10_1126_sciadv_abj8156 crossref_primary_10_1016_j_jmb_2016_02_024 crossref_primary_10_3389_fcell_2023_1177440 crossref_primary_10_1128_mBio_02147_14 crossref_primary_10_1038_srep42591 crossref_primary_10_1083_jcb_201708039 crossref_primary_10_1007_s11154_013_9276_2 crossref_primary_10_3390_biom14121517 crossref_primary_10_1080_15548627_2023_2287932 crossref_primary_10_1016_j_isci_2024_111594 crossref_primary_10_3390_cells8121627 crossref_primary_10_1016_j_ceb_2017_02_011 crossref_primary_10_1080_15548627_2016_1203489 crossref_primary_10_1146_annurev_immunol_042617_053253 crossref_primary_10_1038_s41467_020_19028_w crossref_primary_10_1038_s41419_024_07208_1 crossref_primary_10_1038_cddis_2016_312 crossref_primary_10_1128_MCB_01327_13 crossref_primary_10_1146_annurev_biochem_060815_014556 crossref_primary_10_1194_jlr_M051862 crossref_primary_10_15252_embr_201845889 crossref_primary_10_1038_s41467_022_33933_2 crossref_primary_10_1016_j_bbrc_2017_11_049 crossref_primary_10_1016_j_celrep_2023_112108 crossref_primary_10_1080_15548627_2016_1256521 crossref_primary_10_1016_j_ceb_2021_02_001 crossref_primary_10_1016_j_ceb_2018_06_003 crossref_primary_10_1038_s41579_018_0003_6 crossref_primary_10_1111_tra_12654 crossref_primary_10_1038_s41556_022_00861_8 crossref_primary_10_1002_jat_3393 crossref_primary_10_1016_j_devcel_2019_01_027 crossref_primary_10_1038_ncomms14846 crossref_primary_10_1083_jcb_201402054 crossref_primary_10_15252_embj_201695189 crossref_primary_10_1111_febs_13987 crossref_primary_10_3389_fonc_2021_603224 crossref_primary_10_1007_s00726_014_1787_y crossref_primary_10_1038_ncomms12420 crossref_primary_10_1080_15548627_2021_1969634 crossref_primary_10_1007_s13238_020_00793_9 crossref_primary_10_1242_jcs_223792 crossref_primary_10_1038_s41421_024_00659_y crossref_primary_10_1016_j_cell_2022_03_005 crossref_primary_10_1080_15548627_2020_1817279 crossref_primary_10_1016_j_jmb_2016_12_013 crossref_primary_10_1139_bcb_2014_0115 crossref_primary_10_1080_15548627_2020_1783118 crossref_primary_10_1038_nrm3696 crossref_primary_10_1016_j_cub_2022_01_040 crossref_primary_10_1152_japplphysiol_00550_2015 crossref_primary_10_1016_j_devcel_2014_06_001 crossref_primary_10_1038_s41418_019_0481_8 crossref_primary_10_3389_fonc_2022_841625 crossref_primary_10_1016_j_tplants_2016_11_015 crossref_primary_10_3390_ijms19061775 crossref_primary_10_1016_j_jmb_2016_06_011 crossref_primary_10_24998_maeusabed_355164 crossref_primary_10_1093_plcell_koab263 crossref_primary_10_1007_s00726_014_1775_2 crossref_primary_10_1002_jcp_26583 crossref_primary_10_1146_annurev_cellbio_101011_155756 crossref_primary_10_1083_jcb_201508102 crossref_primary_10_15252_embr_201744559 crossref_primary_10_1111_cmi_12409 crossref_primary_10_1016_j_devcel_2018_03_008 crossref_primary_10_1016_j_bbalip_2019_03_005 crossref_primary_10_1038_s41422_021_00579_6 crossref_primary_10_3389_fcell_2022_892450 crossref_primary_10_3389_fcell_2023_1069256 crossref_primary_10_1080_15548627_2022_2025572 crossref_primary_10_3389_fmmed_2022_971247 crossref_primary_10_1083_jcb_202203045 crossref_primary_10_3389_fcell_2019_00171 crossref_primary_10_1002_1873_3468_13637 crossref_primary_10_7554_eLife_04135 crossref_primary_10_1002_jcp_31366 crossref_primary_10_1080_21541248_2021_1892443 crossref_primary_10_1371_journal_ppat_1007982 crossref_primary_10_1038_s42003_023_05382_0 crossref_primary_10_1007_s11427_023_2443_9 crossref_primary_10_1016_j_canlet_2024_216659 crossref_primary_10_1016_j_jplph_2016_06_001 crossref_primary_10_1016_j_metabol_2023_155629 crossref_primary_10_1080_15548627_2018_1462426 crossref_primary_10_12688_f1000research_22111_1 crossref_primary_10_1083_jcb_201809032 crossref_primary_10_1038_s41421_020_0166_y crossref_primary_10_1038_cddis_2014_243 crossref_primary_10_1242_jcs_158758 crossref_primary_10_3390_biomedicines9111625 crossref_primary_10_1016_j_cub_2017_02_061 crossref_primary_10_3390_cells11233813 crossref_primary_10_1016_j_bbagen_2017_10_021 |
| Cites_doi | 10.1016/j.cell.2012.11.028 10.1126/science.1207056 10.1074/jbc.273.7.3963 10.1016/j.cca.2011.04.023 10.1038/ncb2078 10.1247/csf.28.49 10.4161/auto.6.1.10928 10.1083/jcb.200912089 10.1038/26506 10.1146/annurev-biochem-052709-094552 10.1023/A:1007667802497 10.1016/j.ceb.2009.12.004 10.7554/eLife.00160 10.1016/j.cell.2011.06.022 10.1038/ncb2152 10.1038/ncb1991 10.1242/jcs.112.23.4175 10.1074/jbc.273.51.33889 10.1038/ncb1846 10.1083/jcb.152.4.657 10.1242/jcs.093203 10.1091/mbc.E03-06-0437 10.1091/mbc.E09-04-0345 10.1111/j.1365-2443.2009.01299.x 10.4161/auto.19496 10.1155/2011/713435 10.4161/auto.5.8.10274 10.1083/jcb.200911141 10.1007/s00281-010-0222-z 10.1016/j.cell.2010.04.009 10.1074/jbc.C700195200 10.1083/jcb.200904075 10.1083/jcb.200803137 10.1073/pnas.1014434108 10.1038/35044114 10.1016/j.cmet.2008.04.001 10.1021/jm101144f 10.1021/ml100230n 10.1091/mbc.E09-11-0969 10.1016/j.cell.2005.01.005 10.1016/j.cell.2011.06.025 10.1038/nature03029 10.1242/jcs.03172 10.1038/embor.2008.163 10.1016/j.cell.2012.12.016 10.1073/pnas.0810452105 10.1126/science.1715094 10.1111/j.1600-0854.2010.01086.x 10.1016/j.cub.2011.11.034 10.1091/mbc.10.2.435 10.1091/mbc.E08-03-0309 10.4161/auto.6.6.12709 10.1016/j.molcel.2008.06.001 10.1182/blood-2008-02-137398 10.1016/S0021-9258(19)34116-X 10.1083/jcb.200107045 10.1038/ncb1854 10.1242/jcs.03019 10.1016/j.cell.2011.06.023 10.1073/pnas.0910342106 10.1083/jcb.201111079 10.1038/nature06639 10.1091/mbc.E10-05-0457 10.1016/S1097-2765(00)80455-4 10.1093/emboj/19.21.5720 10.1016/j.febslet.2009.10.053 10.1074/jbc.M801836200 10.1074/jbc.M401461200 10.1074/jbc.M505888200 10.1038/nature11910 10.1083/jcb.201202061 10.1091/mbc.E11-09-0746 10.1038/nprot.2009.151 10.1091/mbc.E07-12-1257 10.1083/jcb.201002108 10.1242/jcs.114.22.3991 10.1083/jcb.200412022 10.4161/auto.3270 10.1073/pnas.1016472108 10.1016/j.ceb.2009.11.014 10.1074/jbc.C000449200 10.1074/jbc.M411091200 10.3410/B3-25 |
| ContentType | Journal Article |
| Copyright | Copyright © 2013, Ge et al. This work is licensed under the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/3.0/ ) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Copyright © 2013, Ge et al 2013 Ge et al |
| Copyright_xml | – notice: Copyright © 2013, Ge et al. This work is licensed under the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/3.0/ ) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: Copyright © 2013, Ge et al 2013 Ge et al |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7X7 7XB 88E 88I 8FE 8FH 8FI 8FJ 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FYUFA GHDGH GNUQQ HCIFZ K9. LK8 M0S M1P M2P M7P PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS Q9U 7X8 5PM DOA |
| DOI | 10.7554/eLife.00947 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Science Database (Alumni Edition) ProQuest SciTech Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection ProQuest Central Natural Science Collection ProQuest One ProQuest Central Korea Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Biological Sciences ProQuest Health & Medical Collection Medical Database Science Database Biological Science Database ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China ProQuest Central Basic MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Science Journals (Alumni Edition) ProQuest Biological Science Collection ProQuest Central Basic ProQuest Science Journals ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest SciTech Collection ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | Publicly Available Content Database CrossRef MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: DOA name: Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 4 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 2050-084X |
| ExternalDocumentID | oai_doaj_org_article_57780319853c45529fb4039188c0715f PMC3736544 23930225 10_7554_eLife_00947 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GrantInformation_xml | – fundername: Human Frontier Science Program grantid: LT000003/2012 – fundername: University of California, Berkeley Miller Institute – fundername: Jane Coffin Childs Fund – fundername: Howard Hughes Medical Institute |
| GroupedDBID | 53G 5VS 7X7 88E 88I 8FE 8FH 8FI 8FJ AAFWJ AAKDD AAYXX ABUWG ACGFO ACGOD ACPRK ADBBV ADRAZ AENEX AFKRA AFPKN ALIPV ALMA_UNASSIGNED_HOLDINGS AOIJS AZQEC BAWUL BBNVY BCNDV BENPR BHPHI BPHCQ BVXVI CCPQU CITATION DIK DWQXO FYUFA GNUQQ GROUPED_DOAJ GX1 HCIFZ HMCUK HYE IAO IEA IHR INH ISR ITC KQ8 LK8 M1P M2P M48 M7P M~E NQS OK1 PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC PSQYO RHI RNS RPM UKHRP CGR CUY CVF ECM EIF NPM PJZUB PPXIY PQGLB 3V. 7XB 8FK K9. PKEHL PQEST PQUKI PRINS Q9U 7X8 5PM PUEGO |
| ID | FETCH-LOGICAL-c541t-b1632d0fda207c8daff32917a82e92351b147b0327d146b7ea7d1caab2bbd8223 |
| IEDL.DBID | DOA |
| ISSN | 2050-084X |
| IngestDate | Wed Aug 27 01:25:49 EDT 2025 Thu Aug 21 14:31:28 EDT 2025 Fri Jul 11 10:55:12 EDT 2025 Fri Jul 25 12:08:56 EDT 2025 Mon Jul 21 05:50:01 EDT 2025 Tue Jul 01 01:29:30 EDT 2025 Thu Apr 24 22:54:42 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Keywords | Human autophagy Mouse autophagosome LC3 lipidation ER–Golgi intermediate compartment |
| Language | English |
| License | http://creativecommons.org/licenses/by/3.0 This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c541t-b1632d0fda207c8daff32917a82e92351b147b0327d146b7ea7d1caab2bbd8223 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| OpenAccessLink | https://doaj.org/article/57780319853c45529fb4039188c0715f |
| PMID | 23930225 |
| PQID | 1966696192 |
| PQPubID | 2045579 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_57780319853c45529fb4039188c0715f pubmedcentral_primary_oai_pubmedcentral_nih_gov_3736544 proquest_miscellaneous_1419344438 proquest_journals_1966696192 pubmed_primary_23930225 crossref_primary_10_7554_eLife_00947 crossref_citationtrail_10_7554_eLife_00947 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2013-08-06 |
| PublicationDateYYYYMMDD | 2013-08-06 |
| PublicationDate_xml | – month: 08 year: 2013 text: 2013-08-06 day: 06 |
| PublicationDecade | 2010 |
| PublicationPlace | England |
| PublicationPlace_xml | – name: England – name: Cambridge |
| PublicationTitle | eLife |
| PublicationTitleAlternate | Elife |
| PublicationYear | 2013 |
| Publisher | eLife Sciences Publications Ltd eLife Sciences Publications, Ltd |
| Publisher_xml | – name: eLife Sciences Publications Ltd – name: eLife Sciences Publications, Ltd |
| References | Axe (bib3) 2008; 182 Ravikumar (bib58) 2010; 12 Kim (bib30) 2013; 152 Kim (bib31) 2011; 13 Peyroche (bib55) 1999; 3 Wieckowski (bib74) 2009; 4 Zoppino (bib83) 2010; 11 Heitman (bib24) 1991; 253 Sun (bib67) 2008; 105 Young (bib79) 2006; 119 Yamamoto (bib75) 2012; 198 Burman (bib5) 2010; 32 Sou (bib64) 2006; 281 von Kleist (bib70) 2011; 146 Hanada (bib22) 2007; 282 Hayashi-Nishino (bib23) 2009; 11 Yla-Anttila (bib78) 2009; 5 Mizushima (bib45) 1998a; 395 Chijiwa (bib8) 1990; 265 Guo (bib17) 2012; 125 Mari (bib40) 2011; 3 Ridley (bib59) 2001; 114 Mizushima (bib46) 1998b; 273 Zoncu (bib82) 2011; 334 Kuma (bib34) 2004; 432 Moreau (bib48) 2011; 146 Stenmark (bib66) 1999; 112 Hokazono (bib25) 2011; 412 Ward (bib71) 2001; 155 Ichimura (bib26) 2000; 408 de Figueiredo (bib9) 1999; 15 Sou (bib65) 2008; 19 Ge (bib13) 2011; 108 van der Vaart (bib69) 2010; 21 Ohashi (bib53) 2010; 21 Zhong (bib81) 2009; 11 Schindler (bib61) 2009; 106 Mizushima (bib44) 2008; 451 Nair (bib49) 2011; 146 Longatti (bib38) 2012; 197 Hamasaki (bib20) 2013; 495 Bravo-Altamirano (bib4) 2011; 2 Kabeya (bib28) 2000; 19 Oh-oka (bib52) 2008; 283 Gao (bib12) 2010; 6 Tanida (bib68) 2004; 279 Yang (bib76) 2010; 22 Fan (bib10) 2011; 108 Shao (bib63) 2007; 3 Mizushima (bib43) 2010; 22 Aridor (bib2) 2000; 275 Sekito (bib62) 2009; 14 Levine (bib36) 2005; 120 Matsunaga (bib41) 2010; 190 Matsunaga (bib42) 2009; 11 Komatsu (bib33) 2005; 169 Kim (bib29) 2005; 280 Puri (bib56) 2003; 14 Cherra (bib7) 2010; 190 Geng (bib15) 2008; 9 Zhang (bib80) 1999; 10 Yen (bib77) 2010; 188 Klionsky (bib32) 2012; 8 Mizushima (bib47) 2001; 152 Mari (bib39) 2010; 190 Hailey (bib19) 2010; 141 Geng (bib16) 2010; 21 Capitani (bib6) 2009; 583 Rubinsztein (bib60) 2012; 22 Itakura (bib27) 2010; 6 Orsi (bib54) 2012; 23 Guo (bib18) 2013; 2 Ragusa (bib57) 2012; 151 Obara (bib51) 2011; 2011 Wei (bib72) 2008; 30 Noda (bib50) 1998; 273 Ge (bib14) 2008; 7 Hamasaki (bib21) 2003; 28 Liu (bib37) 2010; 53 Appenzeller-Herzog (bib1) 2006; 119 Weidberg (bib73) 2011; 80 Fujita (bib11) 2008; 19 Kundu (bib35) 2008; 112 10813364 - Cell Biol Toxicol. 1999;15(5):311-23 22162728 - F1000 Biol Rep. 2011;3:25 11060023 - EMBO J. 2000 Nov 1;19(21):5720-8 20639694 - Autophagy. 2010 Aug;6(6):764-76 11001944 - J Biol Chem. 2000 Nov 17;275(46):35673-6 20861302 - Mol Biol Cell. 2010 Nov 15;21(22):3998-4008 23332761 - Cell. 2013 Jan 17;152(1-2):290-303 19855179 - Autophagy. 2009 Nov;5(8):1180-5 19898463 - Nat Cell Biol. 2009 Dec;11(12):1433-7 20061800 - Autophagy. 2010 Jan;6(1):126-37 16940348 - J Cell Sci. 2006 Sep 15;119(Pt 18):3888-900 9759731 - Nature. 1998 Sep 24;395(6700):395-8 18321988 - Mol Biol Cell. 2008 May;19(5):2092-100 18768753 - Mol Biol Cell. 2008 Nov;19(11):4762-75 11100732 - Nature. 2000 Nov 23;408(6811):488-92 20065092 - J Cell Biol. 2010 Jan 11;188(1):101-14 19050071 - Proc Natl Acad Sci U S A. 2008 Dec 9;105(49):19211-6 19371383 - Genes Cells. 2009 May;14(5):525-38 15525940 - Nature. 2004 Dec 23;432(7020):1032-6 20056399 - Curr Opin Cell Biol. 2010 Apr;22(2):132-9 22053050 - Science. 2011 Nov 4;334(6056):678-83 21617763 - ACS Med Chem Lett. 2011 Feb 14;2(2):154-159 10564636 - J Cell Sci. 1999 Dec;112 ( Pt 23):4175-83 21518905 - Proc Natl Acad Sci U S A. 2011 May 10;108(19):7769-74 23455425 - Nature. 2013 Mar 21;495(7441):389-93 20478256 - Cell. 2010 May 14;141(4):656-67 20713597 - J Cell Biol. 2010 Aug 23;190(4):511-21 19816421 - Nat Protoc. 2009;4(11):1582-90 15623526 - J Biol Chem. 2005 Mar 4;280(9):7758-68 20444982 - Mol Biol Cell. 2010 Jul 1;21(13):2270-84 11266458 - J Cell Biol. 2001 Feb 19;152(4):657-68 21784249 - Cell. 2011 Jul 22;146(2):290-302 23326640 - Elife. 2013;2:e00160 20444978 - Mol Biol Cell. 2010 Jul 1;21(13):2257-69 20860370 - J Med Chem. 2010 Oct 14;53(19):7146-55 15866887 - J Cell Biol. 2005 May 9;169(3):425-34 20855505 - J Cell Biol. 2010 Sep 20;190(6):1005-22 2156866 - J Biol Chem. 1990 Mar 25;265(9):5267-72 18539900 - Blood. 2008 Aug 15;112(4):1493-502 18544538 - J Biol Chem. 2008 Aug 8;283(32):21847-52 11706049 - J Cell Biol. 2001 Nov 12;155(4):557-70 11739631 - J Cell Sci. 2001 Nov;114(Pt 22):3991-4000 19822759 - Proc Natl Acad Sci U S A. 2009 Oct 20;106(42):17775-80 22240478 - Curr Biol. 2012 Jan 10;22(1):R29-34 21784250 - Cell. 2011 Jul 22;146(2):303-17 20034776 - Curr Opin Cell Biol. 2010 Apr;22(2):124-31 15680321 - Cell. 2005 Jan 28;120(2):159-62 20713600 - J Cell Biol. 2010 Aug 23;190(4):533-9 22613832 - J Cell Biol. 2012 May 28;197(5):659-75 16723730 - J Cell Sci. 2006 Jun 1;119(Pt 11):2173-83 10198630 - Mol Cell. 1999 Mar;3(3):275-85 19270696 - Nat Cell Biol. 2009 Apr;11(4):385-96 22966490 - Autophagy. 2012 Apr;8(4):445-544 21548784 - Annu Rev Biochem. 2011;80:125-56 16963840 - Autophagy. 2007 Jan-Feb;3(1):10-6 9950687 - Mol Biol Cell. 1999 Feb;10(2):435-53 14565973 - Mol Biol Cell. 2003 Dec;14(12):5011-8 20545908 - Traffic. 2010 Sep;11(9):1246-61 17986448 - J Biol Chem. 2007 Dec 28;282(52):37298-302 18704115 - EMBO Rep. 2008 Sep;9(9):859-64 21816279 - Cell. 2011 Aug 5;146(3):471-84 21187433 - Proc Natl Acad Sci U S A. 2011 Jan 11;108(2):551-6 18570871 - Mol Cell. 2008 Jun 20;30(6):678-88 22013444 - Int J Cell Biol. 2011;2011:713435 23219485 - Cell. 2012 Dec 21;151(7):1501-12 21549106 - Clin Chim Acta. 2011 Jul 15;412(15-16):1436-40 9852036 - J Biol Chem. 1998 Dec 18;273(51):33889-92 18305538 - Nature. 2008 Feb 28;451(7182):1069-75 16303767 - J Biol Chem. 2006 Feb 10;281(6):3017-24 21258367 - Nat Cell Biol. 2011 Feb;13(2):132-41 18522832 - Cell Metab. 2008 Jun;7(6):508-19 19854180 - FEBS Lett. 2009 Dec 3;583(23):3863-71 20639872 - Nat Cell Biol. 2010 Aug;12(8):747-57 20740284 - Semin Immunopathol. 2010 Dec;32(4):397-413 19270693 - Nat Cell Biol. 2009 Apr;11(4):468-76 22328508 - J Cell Sci. 2012 Apr 1;125(Pt 7):1706-15 22826123 - J Cell Biol. 2012 Jul 23;198(2):219-33 15187094 - J Biol Chem. 2004 Aug 27;279(35):36268-76 12655150 - Cell Struct Funct. 2003 Feb;28(1):49-54 9461583 - J Biol Chem. 1998 Feb 13;273(7):3963-6 18725538 - J Cell Biol. 2008 Aug 25;182(4):685-701 1715094 - Science. 1991 Aug 23;253(5022):905-9 22456507 - Mol Biol Cell. 2012 May;23(10):1860-73 |
| References_xml | – volume: 151 start-page: 1501 year: 2012 ident: bib57 article-title: Architecture of the Atg17 complex as a scaffold for autophagosome biogenesis publication-title: Cell doi: 10.1016/j.cell.2012.11.028 – volume: 334 start-page: 678 year: 2011 ident: bib82 article-title: mTORC1 senses lysosomal amino acids through an inside-out mechanism that requires the vacuolar H(+)-ATPase publication-title: Science doi: 10.1126/science.1207056 – volume: 273 start-page: 3963 year: 1998 ident: bib50 article-title: Tor, a phosphatidylinositol kinase homologue, controls autophagy in yeast publication-title: J Biol Chem doi: 10.1074/jbc.273.7.3963 – volume: 412 start-page: 1436 year: 2011 ident: bib25 article-title: Enzymatic assay of phosphatidylethanolamine in serum using amine oxidase from Arthrobacter sp publication-title: Clin Chim Acta doi: 10.1016/j.cca.2011.04.023 – volume: 12 start-page: 747 year: 2010 ident: bib58 article-title: Plasma membrane contributes to the formation of pre-autophagosomal structures publication-title: Nat Cell Biol doi: 10.1038/ncb2078 – volume: 28 start-page: 49 year: 2003 ident: bib21 article-title: The early secretory pathway contributes to autophagy in yeast publication-title: Cell Struct Funct doi: 10.1247/csf.28.49 – volume: 6 start-page: 126 year: 2010 ident: bib12 article-title: Processing of autophagic protein LC3 by the 20S proteasome publication-title: Autophagy doi: 10.4161/auto.6.1.10928 – volume: 190 start-page: 1005 year: 2010 ident: bib39 article-title: An Atg9-containing compartment that functions in the early steps of autophagosome biogenesis publication-title: J Cell Biol doi: 10.1083/jcb.200912089 – volume: 395 start-page: 395 year: 1998a ident: bib45 article-title: A protein conjugation system essential for autophagy publication-title: Nature doi: 10.1038/26506 – volume: 80 start-page: 125 year: 2011 ident: bib73 article-title: Biogenesis and cargo selectivity of autophagosomes publication-title: Annu Rev Biochem doi: 10.1146/annurev-biochem-052709-094552 – volume: 15 start-page: 311 year: 1999 ident: bib9 article-title: Clofibrate inhibits membrane trafficking to the Golgi complex and induces its retrograde movement to the endoplasmic reticulum publication-title: Cell Biol Toxicol doi: 10.1023/A:1007667802497 – volume: 22 start-page: 132 year: 2010 ident: bib43 article-title: The role of the Atg1/ULK1 complex in autophagy regulation publication-title: Curr Opin Cell Biol doi: 10.1016/j.ceb.2009.12.004 – volume: 2 start-page: e00160 year: 2013 ident: bib18 article-title: A novel GTP-binding protein-adaptor protein complex responsible for export of Vangl2 from the trans Golgi network publication-title: eLife doi: 10.7554/eLife.00160 – volume: 146 start-page: 290 year: 2011 ident: bib49 article-title: SNARE proteins are required for macroautophagy publication-title: Cell doi: 10.1016/j.cell.2011.06.022 – volume: 13 start-page: 132 year: 2011 ident: bib31 article-title: AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1 publication-title: Nat Cell Biol doi: 10.1038/ncb2152 – volume: 11 start-page: 1433 year: 2009 ident: bib23 article-title: A subdomain of the endoplasmic reticulum forms a cradle for autophagosome formation publication-title: Nat Cell Biol doi: 10.1038/ncb1991 – volume: 112 start-page: 4175 issue: Pt 23 year: 1999 ident: bib66 article-title: FYVE-finger proteins–effectors of an inositol lipid publication-title: J Cell Sci doi: 10.1242/jcs.112.23.4175 – volume: 273 start-page: 33889 year: 1998b ident: bib46 article-title: A new protein conjugation system in human. The counterpart of the yeast Apg12p conjugation system essential for autophagy publication-title: J Biol Chem doi: 10.1074/jbc.273.51.33889 – volume: 11 start-page: 385 year: 2009 ident: bib42 article-title: Two Beclin 1-binding proteins, Atg14L and Rubicon, reciprocally regulate autophagy at different stages publication-title: Nat Cell Biol doi: 10.1038/ncb1846 – volume: 152 start-page: 657 year: 2001 ident: bib47 article-title: Dissection of autophagosome formation using Apg5-deficient mouse embryonic stem cells publication-title: J Cell Biol doi: 10.1083/jcb.152.4.657 – volume: 125 start-page: 1706 year: 2012 ident: bib17 article-title: AP1 is essential for generation of autophagosomes from the trans-Golgi network publication-title: J Cell Sci doi: 10.1242/jcs.093203 – volume: 14 start-page: 5011 year: 2003 ident: bib56 article-title: Capacity of the golgi apparatus for biogenesis from the endoplasmic reticulum publication-title: Mol Biol Cell doi: 10.1091/mbc.E03-06-0437 – volume: 21 start-page: 2270 year: 2010 ident: bib69 article-title: Exit from the Golgi is required for the expansion of the autophagosomal phagophore in yeast Saccharomyces cerevisiae publication-title: Mol Biol Cell doi: 10.1091/mbc.E09-04-0345 – volume: 14 start-page: 525 year: 2009 ident: bib62 article-title: Atg17 recruits Atg9 to organize the pre-autophagosomal structure publication-title: Genes Cells doi: 10.1111/j.1365-2443.2009.01299.x – volume: 8 start-page: 445 year: 2012 ident: bib32 article-title: Guidelines for the use and interpretation of assays for monitoring autophagy publication-title: Autophagy doi: 10.4161/auto.19496 – volume: 2011 start-page: 713435 year: 2011 ident: bib51 article-title: Atg14: a key player in orchestrating autophagy publication-title: Int J Cell Biol doi: 10.1155/2011/713435 – volume: 5 start-page: 1180 year: 2009 ident: bib78 article-title: 3D tomography reveals connections between the phagophore and endoplasmic reticulum publication-title: Autophagy doi: 10.4161/auto.5.8.10274 – volume: 190 start-page: 511 year: 2010 ident: bib41 article-title: Autophagy requires endoplasmic reticulum targeting of the PI3-kinase complex via Atg14L publication-title: J Cell Biol doi: 10.1083/jcb.200911141 – volume: 32 start-page: 397 year: 2010 ident: bib5 article-title: Autophagosome formation in mammalian cells publication-title: Semin Immunopathol doi: 10.1007/s00281-010-0222-z – volume: 141 start-page: 656 year: 2010 ident: bib19 article-title: Mitochondria supply membranes for autophagosome biogenesis during starvation publication-title: Cell doi: 10.1016/j.cell.2010.04.009 – volume: 282 start-page: 37298 year: 2007 ident: bib22 article-title: The Atg12–Atg5 conjugate has a novel E3-like activity for protein lipidation in autophagy publication-title: J Biol Chem doi: 10.1074/jbc.C700195200 – volume: 188 start-page: 101 year: 2010 ident: bib77 article-title: The conserved oligomeric Golgi complex is involved in double-membrane vesicle formation during autophagy publication-title: J Cell Biol doi: 10.1083/jcb.200904075 – volume: 182 start-page: 685 year: 2008 ident: bib3 article-title: Autophagosome formation from membrane compartments enriched in phosphatidylinositol 3-phosphate and dynamically connected to the endoplasmic reticulum publication-title: J Cell Biol doi: 10.1083/jcb.200803137 – volume: 108 start-page: 551 year: 2011 ident: bib13 article-title: Flotillins play an essential role in Niemann-Pick C1-like 1-mediated cholesterol uptake publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.1014434108 – volume: 408 start-page: 488 year: 2000 ident: bib26 article-title: A ubiquitin-like system mediates protein lipidation publication-title: Nature doi: 10.1038/35044114 – volume: 7 start-page: 508 year: 2008 ident: bib14 article-title: The cholesterol absorption inhibitor ezetimibe acts by blocking the sterol-induced internalization of NPC1L1 publication-title: Cell Metab doi: 10.1016/j.cmet.2008.04.001 – volume: 53 start-page: 7146 year: 2010 ident: bib37 article-title: Discovery of 1-(4-(4-propionylpiperazin-1-yl)-3-(trifluoromethyl)phenyl)-9-(quinolin-3-yl)benz o[h][1,6]naphthyridin-2(1H)-one as a highly potent, selective mammalian target of rapamycin (mTOR) inhibitor for the treatment of cancer publication-title: J Med Chem doi: 10.1021/jm101144f – volume: 2 start-page: 154 year: 2011 ident: bib4 article-title: Synthesis and structure-activity relationships of benzothienothiazepinone inhibitors of protein kinase D publication-title: ACS Med Chem Lett doi: 10.1021/ml100230n – volume: 21 start-page: 2257 year: 2010 ident: bib16 article-title: Post-Golgi Sec proteins are required for autophagy in Saccharomyces cerevisiae publication-title: Mol Biol Cell doi: 10.1091/mbc.E09-11-0969 – volume: 120 start-page: 159 year: 2005 ident: bib36 article-title: Eating oneself and uninvited guests: autophagy-related pathways in cellular defense publication-title: Cell doi: 10.1016/j.cell.2005.01.005 – volume: 146 start-page: 471 year: 2011 ident: bib70 article-title: Role of the clathrin terminal domain in regulating coated pit dynamics revealed by small molecule inhibition publication-title: Cell doi: 10.1016/j.cell.2011.06.025 – volume: 432 start-page: 1032 year: 2004 ident: bib34 article-title: The role of autophagy during the early neonatal starvation period publication-title: Nature doi: 10.1038/nature03029 – volume: 119 start-page: 3888 year: 2006 ident: bib79 article-title: Starvation and ULK1-dependent cycling of mammalian Atg9 between the TGN and endosomes publication-title: J Cell Sci doi: 10.1242/jcs.03172 – volume: 9 start-page: 859 year: 2008 ident: bib15 article-title: The Atg8 and Atg12 ubiquitin-like conjugation systems in macroautophagy. ‘Protein modifications: beyond the usual suspects’ review series publication-title: EMBO Rep doi: 10.1038/embor.2008.163 – volume: 152 start-page: 290 year: 2013 ident: bib30 article-title: Differential regulation of distinct Vps34 complexes by AMPK in nutrient stress and autophagy publication-title: Cell doi: 10.1016/j.cell.2012.12.016 – volume: 105 start-page: 19211 year: 2008 ident: bib67 article-title: Identification of Barkor as a mammalian autophagy-specific factor for Beclin 1 and class III phosphatidylinositol 3-kinase publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0810452105 – volume: 253 start-page: 905 year: 1991 ident: bib24 article-title: Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast publication-title: Science doi: 10.1126/science.1715094 – volume: 11 start-page: 1246 year: 2010 ident: bib83 article-title: Autophagosome formation depends on the small GTPase Rab1 and functional ER exit sites publication-title: Traffic doi: 10.1111/j.1600-0854.2010.01086.x – volume: 22 start-page: R29 year: 2012 ident: bib60 article-title: Mechanisms of autophagosome biogenesis publication-title: Curr Biol doi: 10.1016/j.cub.2011.11.034 – volume: 10 start-page: 435 year: 1999 ident: bib80 article-title: Morphological and functional association of Sec22b/ERS-24 with the pre-Golgi intermediate compartment publication-title: Mol Biol Cell doi: 10.1091/mbc.10.2.435 – volume: 19 start-page: 4762 year: 2008 ident: bib65 article-title: The Atg8 conjugation system is indispensable for proper development of autophagic isolation membranes in mice publication-title: Mol Biol Cell doi: 10.1091/mbc.E08-03-0309 – volume: 6 start-page: 764 year: 2010 ident: bib27 article-title: Characterization of autophagosome formation site by a hierarchical analysis of mammalian Atg proteins publication-title: Autophagy doi: 10.4161/auto.6.6.12709 – volume: 30 start-page: 678 year: 2008 ident: bib72 article-title: JNK1-mediated phosphorylation of Bcl-2 regulates starvation-induced autophagy publication-title: Mol Cell doi: 10.1016/j.molcel.2008.06.001 – volume: 112 start-page: 1493 year: 2008 ident: bib35 article-title: Ulk1 plays a critical role in the autophagic clearance of mitochondria and ribosomes during reticulocyte maturation publication-title: Blood doi: 10.1182/blood-2008-02-137398 – volume: 265 start-page: 5267 year: 1990 ident: bib8 article-title: Inhibition of forskolin-induced neurite outgrowth and protein phosphorylation by a newly synthesized selective inhibitor of cyclic AMP-dependent protein kinase, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), of PC12D pheochromocytoma cells publication-title: J Biol Chem doi: 10.1016/S0021-9258(19)34116-X – volume: 155 start-page: 557 year: 2001 ident: bib71 article-title: Maintenance of Golgi structure and function depends on the integrity of ER export publication-title: J Cell Biol doi: 10.1083/jcb.200107045 – volume: 11 start-page: 468 year: 2009 ident: bib81 article-title: Distinct regulation of autophagic activity by Atg14L and Rubicon associated with Beclin 1-phosphatidylinositol-3-kinase complex publication-title: Nat Cell Biol doi: 10.1038/ncb1854 – volume: 119 start-page: 2173 year: 2006 ident: bib1 article-title: The ER-Golgi intermediate compartment (ERGIC): in search of its identity and function publication-title: J Cell Sci doi: 10.1242/jcs.03019 – volume: 146 start-page: 303 year: 2011 ident: bib48 article-title: Autophagosome precursor maturation requires homotypic fusion publication-title: Cell doi: 10.1016/j.cell.2011.06.023 – volume: 106 start-page: 17775 year: 2009 ident: bib61 article-title: In vitro reconstitution of ER-stress induced ATF6 transport in COPII vesicles publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0910342106 – volume: 197 start-page: 659 year: 2012 ident: bib38 article-title: TBC1D14 regulates autophagosome formation via Rab11- and ULK1-positive recycling endosomes publication-title: J Cell Biol doi: 10.1083/jcb.201111079 – volume: 451 start-page: 1069 year: 2008 ident: bib44 article-title: Autophagy fights disease through cellular self-digestion publication-title: Nature doi: 10.1038/nature06639 – volume: 21 start-page: 3998 year: 2010 ident: bib53 article-title: Membrane delivery to the yeast autophagosome from the Golgi-endosomal system publication-title: Mol Biol Cell doi: 10.1091/mbc.E10-05-0457 – volume: 3 start-page: 275 year: 1999 ident: bib55 article-title: Brefeldin A acts to stabilize an abortive ARF-GDP-Sec7 domain protein complex: involvement of specific residues of the Sec7 domain publication-title: Mol Cell doi: 10.1016/S1097-2765(00)80455-4 – volume: 19 start-page: 5720 year: 2000 ident: bib28 article-title: LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing publication-title: EMBO J doi: 10.1093/emboj/19.21.5720 – volume: 583 start-page: 3863 year: 2009 ident: bib6 article-title: The KDEL receptor: new functions for an old protein publication-title: FEBS Lett doi: 10.1016/j.febslet.2009.10.053 – volume: 283 start-page: 21847 year: 2008 ident: bib52 article-title: Physiological pH and acidic phospholipids contribute to substrate specificity in lipidation of Atg8 publication-title: J Biol Chem doi: 10.1074/jbc.M801836200 – volume: 279 start-page: 36268 year: 2004 ident: bib68 article-title: HsAtg4B/HsApg4B/autophagin-1 cleaves the carboxyl termini of three human Atg8 homologues and delipidates microtubule-associated protein light chain 3- and GABAA receptor-associated protein-phospholipid conjugates publication-title: J Biol Chem doi: 10.1074/jbc.M401461200 – volume: 281 start-page: 3017 year: 2006 ident: bib64 article-title: Phosphatidylserine in addition to phosphatidylethanolamine is an in vitro target of the mammalian Atg8 modifiers, LC3, GABARAP, and GATE-16 publication-title: J Biol Chem doi: 10.1074/jbc.M505888200 – volume: 495 start-page: 389 year: 2013 ident: bib20 article-title: Autophagosomes form at ER-mitochondria contact sites publication-title: Nature doi: 10.1038/nature11910 – volume: 198 start-page: 219 year: 2012 ident: bib75 article-title: Atg9 vesicles are an important membrane source during early steps of autophagosome formation publication-title: J Cell Biol doi: 10.1083/jcb.201202061 – volume: 23 start-page: 1860 year: 2012 ident: bib54 article-title: Dynamic and transient interactions of Atg9 with autophagosomes, but not membrane integration, are required for autophagy publication-title: Mol Biol Cell doi: 10.1091/mbc.E11-09-0746 – volume: 4 start-page: 1582 year: 2009 ident: bib74 article-title: Isolation of mitochondria-associated membranes and mitochondria from animal tissues and cells publication-title: Nat Protoc doi: 10.1038/nprot.2009.151 – volume: 19 start-page: 2092 year: 2008 ident: bib11 article-title: The Atg16L complex specifies the site of LC3 lipidation for membrane biogenesis in autophagy publication-title: Mol Biol Cell doi: 10.1091/mbc.E07-12-1257 – volume: 190 start-page: 533 year: 2010 ident: bib7 article-title: Regulation of the autophagy protein LC3 by phosphorylation publication-title: J Cell Biol doi: 10.1083/jcb.201002108 – volume: 114 start-page: 3991 year: 2001 ident: bib59 article-title: FENS-1 and DFCP1 are FYVE domain-containing proteins with distinct functions in the endosomal and Golgi compartments publication-title: J Cell Sci doi: 10.1242/jcs.114.22.3991 – volume: 169 start-page: 425 year: 2005 ident: bib33 article-title: Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice publication-title: J Cell Biol doi: 10.1083/jcb.200412022 – volume: 3 start-page: 10 year: 2007 ident: bib63 article-title: Stimulation of ATG12–ATG5 conjugation by ribonucleic acid publication-title: Autophagy doi: 10.4161/auto.3270 – volume: 108 start-page: 7769 year: 2011 ident: bib10 article-title: Autophagosome targeting and membrane curvature sensing by Barkor/Atg14(L) publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.1016472108 – volume: 22 start-page: 124 year: 2010 ident: bib76 article-title: Mammalian autophagy: core molecular machinery and signaling regulation publication-title: Curr Opin Cell Biol doi: 10.1016/j.ceb.2009.11.014 – volume: 275 start-page: 35673 year: 2000 ident: bib2 article-title: Kinase signaling initiates coat complex II (COPII) recruitment and export from the mammalian endoplasmic reticulum publication-title: J Biol Chem doi: 10.1074/jbc.C000449200 – volume: 280 start-page: 7758 year: 2005 ident: bib29 article-title: Uncoupled packaging of amyloid precursor protein and presenilin 1 into coat protein complex II vesicles publication-title: J Biol Chem doi: 10.1074/jbc.M411091200 – volume: 3 start-page: 25 year: 2011 ident: bib40 article-title: The puzzling origin of the autophagosomal membrane publication-title: F1000 Biol Rep doi: 10.3410/B3-25 – reference: 21187433 - Proc Natl Acad Sci U S A. 2011 Jan 11;108(2):551-6 – reference: 16963840 - Autophagy. 2007 Jan-Feb;3(1):10-6 – reference: 20861302 - Mol Biol Cell. 2010 Nov 15;21(22):3998-4008 – reference: 20065092 - J Cell Biol. 2010 Jan 11;188(1):101-14 – reference: 15187094 - J Biol Chem. 2004 Aug 27;279(35):36268-76 – reference: 18570871 - Mol Cell. 2008 Jun 20;30(6):678-88 – reference: 11266458 - J Cell Biol. 2001 Feb 19;152(4):657-68 – reference: 21617763 - ACS Med Chem Lett. 2011 Feb 14;2(2):154-159 – reference: 19898463 - Nat Cell Biol. 2009 Dec;11(12):1433-7 – reference: 20056399 - Curr Opin Cell Biol. 2010 Apr;22(2):132-9 – reference: 12655150 - Cell Struct Funct. 2003 Feb;28(1):49-54 – reference: 14565973 - Mol Biol Cell. 2003 Dec;14(12):5011-8 – reference: 11001944 - J Biol Chem. 2000 Nov 17;275(46):35673-6 – reference: 22613832 - J Cell Biol. 2012 May 28;197(5):659-75 – reference: 19855179 - Autophagy. 2009 Nov;5(8):1180-5 – reference: 20545908 - Traffic. 2010 Sep;11(9):1246-61 – reference: 16723730 - J Cell Sci. 2006 Jun 1;119(Pt 11):2173-83 – reference: 19371383 - Genes Cells. 2009 May;14(5):525-38 – reference: 19816421 - Nat Protoc. 2009;4(11):1582-90 – reference: 22966490 - Autophagy. 2012 Apr;8(4):445-544 – reference: 23326640 - Elife. 2013;2:e00160 – reference: 16940348 - J Cell Sci. 2006 Sep 15;119(Pt 18):3888-900 – reference: 23332761 - Cell. 2013 Jan 17;152(1-2):290-303 – reference: 15525940 - Nature. 2004 Dec 23;432(7020):1032-6 – reference: 10198630 - Mol Cell. 1999 Mar;3(3):275-85 – reference: 21816279 - Cell. 2011 Aug 5;146(3):471-84 – reference: 21258367 - Nat Cell Biol. 2011 Feb;13(2):132-41 – reference: 20478256 - Cell. 2010 May 14;141(4):656-67 – reference: 1715094 - Science. 1991 Aug 23;253(5022):905-9 – reference: 20034776 - Curr Opin Cell Biol. 2010 Apr;22(2):124-31 – reference: 21784249 - Cell. 2011 Jul 22;146(2):290-302 – reference: 21549106 - Clin Chim Acta. 2011 Jul 15;412(15-16):1436-40 – reference: 18321988 - Mol Biol Cell. 2008 May;19(5):2092-100 – reference: 18522832 - Cell Metab. 2008 Jun;7(6):508-19 – reference: 17986448 - J Biol Chem. 2007 Dec 28;282(52):37298-302 – reference: 10813364 - Cell Biol Toxicol. 1999;15(5):311-23 – reference: 22240478 - Curr Biol. 2012 Jan 10;22(1):R29-34 – reference: 18704115 - EMBO Rep. 2008 Sep;9(9):859-64 – reference: 9950687 - Mol Biol Cell. 1999 Feb;10(2):435-53 – reference: 11100732 - Nature. 2000 Nov 23;408(6811):488-92 – reference: 16303767 - J Biol Chem. 2006 Feb 10;281(6):3017-24 – reference: 20639694 - Autophagy. 2010 Aug;6(6):764-76 – reference: 19822759 - Proc Natl Acad Sci U S A. 2009 Oct 20;106(42):17775-80 – reference: 23219485 - Cell. 2012 Dec 21;151(7):1501-12 – reference: 20444978 - Mol Biol Cell. 2010 Jul 1;21(13):2257-69 – reference: 20639872 - Nat Cell Biol. 2010 Aug;12(8):747-57 – reference: 20061800 - Autophagy. 2010 Jan;6(1):126-37 – reference: 18539900 - Blood. 2008 Aug 15;112(4):1493-502 – reference: 9759731 - Nature. 1998 Sep 24;395(6700):395-8 – reference: 11706049 - J Cell Biol. 2001 Nov 12;155(4):557-70 – reference: 22162728 - F1000 Biol Rep. 2011;3:25 – reference: 22053050 - Science. 2011 Nov 4;334(6056):678-83 – reference: 20713600 - J Cell Biol. 2010 Aug 23;190(4):533-9 – reference: 19270693 - Nat Cell Biol. 2009 Apr;11(4):468-76 – reference: 21784250 - Cell. 2011 Jul 22;146(2):303-17 – reference: 21548784 - Annu Rev Biochem. 2011;80:125-56 – reference: 18768753 - Mol Biol Cell. 2008 Nov;19(11):4762-75 – reference: 15680321 - Cell. 2005 Jan 28;120(2):159-62 – reference: 20855505 - J Cell Biol. 2010 Sep 20;190(6):1005-22 – reference: 15623526 - J Biol Chem. 2005 Mar 4;280(9):7758-68 – reference: 9461583 - J Biol Chem. 1998 Feb 13;273(7):3963-6 – reference: 18305538 - Nature. 2008 Feb 28;451(7182):1069-75 – reference: 21518905 - Proc Natl Acad Sci U S A. 2011 May 10;108(19):7769-74 – reference: 15866887 - J Cell Biol. 2005 May 9;169(3):425-34 – reference: 22826123 - J Cell Biol. 2012 Jul 23;198(2):219-33 – reference: 11739631 - J Cell Sci. 2001 Nov;114(Pt 22):3991-4000 – reference: 20740284 - Semin Immunopathol. 2010 Dec;32(4):397-413 – reference: 22013444 - Int J Cell Biol. 2011;2011:713435 – reference: 9852036 - J Biol Chem. 1998 Dec 18;273(51):33889-92 – reference: 2156866 - J Biol Chem. 1990 Mar 25;265(9):5267-72 – reference: 22456507 - Mol Biol Cell. 2012 May;23(10):1860-73 – reference: 11060023 - EMBO J. 2000 Nov 1;19(21):5720-8 – reference: 19854180 - FEBS Lett. 2009 Dec 3;583(23):3863-71 – reference: 20860370 - J Med Chem. 2010 Oct 14;53(19):7146-55 – reference: 22328508 - J Cell Sci. 2012 Apr 1;125(Pt 7):1706-15 – reference: 19050071 - Proc Natl Acad Sci U S A. 2008 Dec 9;105(49):19211-6 – reference: 19270696 - Nat Cell Biol. 2009 Apr;11(4):385-96 – reference: 18725538 - J Cell Biol. 2008 Aug 25;182(4):685-701 – reference: 18544538 - J Biol Chem. 2008 Aug 8;283(32):21847-52 – reference: 23455425 - Nature. 2013 Mar 21;495(7441):389-93 – reference: 10564636 - J Cell Sci. 1999 Dec;112 ( Pt 23):4175-83 – reference: 20713597 - J Cell Biol. 2010 Aug 23;190(4):511-21 – reference: 20444982 - Mol Biol Cell. 2010 Jul 1;21(13):2270-84 |
| SSID | ssj0000748819 |
| Score | 2.5107355 |
| Snippet | Autophagy is a catabolic process for bulk degradation of cytosolic materials mediated by double-membraned autophagosomes. The membrane determinant to initiate... |
| SourceID | doaj pubmedcentral proquest pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | e00947 |
| SubjectTerms | autophagosome Autophagy Biochemistry Biosynthesis Cell Biology Endoplasmic reticulum Endoplasmic Reticulum - metabolism ER–Golgi intermediate compartment Fibroblasts Golgi apparatus Golgi Apparatus - metabolism Kinases LC3 lipidation Lipid Metabolism Membranes Phagocytosis Phagosomes Phagosomes - metabolism Physiology Proteins |
| SummonAdditionalLinks | – databaseName: Health & Medical Collection dbid: 7X7 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3NbtQwELagCIlLxT-BgozUE1Jo4p_Ye6qgaqlQ4YCotLfIju0l0m6y3exKcOMdeEOepDNONrCoIqco9sHKjD3fjGe-IeRwYnKtDQe3xBUmFUKp1ATLU8cLy1lwYOSxOPnT5-L8UnycyukQcOuGtMrtmRgPatdWGCM_Ak0pignC_ePlVYpdo_B2dWihcZvcQeoyTOlSUzXGWMA8arB4fVmeAsN55C_q4N9iOp3aMUSRr_8mkPlvruRfxufsPtkfUCN914v5Abnlm4fkbt9H8scj8h2ETU-__P7560M7n9UUOSBWsSZk7WmfZR6TyWndUUNh29KFX4Cb3HjaB-8pQFcKUJBenHA6r5d132mJggosaRuo2SD_gJm1Xbvw1NbtDI_IuntMLs9Ov56cp0NLhbSSIl-nFuAXc1lwhmWq0s6EwBl4bEYzD1BP5jYXymacKQdHqFXewEtljGXWOsAS_AnZa9rGPyM0Z4Xx4F0WPmQiaGbgCZlWzGBU0dmEvNn-37Ia-Max7cW8BL8DhVFGYZRRGAk5HCcve5qNm6e9R0GNU5AbO35oV7Ny2GqlVEpjbRYAkUpIySbBCuTB17oCPCVDQg62Yi6HDduVf9QrIa_HYdhqeH8C4mg3MEcA2hVCcJ2Qp71WjCtBJjmAQzIhakdfdpa6O9LU3yKdN1e8kEI8__-yXpB7LHbi0GlWHJC99WrjXwIeWttXUemvAXVuDic priority: 102 providerName: ProQuest – databaseName: Scholars Portal Journals: Open Access dbid: M48 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3NbtQwEB6VIiQuiPIbaJGRekLKktiO7T1VULVUqOWAWKm3yI7tJdJusuyP1N54B96QJ-nYya7Yao_kFMWO5HhmPN84428Ajoc6V0ozDEus0CnnUqbaG5ZaJgyj3qKTD4eTr76JixH_el1c78G6GGc_gYudoV2oJzWaTwY3v25P0OARvw4kesOP7rL2bhBy5OQDeIguSQYLvepxflySJeppPuzO591_Z8sjReL-XWjzftLkP17o_Ck86eEj-dTJ-wD2XPMMHnUFJW-fww1KnZx9__v7z5d2Mq5JIIOYx8MhS0e6dPOYVU7qBdEE7ZdM3RTj5caRbhefIIYliAnJ5Skjk3pWdyWXCOrCjLSe6FUgItDjdtFOHTF1Ow5rZb14AaPzsx-nF2lfWyGtCp4vU4M4jNrMW00zWSmrvWcUQzetqEPMV-Qm59JkjEqLa6mRTuNNpbWhxlgEFewl7Ddt414DyanQDsNM4XzGvaIaL58pSXXYXrQmgQ_r-S2rnng81L-YlBiABGGUURhlFEYCx5vOs45vY3e3z0FQmy6BJDs-aOfjsre5spBShUNaiEgqXhR06A0PhPhKVQisCp_A4VrM5VrxSlyRhBiGsDKB95tmtLnwIwXF0a6wD0fYyzlnKoFXnVZsRhIo5RAXFQnILX3ZGup2S1P_jLzeTDJRcP7mf3zbW3hMY-EOlWbiEPaX85U7Qvi0NO-iadwBbwkcUQ priority: 102 providerName: Scholars Portal |
| Title | The ER–Golgi intermediate compartment is a key membrane source for the LC3 lipidation step of autophagosome biogenesis |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/23930225 https://www.proquest.com/docview/1966696192 https://www.proquest.com/docview/1419344438 https://pubmed.ncbi.nlm.nih.gov/PMC3736544 https://doaj.org/article/57780319853c45529fb4039188c0715f |
| Volume | 2 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3NatwwEB7alEIvJf13mywq5FRwa0uypT0mYZNQklBCA3szkiVtDbv2kt2F9tZ36Bv2STKSnGW3BHqJD8ZYOsia0cw38ugbgIOhyqVUDMMSU6qUcyFS5TRLDSs1o86gk_eHky8uy7Nr_nVcjDdKffmcsEgPHCcOA3Yh_UkbdCs1Lwo6dJp7VnMpa_SOhfPWF33eRjAVbLBAxcyH8UCeQJf5xZ43zn72iXRiywUFpv774OW_WZIbbudkF573eJEcxnG-gEe2fQlPYwXJX6_gJ4qZjK7-_v5z2k0nDfHsDzfhNMjSkphfHtLISbMgiuCCJTM7wwC5tSRu2xMErQRBIDk_ZmTazJtYY4mg8Oekc0StPPOAmnSLbmaJbrqJN47N4jVcn4y-H5-lfTGFtC54vkw1Ai9qMmcUzUQtjXKOUYzVlKQWQV6R65wLnTEqDBpPLazCh1opTbU2iCLYG9hpu9a-A5LTUlmMK0vrMu4kVXi5TAqq_H6i0Ql8upvfqu6Zxn3Bi2mFEYcXRhWEUQVhJHCw7jyPBBv3dzvyglp38azY4QXqStXrSvU_XUlg707MVb9UFxWaoLIc-jgygY_rZlxk_s8JiqNbYR-OOJdzzmQCb6NWrEfiOeQQCBUJiC192Rrqdkvb_AhE3kywsuD8_UN82wd4RkOlDplm5R7sLG9Wdh_x0lIP4LEYiwE8ORpdfrsahIWC9wsubwF0qBd_ |
| linkProvider | Directory of Open Access Journals |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1bb9MwFD4anRC8IO4EBhhpvCCFJbYTuw8IsdHRsa5C0ybtLbMTu0Rqk9KLYG_8B_4HP4pfwnGSBoom3panKLYiy-f2HftcALa7KpRSMXRLslj5nAvhK6uZn7FYM2ozNPIuOfloGPdP-cez6GwDfq5yYVxY5UonVoo6K1N3Rr6DnBLHXQf3306_-K5rlLtdXbXQqNni0Fx8RZdt_ubgPdL3JaX7vZO9vt90FfDTiIcLXyMCoVlgM0UDkcpMWcsoOi1KUoNoJwp1yIUOGBUZahEtjMKXVClNtc7QnDL87zXY5AxdmQ5s7vaGn47bUx00yBJtbJ0IKNBU75hBbs1rF8An1kxf1SHgMlj7b3TmX-Zu_zbcanAqeVcz1h3YMMVduF53rry4B9-QvUjv-Nf3Hx_K8SgnrurErMpCWRhSx7VX4esknxNFUFGQiZmgY14YUl8XEATLBMEnGewxMs6ned3biSDTTUlpiVq6igdqVM7LiSE6L0dOKefz-3B6Jdv9ADpFWZhHQEIaK4P-bGxswK2kCh8bSEGVO8fMtAevVvubpE2Fc9doY5ygp-OIkVTESCpieLDdTp7WhT0un7brCNVOcdW4qw_lbJQ0wp1EQkiXDYbQJ-VRRLtWc1d5X8oUEVxkPdhakTlpVMQ8-cPQHrxoh1G43Y0NkqNc4hyO-JpzzqQHD2uuaFfiatchAIs8EGv8srbU9ZEi_1wVEGeCxRHnj_-_rOdwo39yNEgGB8PDJ3CTVn1ApB_EW9BZzJbmKaKxhX7WiACB86uWut_34Uyc |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB6VIhCXijcpBYxULkhhE9uJvQeEoO3S0qVCiEp7S-3EXiLtJss-BL3xH_g3_Bx-CeO8YFHFrTlFySiyMq9v7HkA7PZVKKViGJZksfI5F8JXVjM_Y7Fm1Gbo5F1x8vuT-PCUvxtFow342dbCuLTK1iZWhjorU7dH3kNJieO-g_s926RFfNgfvJp98d0EKXfS2o7TqEXk2Jx_xfBt8fJoH3n9jNLBwae9Q7-ZMOCnEQ-XvkY0QrPAZooGIpWZspZRDGCUpAaRTxTqkAsdMCoytChaGIU3qVKaap2ha2X43StwVSCl0zExEt3-Drpmid62LgkU6LR7Zphb88Kl8ok1J1jNCrgI4P6bp_mX4xvchK0GsZLXtYjdgg1T3IZr9QzL8zvwDQWNHHz89f3H23IyzonrPzGv6lGWhtQZ7lUiO8kXRBE0GWRqphiiF4bUBwcEYTNBGEqGe4xM8lleT3kiKH4zUlqiVq73gRqXi3JqiM7LsTPP-eIunF7Kz74Hm0VZmAdAQhorg5FtbGzAraQKLxtIQZXb0cy0B8_b_5ukTa9zN3JjkmDM45iRVMxIKmZ4sNsRz-oWHxeTvXGM6khcX-7qQTkfJ42aJ5EQ0tWFIQhKeRTRvtXc9eCXMkUsF1kPdlo2J42xWCR_RNuDp91rVHN3doPsKFdIwxFpc86Z9OB-LRXdSlwXO4RikQdiTV7Wlrr-psg_V63EmWBxxPn2_5f1BK6jriXDo5Pjh3CDVgNBpB_EO7C5nK_MI4RlS_24kn8CZ5etcL8Bh3FPbA |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=The+ER%E2%80%93Golgi+intermediate+compartment+is+a+key+membrane+source+for+the+LC3+lipidation+step+of+autophagosome+biogenesis&rft.jtitle=eLife&rft.au=Liang+Ge&rft.au=David+Melville&rft.au=Min+Zhang&rft.au=Randy+Schekman&rft.date=2013-08-06&rft.pub=eLife+Sciences+Publications+Ltd&rft.eissn=2050-084X&rft.volume=2&rft_id=info:doi/10.7554%2FeLife.00947&rft.externalDBID=DOA&rft.externalDocID=oai_doaj_org_article_57780319853c45529fb4039188c0715f |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2050-084X&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2050-084X&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2050-084X&client=summon |