Inhibition of lysosome degradation on autophagosome formation and responses to GMI, an immunomodulatory protein from Ganoderma microsporum

BACKGROUND AND PURPOSE Autophagic cell death is considered a self‐destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. T...

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Published inBritish journal of pharmacology Vol. 167; no. 6; pp. 1287 - 1300
Main Authors Hsin, I‐Lun, Sheu, Gwo‐Tarng, Jan, Ming‐Shiou, Sun, Hai‐Lun, Wu, Tzu‐Chin, Chiu, Ling‐Yen, Lue, Ko‐Huang, Ko, Jiunn‐Liang
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.11.2012
Nature Publishing Group
Subjects
Apoptosis
ATP6V0A1
autophagic cell death
autophagic flux
autophagy
Autophagy - drug effects
Biological and medical sciences
Cell Line, Tumor
Chloroquine - pharmacology
Fungal Proteins - pharmacology
Ganoderma
Gene Silencing
GMI
Humans
Immunologic Factors - pharmacology
immunomodulatory protein
Kinases
Lung cancer
lysosome
Lysosomes - drug effects
Macrolides - pharmacology
Medical sciences
Microsporum
mTOR
Phagosomes - drug effects
Pharmacology. Drug treatments
PKB
Proto-Oncogene Proteins c-akt - metabolism
Research Papers
TOR Serine-Threonine Kinases - metabolism
Vacuolar Proton-Translocating ATPases - genetics
V‐ATPases
autophagic flux
GMI
autophagic cell death
autophagy
Enzyme
PKB
Adenosinetriphosphatase
Lysosome
immunomodulatory protein
Microsporum
Basidiomycota
Fungi
Immunomodulator
Cell death
V-ATPases
Mammalian target of rapamycin
mTOR
Hydrolases
Fungi Imperfecti
Ganoderma
ATP6V0A1
Online AccessGet full text
ISSN0007-1188
1476-5381
1476-5381
DOI10.1111/j.1476-5381.2012.02073.x

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Abstract BACKGROUND AND PURPOSE Autophagic cell death is considered a self‐destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI‐mediated cell death. EXPERIMENTAL APPROACH Western blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI‐mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro. KEY RESULTS Lysosome inhibitors bafilomycin‐A1 and chloroquine increased GMI‐mediated autophagic cell death. GMI and bafilomycin‐A1 co‐treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H+‐ATPases (V‐ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI‐mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI‐treated CaLu‐1/GFP‐LC3 lung cancer cells. CONCLUSION AND IMPLICATIONS We demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome‐lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.
AbstractList Autophagic cell death is considered a self-destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI-mediated cell death.BACKGROUND AND PURPOSEAutophagic cell death is considered a self-destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI-mediated cell death.Western blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI-mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro.EXPERIMENTAL APPROACHWestern blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI-mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro.Lysosome inhibitors bafilomycin-A1 and chloroquine increased GMI-mediated autophagic cell death. GMI and bafilomycin-A1 co-treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H(+)-ATPases (V-ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI-mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI-treated CaLu-1/GFP-LC3 lung cancer cells.KEY RESULTSLysosome inhibitors bafilomycin-A1 and chloroquine increased GMI-mediated autophagic cell death. GMI and bafilomycin-A1 co-treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H(+)-ATPases (V-ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI-mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI-treated CaLu-1/GFP-LC3 lung cancer cells.We demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome-lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.CONCLUSION AND IMPLICATIONSWe demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome-lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.
Autophagic cell death is considered a self-destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI-mediated cell death. Western blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI-mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro. Lysosome inhibitors bafilomycin-A1 and chloroquine increased GMI-mediated autophagic cell death. GMI and bafilomycin-A1 co-treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H(+)-ATPases (V-ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI-mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI-treated CaLu-1/GFP-LC3 lung cancer cells. We demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome-lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.
BACKGROUND AND PURPOSE Autophagic cell death is considered a self‐destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI‐mediated cell death. EXPERIMENTAL APPROACH Western blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI‐mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro. KEY RESULTS Lysosome inhibitors bafilomycin‐A1 and chloroquine increased GMI‐mediated autophagic cell death. GMI and bafilomycin‐A1 co‐treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H+‐ATPases (V‐ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI‐mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI‐treated CaLu‐1/GFP‐LC3 lung cancer cells. CONCLUSION AND IMPLICATIONS We demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome‐lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.
BACKGROUND AND PURPOSE Autophagic cell death is considered a self-destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI-mediated cell death. EXPERIMENTAL APPROACH Western blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI-mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro. KEY RESULTS Lysosome inhibitors bafilomycin-A1 and chloroquine increased GMI-mediated autophagic cell death. GMI and bafilomycin-A1 co-treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H super(+)-ATPases (V-ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI-mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI-treated CaLu-1/GFP-LC3 lung cancer cells. CONCLUSION AND IMPLICATIONS We demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome-lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.
BACKGROUND AND PURPOSE Autophagic cell death is considered a self-destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum, induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI-mediated cell death. EXPERIMENTAL APPROACH Western blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI-mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro. KEY RESULTS Lysosome inhibitors bafilomycin-A1 and chloroquine increased GMI-mediated autophagic cell death. GMI and bafilomycin-A1 co-treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H+-ATPases (V-ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI-mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI-treated CaLu-1/GFP-LC3 lung cancer cells. CONCLUSION AND IMPLICATIONS We demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome-lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.
BACKGROUND AND PURPOSE Autophagic cell death is considered a self‐destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant fungal immunomodulatory protein cloned from Ganoderma microsporum , induced autophagic cell death in lung cancer cells. The aim of this study was to examine the role of autophagosome accumulation in GMI‐mediated cell death. EXPERIMENTAL APPROACH Western blot analysis, flow cytometry and confocal microscopy were used to evaluate the effects of different treatments, including silencing of ATP6V0A1 by use of short hairpin RNAi, on GMI‐mediated cell death, lung cancer cell viability and autophagosome accumulation in vitro . KEY RESULTS Lysosome inhibitors bafilomycin‐A1 and chloroquine increased GMI‐mediated autophagic cell death. GMI and bafilomycin‐A1 co‐treatment induced the accumulation of large amounts of autophagosomes, but did not significantly induce apoptosis. GMI elicited autophagy through the PKB (Akt)/mammalian target of rapamycin signalling pathway. Silencing of ATP6V0A1, one subunit of vesicular H + ‐ATPases (V‐ATPases) that mediates lysosome acidification, spontaneously induced autophagosome accumulation, but did not affect lysosome acidity. GMI‐mediated autophagosome accumulation and cytotoxicity was increased in shATP6V0A1 lung cancer cells. Furthermore, ATP6V0A1 silencing decreased autophagosome and lysosome fusion in GMI‐treated CaLu‐1/GFP‐LC3 lung cancer cells. CONCLUSION AND IMPLICATIONS We demonstrated that autophagosome accumulation induces autophagic cell death in a GMI treatment model, and ATP6V0A1 plays an important role in mediating autophagosome‐lysosome fusion. Our findings provide new insights into the mechanisms involved in the induction of autophagic cell death.
Author Sheu, Gwo‐Tarng
Hsin, I‐Lun
Ko, Jiunn‐Liang
Wu, Tzu‐Chin
Lue, Ko‐Huang
Jan, Ming‐Shiou
Sun, Hai‐Lun
Chiu, Ling‐Yen
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https://www.ncbi.nlm.nih.gov/pubmed/22708544$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1271/bbb.60232
10.1016/j.cell.2011.07.030
10.1016/j.molcel.2011.04.024
10.1038/446745a
10.4161/auto.6845
10.1016/j.cmet.2007.11.001
10.1038/emboj.2011.335
10.1038/jid.2009.80
10.1038/emboj.2011.355
10.4161/auto.7.5.14226
10.1016/j.molcel.2006.12.009
10.1021/jf103068w
10.1038/nrclinonc.2011.71
10.1016/j.procbio.2010.06.006
10.1158/0008-5472.CAN-10-1626
10.1016/j.bcp.2007.07.025
10.1016/j.ceca.2011.04.001
10.1126/scisignal.2001017
10.1002/mc.20161
10.4161/auto.7.8.15698
10.1083/jcb.200212004
10.1038/emboj.2011.257
10.1038/ncb1730
10.1247/csf.23.33
10.1158/1078-0432.CCR-10-1948
10.1093/carcin/bgr031
10.4161/auto.5939
10.1038/nrm2239
10.1152/physiol.00005.2004
10.1038/ncb0910-814
10.1016/j.cell.2010.01.028
10.1074/jbc.274.19.12951
10.1016/j.cell.2008.04.037
10.1016/S1387-2656(07)13010-6
10.1016/j.fct.2008.01.044
10.1158/0008-5472.CAN-09-2190
10.4161/auto.1.2.1697
10.4161/auto.5338
10.1038/cdd.2010.53
ContentType Journal Article
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ID FETCH-LOGICAL-c6313-251b5c6c7cc04598ec143f4b69ce13e9387bcfbcbe71d073287acfe19487332d3
ISSN 0007-1188
1476-5381
IngestDate Thu Aug 21 18:29:37 EDT 2025
Fri Jul 11 09:20:22 EDT 2025
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Fri Jul 25 19:38:08 EDT 2025
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IsDoiOpenAccess false
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Issue 6
Keywords autophagic flux
GMI
autophagic cell death
autophagy
Enzyme
PKB
Adenosinetriphosphatase
Lysosome
immunomodulatory protein
Microsporum
Basidiomycota
Fungi
Immunomodulator
Cell death
V-ATPases
Mammalian target of rapamycin
mTOR
Hydrolases
Fungi Imperfecti
Ganoderma
ATP6V0A1
Language English
License CC BY 4.0
2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.
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Notes The two corresponding authors contributed equally to this work.
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References 2010; 12
2006; 70
2009; 69
2008a; 4
2007; 446
2010; 17
2010a; 58
2011; 30
2011; 32
2008; 10
2010; 140
2007; 74
2008; 4
2011; 17
2007; 13
2011; 8
1998; 23
2011; 7
2008b; 4
2011; 146
2006; 45
2004; 19
2011; 50
2003; 162
1999; 274
2011; 42
2007; 8
2007; 6
2008; 46
2005; 1
2010; 3
2009; 129
2010; 70
2008; 133
2010b; 45
2007; 25
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e_1_2_8_25_1
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e_1_2_8_27_1
e_1_2_8_3_1
e_1_2_8_2_1
e_1_2_8_5_1
e_1_2_8_4_1
e_1_2_8_7_1
e_1_2_8_6_1
e_1_2_8_8_1
e_1_2_8_20_1
Geng Y (e_1_2_8_9_1) 2010; 12
e_1_2_8_21_1
e_1_2_8_22_1
e_1_2_8_23_1
e_1_2_8_41_1
e_1_2_8_40_1
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21062993 - Sci Signal. 2010;3(147):ra81
18454141 - Nat Cell Biol. 2008 Jun;10(6):676-87
12876274 - J Cell Biol. 2003 Jul 21;162(2):211-22
15304635 - Physiology (Bethesda). 2004 Aug;19:207-15
21490426 - Autophagy. 2011 Aug;7(8):873-82
22009224 - EMBO J. 2011 Oct 19;30(20):4113-5
18188003 - Autophagy. 2008 Feb;4(2):151-75
18758232 - Autophagy. 2008 Oct;4(7):849-50
20508647 - Cell Death Differ. 2010 Dec;17(12):1867-81
21587219 - Nat Rev Clin Oncol. 2011 Sep;8(9):528-39
21884931 - Cell. 2011 Sep 2;146(5):682-95
18054315 - Cell Metab. 2007 Dec;6(6):458-71
18510934 - Cell. 2008 May 30;133(5):916-27
17875480 - Biotechnol Annu Rev. 2007;13:265-301
20144757 - Cell. 2010 Feb 5;140(3):313-26
19920197 - Cancer Res. 2009 Dec 1;69(23):8967-76
18376137 - Autophagy. 2008 Jul;4(5):621-8
21934648 - EMBO J. 2011 Oct 19;30(20):4126-41
17090952 - Biosci Biotechnol Biochem. 2006 Nov;70(11):2627-34
20876807 - Cancer Res. 2010 Oct 1;70(19):7699-709
21690574 - Clin Cancer Res. 2011 Aug 15;17(16):5353-66
17720143 - Biochem Pharmacol. 2007 Nov 15;74(10):1541-54
20406898 - Neuro Oncol. 2010 May;12(5):473-81
21317301 - Carcinogenesis. 2011 Jul;32(7):955-63
21571367 - Cell Calcium. 2011 Sep;50(3):242-50
17244528 - Mol Cell. 2007 Jan 26;25(2):193-205
10224039 - J Biol Chem. 1999 May 7;274(19):12951-4
16402390 - Mol Carcinog. 2006 Apr;45(4):220-9
16874052 - Autophagy. 2005 Jul;1(2):84-91
18329152 - Food Chem Toxicol. 2008 May;46(5):1851-9
21150268 - Autophagy. 2011 May;7(5):457-65
17717517 - Nat Rev Mol Cell Biol. 2007 Sep;8(9):741-52
9639028 - Cell Struct Funct. 1998 Feb;23(1):33-42
21700220 - Mol Cell. 2011 Jun 24;42(6):731-43
21028821 - J Agric Food Chem. 2010 Nov 24;58(22):12014-21
21804531 - EMBO J. 2011 Aug 17;30(16):3242-58
19357706 - J Invest Dermatol. 2009 Oct;129(10):2419-26
20811353 - Nat Cell Biol. 2010 Sep;12(9):814-22
17429391 - Nature. 2007 Apr 12;446(7137):745-7
References_xml – volume: 140
  start-page: 313
  year: 2010
  end-page: 326
  article-title: Methods in mammalian autophagy research
  publication-title: Cell
– volume: 70
  start-page: 7699
  year: 2010
  end-page: 7709
  article-title: Inhibition of autophagy enhances anticancer effects of atorvastatin in digestive malignancies
  publication-title: Cancer Res
– volume: 19
  start-page: 207
  year: 2004
  end-page: 215
  article-title: The pH of the secretory pathway: measurement, determinants, and regulation
  publication-title: Physiology (Bethesda)
– volume: 129
  start-page: 2419
  year: 2009
  end-page: 2426
  article-title: Hydroxychloroquine modulates metabolic activity and proliferation and induces autophagic cell death of human dermal fibroblasts
  publication-title: J Invest Dermatol
– volume: 32
  start-page: 955
  year: 2011
  end-page: 963
  article-title: The multiple roles of autophagy in cancer
  publication-title: Carcinogenesis
– volume: 12
  start-page: 814
  year: 2010
  end-page: 822
  article-title: Eaten alive: a history of macroautophagy
  publication-title: Nat Cell Biol
– volume: 70
  start-page: 2627
  year: 2006
  end-page: 2634
  article-title: Functional expression of FIP‐gts, a fungal immunomodulatory protein from Ganoderma tsugae in Sf21 insect cells
  publication-title: Biosci Biotechnol Biochem
– volume: 10
  start-page: 676
  year: 2008
  end-page: 687
  article-title: Regulation of autophagy by cytoplasmic p53
  publication-title: Nat Cell Biol
– volume: 17
  start-page: 1867
  year: 2010
  end-page: 1881
  article-title: Arsenic trioxide induces a beclin‐1‐independent autophagic pathway via modulation of SnoN/SkiL expression in ovarian carcinoma cells
  publication-title: Cell Death Differ
– volume: 23
  start-page: 33
  year: 1998
  end-page: 42
  article-title: Bafilomycin A1 prevents maturation of autophagic vacuoles by inhibiting fusion between autophagosomes and lysosomes in rat hepatoma cell line, H‐4‐II‐E cells
  publication-title: Cell Struct Funct
– volume: 50
  start-page: 242
  year: 2011
  end-page: 250
  article-title: A dual role for Ca(2+) in autophagy regulation
  publication-title: Cell Calcium
– volume: 42
  start-page: 731
  year: 2011
  end-page: 743
  article-title: Distinct autophagosomal‐lysosomal fusion mechanism revealed by thapsigargin‐induced autophagy arrest
  publication-title: Mol Cell
– volume: 4
  start-page: 621
  year: 2008
  end-page: 628
  article-title: Utilizing flow cytometry to monitor autophagy in living mammalian cells
  publication-title: Autophagy
– volume: 45
  start-page: 220
  year: 2006
  end-page: 229
  article-title: Transcriptionally mediated inhibition of telomerase of fungal immunomodulatory protein from in A549 human lung adenocarcinoma cell line
  publication-title: Mol Carcinog
– volume: 12
  start-page: 473
  year: 2010
  end-page: 481
  article-title: Chloroquine‐induced autophagic vacuole accumulation and cell death in glioma cells is p53 independent
  publication-title: Neuro Oncol
– volume: 17
  start-page: 5353
  year: 2011
  end-page: 5366
  article-title: PM02734 (elisidepsin) induces caspase‐independent cell death associated with features of autophagy, inhibition of the Akt/mTOR signaling pathway, and activation of death‐associated protein kinase
  publication-title: Clin Cancer Res
– volume: 30
  start-page: 3242
  year: 2011
  end-page: 3258
  article-title: Regulation of TFEB and V‐ATPases by mTORC1
  publication-title: EMBO J
– volume: 8
  start-page: 741
  year: 2007
  end-page: 752
  article-title: Self‐eating and self‐killing: crosstalk between autophagy and apoptosis
  publication-title: Nat Rev Mol Cell Biol
– volume: 74
  start-page: 1541
  year: 2007
  end-page: 1554
  article-title: Nuclear translocation of telomerase reverse transcriptase and calcium signaling in repression of telomerase activity in human lung cancer cells by fungal immunomodulatory protein from
  publication-title: Biochem Pharmacol
– volume: 7
  start-page: 873
  year: 2011
  end-page: 882
  article-title: GMI, an immunomodulatory protein from , induces autophagy in non‐small cell lung cancer cells
  publication-title: Autophagy
– volume: 1
  start-page: 84
  year: 2005
  end-page: 91
  article-title: Lysosomal turnover, but not a cellular level, of endogenous LC3 is a marker for autophagy
  publication-title: Autophagy
– volume: 30
  start-page: 4126
  year: 2011
  end-page: 4141
  article-title: The V‐ATPase proteolipid cylinder promotes the lipid‐mixing stage of SNARE‐dependent fusion of yeast vacuoles
  publication-title: EMBO J
– volume: 3
  start-page: ra81
  year: 2010
  article-title: Akt and autophagy cooperate to promote survival of drug‐resistant glioma
  publication-title: Sci Signal
– volume: 146
  start-page: 682
  year: 2011
  end-page: 695
  article-title: Autophagy and aging
  publication-title: Cell
– volume: 7
  start-page: 457
  year: 2011
  end-page: 465
  article-title: Autophagic cell death: Loch Ness monster or endangered species?
  publication-title: Autophagy
– volume: 446
  start-page: 745
  year: 2007
  end-page: 747
  article-title: Cell biology: autophagy and cancer
  publication-title: Nature
– volume: 4
  start-page: 151
  year: 2008a
  end-page: 175
  article-title: Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
  publication-title: Autophagy
– volume: 58
  start-page: 12014
  year: 2010a
  end-page: 12021
  article-title: GMI, a Ganoderma immunomodulatory protein, down‐regulates tumor necrosis factor alpha‐induced expression of matrix metalloproteinase 9 via NF‐kappaB pathway in human alveolar epithelial A549 cells
  publication-title: J Agric Food Chem
– volume: 133
  start-page: 916
  year: 2008
  end-page: 927
  article-title: Live imaging of neuronal degradation by microglia reveals a role for v0‐ATPase a1 in phagosomal fusion
  publication-title: Cell
– volume: 4
  start-page: 849
  year: 2008b
  end-page: 950
  article-title: Does bafilomycin A1 block the fusion of autophagosomes with lysosomes?
  publication-title: Autophagy
– volume: 45
  start-page: 1537
  year: 2010b
  end-page: 1542
  article-title: A new immunomodulatory protein from inhibits epidermal growth factor mediated migration and invasion in A549 lung cancer cells
  publication-title: Process Biochem
– volume: 274
  start-page: 12951
  year: 1999
  end-page: 12954
  article-title: Structure and properties of the vacuolar (H+)‐ATPases
  publication-title: J Biol Chem
– volume: 162
  start-page: 211
  year: 2003
  end-page: 222
  article-title: Vacuole membrane fusion: V0 functions after trans‐SNARE pairing and is coupled to the Ca2+‐releasing channel
  publication-title: J Cell Biol
– volume: 13
  start-page: 265
  year: 2007
  end-page: 301
  article-title: Ganoderma lucidum and its pharmaceutically active compounds
  publication-title: Biotechnol Annu Rev
– volume: 69
  start-page: 8967
  year: 2009
  end-page: 8976
  article-title: Perifosine inhibits mammalian target of rapamycin signaling through facilitating degradation of major components in the mTOR axis and induces autophagy
  publication-title: Cancer Res
– volume: 46
  start-page: 1851
  year: 2008
  end-page: 1859
  article-title: Induction of premature senescence in human lung cancer by fungal immunomodulatory protein from
  publication-title: Food Chem Toxicol
– volume: 6
  start-page: 458
  year: 2007
  end-page: 471
  article-title: FoxO3 controls autophagy in skeletal muscle
  publication-title: Cell Metab
– volume: 30
  start-page: 4113
  year: 2011
  end-page: 4115
  article-title: Duelling functions of the V‐ATPase
  publication-title: EMBO J
– volume: 25
  start-page: 193
  year: 2007
  end-page: 205
  article-title: Control of macroautophagy by calcium, calmodulin‐dependent kinase kinase‐beta, and Bcl‐2
  publication-title: Mol Cell
– volume: 8
  start-page: 528
  year: 2011
  end-page: 539
  article-title: Autophagy as a target for anticancer therapy
  publication-title: Nat Rev Clin Oncol
– ident: e_1_2_8_13_1
  doi: 10.1271/bbb.60232
– ident: e_1_2_8_31_1
  doi: 10.1016/j.cell.2011.07.030
– ident: e_1_2_8_8_1
  doi: 10.1016/j.molcel.2011.04.024
– ident: e_1_2_8_16_1
  doi: 10.1038/446745a
– ident: e_1_2_8_15_1
  doi: 10.4161/auto.6845
– ident: e_1_2_8_24_1
  doi: 10.1016/j.cmet.2007.11.001
– ident: e_1_2_8_36_1
  doi: 10.1038/emboj.2011.335
– ident: e_1_2_8_29_1
  doi: 10.1038/jid.2009.80
– ident: e_1_2_8_32_1
  doi: 10.1038/emboj.2011.355
– ident: e_1_2_8_33_1
  doi: 10.4161/auto.7.5.14226
– ident: e_1_2_8_10_1
  doi: 10.1016/j.molcel.2006.12.009
– ident: e_1_2_8_20_1
  doi: 10.1021/jf103068w
– ident: e_1_2_8_12_1
  doi: 10.1038/nrclinonc.2011.71
– ident: e_1_2_8_21_1
  doi: 10.1016/j.procbio.2010.06.006
– ident: e_1_2_8_40_1
  doi: 10.1158/0008-5472.CAN-10-1626
– ident: e_1_2_8_18_1
  doi: 10.1016/j.bcp.2007.07.025
– ident: e_1_2_8_4_1
  doi: 10.1016/j.ceca.2011.04.001
– ident: e_1_2_8_5_1
  doi: 10.1126/scisignal.2001017
– ident: e_1_2_8_17_1
  doi: 10.1002/mc.20161
– ident: e_1_2_8_11_1
  doi: 10.4161/auto.7.8.15698
– ident: e_1_2_8_2_1
  doi: 10.1083/jcb.200212004
– ident: e_1_2_8_27_1
  doi: 10.1038/emboj.2011.257
– ident: e_1_2_8_38_1
  doi: 10.1038/ncb1730
– ident: e_1_2_8_39_1
  doi: 10.1247/csf.23.33
– ident: e_1_2_8_22_1
  doi: 10.1158/1078-0432.CCR-10-1948
– ident: e_1_2_8_30_1
  doi: 10.1093/carcin/bgr031
– ident: e_1_2_8_34_1
  doi: 10.4161/auto.5939
– ident: e_1_2_8_23_1
  doi: 10.1038/nrm2239
– ident: e_1_2_8_26_1
  doi: 10.1152/physiol.00005.2004
– ident: e_1_2_8_41_1
  doi: 10.1038/ncb0910-814
– ident: e_1_2_8_25_1
  doi: 10.1016/j.cell.2010.01.028
– ident: e_1_2_8_6_1
  doi: 10.1074/jbc.274.19.12951
– ident: e_1_2_8_28_1
  doi: 10.1016/j.cell.2008.04.037
– ident: e_1_2_8_3_1
  doi: 10.1016/S1387-2656(07)13010-6
– ident: e_1_2_8_19_1
  doi: 10.1016/j.fct.2008.01.044
– volume: 12
  start-page: 473
  year: 2010
  ident: e_1_2_8_9_1
  article-title: Chloroquine‐induced autophagic vacuole accumulation and cell death in glioma cells is p53 independent
  publication-title: Neuro Oncol
– ident: e_1_2_8_7_1
  doi: 10.1158/0008-5472.CAN-09-2190
– ident: e_1_2_8_37_1
  doi: 10.4161/auto.1.2.1697
– ident: e_1_2_8_14_1
  doi: 10.4161/auto.5338
– ident: e_1_2_8_35_1
  doi: 10.1038/cdd.2010.53
– reference: 21934648 - EMBO J. 2011 Oct 19;30(20):4126-41
– reference: 18454141 - Nat Cell Biol. 2008 Jun;10(6):676-87
– reference: 21150268 - Autophagy. 2011 May;7(5):457-65
– reference: 17429391 - Nature. 2007 Apr 12;446(7137):745-7
– reference: 21028821 - J Agric Food Chem. 2010 Nov 24;58(22):12014-21
– reference: 18329152 - Food Chem Toxicol. 2008 May;46(5):1851-9
– reference: 21062993 - Sci Signal. 2010;3(147):ra81
– reference: 18758232 - Autophagy. 2008 Oct;4(7):849-50
– reference: 21587219 - Nat Rev Clin Oncol. 2011 Sep;8(9):528-39
– reference: 18188003 - Autophagy. 2008 Feb;4(2):151-75
– reference: 16874052 - Autophagy. 2005 Jul;1(2):84-91
– reference: 17244528 - Mol Cell. 2007 Jan 26;25(2):193-205
– reference: 21571367 - Cell Calcium. 2011 Sep;50(3):242-50
– reference: 21884931 - Cell. 2011 Sep 2;146(5):682-95
– reference: 15304635 - Physiology (Bethesda). 2004 Aug;19:207-15
– reference: 19920197 - Cancer Res. 2009 Dec 1;69(23):8967-76
– reference: 10224039 - J Biol Chem. 1999 May 7;274(19):12951-4
– reference: 17717517 - Nat Rev Mol Cell Biol. 2007 Sep;8(9):741-52
– reference: 21690574 - Clin Cancer Res. 2011 Aug 15;17(16):5353-66
– reference: 20876807 - Cancer Res. 2010 Oct 1;70(19):7699-709
– reference: 20811353 - Nat Cell Biol. 2010 Sep;12(9):814-22
– reference: 18510934 - Cell. 2008 May 30;133(5):916-27
– reference: 18376137 - Autophagy. 2008 Jul;4(5):621-8
– reference: 20508647 - Cell Death Differ. 2010 Dec;17(12):1867-81
– reference: 19357706 - J Invest Dermatol. 2009 Oct;129(10):2419-26
– reference: 18054315 - Cell Metab. 2007 Dec;6(6):458-71
– reference: 12876274 - J Cell Biol. 2003 Jul 21;162(2):211-22
– reference: 16402390 - Mol Carcinog. 2006 Apr;45(4):220-9
– reference: 21700220 - Mol Cell. 2011 Jun 24;42(6):731-43
– reference: 9639028 - Cell Struct Funct. 1998 Feb;23(1):33-42
– reference: 17875480 - Biotechnol Annu Rev. 2007;13:265-301
– reference: 21490426 - Autophagy. 2011 Aug;7(8):873-82
– reference: 20406898 - Neuro Oncol. 2010 May;12(5):473-81
– reference: 22009224 - EMBO J. 2011 Oct 19;30(20):4113-5
– reference: 17090952 - Biosci Biotechnol Biochem. 2006 Nov;70(11):2627-34
– reference: 17720143 - Biochem Pharmacol. 2007 Nov 15;74(10):1541-54
– reference: 20144757 - Cell. 2010 Feb 5;140(3):313-26
– reference: 21317301 - Carcinogenesis. 2011 Jul;32(7):955-63
– reference: 21804531 - EMBO J. 2011 Aug 17;30(16):3242-58
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Snippet BACKGROUND AND PURPOSE Autophagic cell death is considered a self‐destructive process that results from large amounts of autophagic flux. In our previous...
BACKGROUND AND PURPOSE Autophagic cell death is considered a self‐destructive process that results from large amounts of autophagic flux. In our previous...
Autophagic cell death is considered a self-destructive process that results from large amounts of autophagic flux. In our previous study, GMI, a recombinant...
BACKGROUND AND PURPOSE Autophagic cell death is considered a self-destructive process that results from large amounts of autophagic flux. In our previous...
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pubmed
pascalfrancis
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wiley
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SubjectTerms Apoptosis
ATP6V0A1
autophagic cell death
autophagic flux
autophagy
Autophagy - drug effects
Biological and medical sciences
Cell Line, Tumor
Chloroquine - pharmacology
Fungal Proteins - pharmacology
Ganoderma
Gene Silencing
GMI
Humans
Immunologic Factors - pharmacology
immunomodulatory protein
Kinases
Lung cancer
lysosome
Lysosomes - drug effects
Macrolides - pharmacology
Medical sciences
Microsporum
mTOR
Phagosomes - drug effects
Pharmacology. Drug treatments
PKB
Proto-Oncogene Proteins c-akt - metabolism
Research Papers
TOR Serine-Threonine Kinases - metabolism
Vacuolar Proton-Translocating ATPases - genetics
V‐ATPases
Title Inhibition of lysosome degradation on autophagosome formation and responses to GMI, an immunomodulatory protein from Ganoderma microsporum
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1476-5381.2012.02073.x
https://www.ncbi.nlm.nih.gov/pubmed/22708544
https://www.proquest.com/docview/1766586219
https://www.proquest.com/docview/1239054772
https://www.proquest.com/docview/1776648590
https://pubmed.ncbi.nlm.nih.gov/PMC3504994
Volume 167
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