Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function
Endonuclease G and heart disease Elevated left ventricular mass, a highly heritable trait, is an important risk factor for heart failure and death. Stuart Cook and colleagues genetically dissect a locus in the rat associated with blood-pressure-independent cardiac hypertrophy and identify endonuclea...
Saved in:
| Published in | Nature (London) Vol. 478; no. 7367; pp. 114 - 118 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
06.10.2011
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Endonuclease G and heart disease
Elevated left ventricular mass, a highly heritable trait, is an important risk factor for heart failure and death. Stuart Cook and colleagues genetically dissect a locus in the rat associated with blood-pressure-independent cardiac hypertrophy and identify endonuclease G (ENDOG) as a key regulator of hypertrophy at this locus. They further show that the
Endog
gene is involved in proper mitochondrial function and is modulated by ERR-α and PGC1α, master regulators of mitochondrial and cardiac function. Loss of function of ENDOG causes impaired mitochondrial respiration and increased production of reactive oxygen species, which may contribute to the observed cardiac hypertrophy.
Left ventricular mass (LVM) is a highly heritable trait
1
and an independent risk factor for all-cause mortality
2
. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation
3
, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood
4
,
5
. Unbiased systems genetics approaches in the rat
6
,
7
now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (
Endog
), which previously was implicated in apoptosis
8
but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in
Endog
that is associated with increased LVM and impaired cardiac function. Inhibition of
Endog
in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated
ENDOG
in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of
ENDOG
by ERR-α and PGC1α (which are master regulators of mitochondrial and cardiac function)
9
,
10
,
11
, interaction of ENDOG with the mitochondrial genome and
ENDOG
-mediated regulation of mitochondrial mass. At baseline, the
Endog
-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for
Endog
in maladaptive cardiac hypertrophy. |
|---|---|
| AbstractList | Left ventricular mass (LVM) is a highly heritable trait
1
and an independent risk factor for all-cause mortality
2
. To date, genome-wide association studies (GWASs) have not identified the genetic factors underlying LVM variation
3
and the regulatory mechanisms for blood pressure (BP)-independent cardiac hypertrophy remain poorly understood
4
,
5
. Unbiased systems-genetics approaches in the rat
6
,
7
now provide a powerful complementary tool to GWAS and we applied integrative genomics to dissect a highly replicated, BP-independent LVM locus on rat chromosome 3p. We identified endonuclease G (
Endog
), previously implicated in apoptosis
8
but not hypertrophy, as the gene at the locus and demonstrated loss-of-function mutation in
Endog
associated with increased LVM and impaired cardiac function. Inhibition of
Endog
in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly inferred
ENDOG
in fundamental mitochondrial processes unrelated to apoptosis. We showed direct regulation of
ENDOG
by
ERR
α and
PGC1
α, master regulators of mitochondrial and cardiac function
9
,
10
,
11
, interaction of ENDOG with the mitochondrial genome and
ENDOG
-mediated regulation of mitochondrial mass. At baseline,
Endog
deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated reactive oxygen species (ROS), which was associated with enlarged and steatotic cardiomyocytes. Our studies establish further the link between mitochondrial dysfunction, ROS and heart disease and demonstrate a new role for
Endog
in maladaptive cardiac hypertrophy. Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood. Unbiased systems genetics approaches in the rat now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-α and PGC1α (which are master regulators of mitochondrial and cardiac function), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy. [PUBLICATION ABSTRACT] Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood. Unbiased systems genetics approaches in the rat now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-α and PGC1α (which are master regulators of mitochondrial and cardiac function), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy.Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood. Unbiased systems genetics approaches in the rat now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-α and PGC1α (which are master regulators of mitochondrial and cardiac function), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy. Endonuclease G and heart disease Elevated left ventricular mass, a highly heritable trait, is an important risk factor for heart failure and death. Stuart Cook and colleagues genetically dissect a locus in the rat associated with blood-pressure-independent cardiac hypertrophy and identify endonuclease G (ENDOG) as a key regulator of hypertrophy at this locus. They further show that the Endog gene is involved in proper mitochondrial function and is modulated by ERR-α and PGC1α, master regulators of mitochondrial and cardiac function. Loss of function of ENDOG causes impaired mitochondrial respiration and increased production of reactive oxygen species, which may contribute to the observed cardiac hypertrophy. Left ventricular mass (LVM) is a highly heritable trait 1 and an independent risk factor for all-cause mortality 2 . So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation 3 , and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood 4 , 5 . Unbiased systems genetics approaches in the rat 6 , 7 now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G ( Endog ), which previously was implicated in apoptosis 8 but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-α and PGC1α (which are master regulators of mitochondrial and cardiac function) 9 , 10 , 11 , interaction of ENDOG with the mitochondrial genome and ENDOG -mediated regulation of mitochondrial mass. At baseline, the Endog -deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy. Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood. Unbiased systems genetics approaches in the rat now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-α and PGC1α (which are master regulators of mitochondrial and cardiac function), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy. Left ventricular mass (LVM) is a highly heritable trait (1) and an independent risk factor for all-cause mortality (2). So far, genomewide association studies have not identified the genetic factors that underlie LVM variation (3), and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood (4,5). Unbiased systems genetics approaches in the rat (6,7) now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis (8) but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-α and PGC1a (which are master regulators of mitochondrial and cardiac function) (9-11), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endogin maladaptive cardiac hypertrophy. |
| Audience | Academic |
| Author | Ye, Junmei McDermott-Roe, Chris Buchan, Rachel Jacob, Howard Sanchis, Daniel Lu, Han Pravenec, Michal Braithwaite, Adam Comella, Joan X. Barton, Paul J. R. Rowe, Glenn C. Mancini, Massimiliano Sun, Xi-Ming Hauton, David Zhang, Jisheng Felkin, Leanne E. Zidek, Vaclav Serafín, Anna Serikawa, Tadao Papousek, Frantisek Cañas, Xavier Kolar, Frantisek Bottolo, Leonardo Martí, Ramon Hubner, Norbert Muckett, Phil Ahmed, Rizwan Arany, Zoltan Cook, Stuart A. García-Arumí, Elena García-Dorado, David Ware, James Ruiz-Meana, Marisol Petretto, Enrico Cardona, Maria |
| AuthorAffiliation | 3 Platform of Applied Research on Laboratory Animal Barcelona Science Park, Baldiri Reixac, 4, 08028 Barcelona, Spain 10 Department of Physiology, Medical College of Wisconsin, Milwaukee WI 53226, U.S.A 8 Max-Delbrück Center for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin, Germany 9 CC4, Campus Charité Mitte, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany 1 Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK 11 Institute of Laboratory Animals, Graduate School of Medicine, Kyoto University, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan 16 Cardiovascular Biomedical Research Unit, Royal Brompton and Harefield NHS Trust, Sydney Street, London, SW3 6NP 14 Cell Signaling & Apoptosis Group at CIBERNED and Vall d’Hebron Institut of Research (VHIR) and Dept Biochemistry-molecular Biology and Institut de Neurociencies at Universitat Autonoma de Barcelona, B |
| AuthorAffiliation_xml | – name: 1 Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK – name: 2 Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Av Rovira Roure, 80, 25198 Lleida, Spain – name: 10 Department of Physiology, Medical College of Wisconsin, Milwaukee WI 53226, U.S.A – name: 16 Cardiovascular Biomedical Research Unit, Royal Brompton and Harefield NHS Trust, Sydney Street, London, SW3 6NP – name: 4 Cardiovascular Institute, Beth Israel Deaconess Medical Institute, CLS906, 3 Blackfan Circle, Boston MA 02215, USA – name: 3 Platform of Applied Research on Laboratory Animal Barcelona Science Park, Baldiri Reixac, 4, 08028 Barcelona, Spain – name: 5 Department of Radiological, Oncological and Anatomo-Pathological Sciences, Sapienza, University of Rome, Italy – name: 6 School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT – name: 9 CC4, Campus Charité Mitte, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany – name: 14 Cell Signaling & Apoptosis Group at CIBERNED and Vall d’Hebron Institut of Research (VHIR) and Dept Biochemistry-molecular Biology and Institut de Neurociencies at Universitat Autonoma de Barcelona, Barcelona, Spain – name: 15 Heart Science Centre, National Heart and Lung Institute, Imperial College London, Harefield Hospital, Harefield, Middlesex, UB9 6JH, UK – name: 12 Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083, 142 20 Prague 4, Czech Republic – name: 7 Unitat de Patologia Mitocondrial i Neuromuscular, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain – name: 11 Institute of Laboratory Animals, Graduate School of Medicine, Kyoto University, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan – name: 17 Department of Epidemiology and Biostatistics, Faculty of Medicine, Imperial College London, Praed Street, London W2 1PG, UK – name: 8 Max-Delbrück Center for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin, Germany – name: 13 Grup de Patologia Cardiovascular, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain |
| Author_xml | – sequence: 1 givenname: Chris surname: McDermott-Roe fullname: McDermott-Roe, Chris organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 2 givenname: Junmei surname: Ye fullname: Ye, Junmei organization: Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Avenida Rovira Roure 80 – sequence: 3 givenname: Rizwan surname: Ahmed fullname: Ahmed, Rizwan organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 4 givenname: Xi-Ming surname: Sun fullname: Sun, Xi-Ming organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 5 givenname: Anna surname: Serafín fullname: Serafín, Anna organization: Platform of Applied Research on Laboratory Animal, Barcelona Science Park, Baldiri Reixac 4 – sequence: 6 givenname: James surname: Ware fullname: Ware, James organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 7 givenname: Leonardo surname: Bottolo fullname: Bottolo, Leonardo organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 8 givenname: Phil surname: Muckett fullname: Muckett, Phil organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 9 givenname: Xavier surname: Cañas fullname: Cañas, Xavier organization: Platform of Applied Research on Laboratory Animal, Barcelona Science Park, Baldiri Reixac 4 – sequence: 10 givenname: Jisheng surname: Zhang fullname: Zhang, Jisheng organization: Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Avenida Rovira Roure 80 – sequence: 11 givenname: Glenn C. surname: Rowe fullname: Rowe, Glenn C. organization: Cardiovascular Institute, Beth Israel Deaconess Medical Institute, CLS906, 3 Blackfan Circle – sequence: 12 givenname: Rachel surname: Buchan fullname: Buchan, Rachel organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 13 givenname: Han surname: Lu fullname: Lu, Han organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 14 givenname: Adam surname: Braithwaite fullname: Braithwaite, Adam organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital – sequence: 15 givenname: Massimiliano surname: Mancini fullname: Mancini, Massimiliano organization: Department of Radiological, Oncological and Anatomo-Pathological Sciences, University of Rome – sequence: 16 givenname: David surname: Hauton fullname: Hauton, David organization: School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston – sequence: 17 givenname: Ramon surname: Martí fullname: Martí, Ramon organization: Unitat de Patologia Mitocondrial i Neuromuscular CIBERER, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona – sequence: 18 givenname: Elena surname: García-Arumí fullname: García-Arumí, Elena organization: Unitat de Patologia Mitocondrial i Neuromuscular CIBERER, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona – sequence: 19 givenname: Norbert surname: Hubner fullname: Hubner, Norbert organization: Max-Delbrück Center for Molecular Medicine, Robert-Rössle-Strasse 10, CC4, Campus Charité Mitte, Charité-Universitätsmedizin Berlin, Charitéplatz 1 – sequence: 20 givenname: Howard surname: Jacob fullname: Jacob, Howard organization: Department of Physiology, Medical College of Wisconsin – sequence: 21 givenname: Tadao surname: Serikawa fullname: Serikawa, Tadao organization: Institute of Laboratory Animals, Graduate School of Medicine, Kyoto University, Yoshidakonoe-cho – sequence: 22 givenname: Vaclav surname: Zidek fullname: Zidek, Vaclav organization: Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083 – sequence: 23 givenname: Frantisek surname: Papousek fullname: Papousek, Frantisek organization: Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083 – sequence: 24 givenname: Frantisek surname: Kolar fullname: Kolar, Frantisek organization: Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083 – sequence: 25 givenname: Maria surname: Cardona fullname: Cardona, Maria organization: Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Avenida Rovira Roure 80 – sequence: 26 givenname: Marisol surname: Ruiz-Meana fullname: Ruiz-Meana, Marisol organization: Grup de Patologia Cardiovascular, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Pg. Vall d’Hebron, 119 – sequence: 27 givenname: David surname: García-Dorado fullname: García-Dorado, David organization: Grup de Patologia Cardiovascular, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Pg. Vall d’Hebron, 119 – sequence: 28 givenname: Joan X. surname: Comella fullname: Comella, Joan X. organization: Cell Signaling & Apoptosis Group at CIBERNED and Vall d’Hebron Institute of Research (VHIR), Pg. Vall d'Hebron, 119-129, Department of Biochemistry and Molecular Biology and the Institut de Neurociencies at Universitat Autonoma de Barcelona – sequence: 29 givenname: Leanne E. surname: Felkin fullname: Felkin, Leanne E. organization: Heart Science Centre, National Heart and Lung Institute, Imperial College London, Harefield Hospital – sequence: 30 givenname: Paul J. R. surname: Barton fullname: Barton, Paul J. R. organization: Heart Science Centre, National Heart and Lung Institute, Imperial College London, Harefield Hospital, Cardiovascular Biomedical Research Unit, Royal Brompton and Harefield NHS Trust – sequence: 31 givenname: Zoltan surname: Arany fullname: Arany, Zoltan organization: Cardiovascular Institute, Beth Israel Deaconess Medical Institute, CLS906, 3 Blackfan Circle – sequence: 32 givenname: Michal surname: Pravenec fullname: Pravenec, Michal organization: Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083 – sequence: 33 givenname: Enrico surname: Petretto fullname: Petretto, Enrico organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Department of Epidemiology and Biostatistics, Faculty of Medicine, Imperial College London – sequence: 34 givenname: Daniel surname: Sanchis fullname: Sanchis, Daniel email: daniel.sanchis@cmb.udl.cat organization: Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Avenida Rovira Roure 80 – sequence: 35 givenname: Stuart A. surname: Cook fullname: Cook, Stuart A. email: stuart.cook@imperial.ac.uk organization: Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Cardiovascular Biomedical Research Unit, Royal Brompton and Harefield NHS Trust |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24569712$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21979051$$D View this record in MEDLINE/PubMed |
| BookMark | eNp10s9v0zAUB3ALDbGucOKOoiGEEGTY-WX7glRVY0yaQIKhHa1Xx249JXZmJxP973Fp2VoUfLEcf_J1nPdO0JF1ViH0kuAzgnP20UI_eEVwwfETNCEFrdKiYvQITTDOWIpZXh2jkxBuMcYlocUzdJwRTnlcTNDNua2dHWSjIKjkIjEhgcS6e9UkteqVb40F2ydOJxJ8bUAmq3WnfO9dt1onYOukNb2TK2drb6BJ9GBlb5x9jp5qaIJ6sZun6Ofn8-v5l_Tq28XlfHaVyopWfco4MM4oryilJSlLxRaZJBqkVouCVEUBEmrJS81JKeOoMXCSac3LjGQ5I_kUfdrmdsOiVbVUtvfQiM6bFvxaODDicMealVi6e5ETxstiE_B2F-Dd3aBCL1oTpGoasMoNQTBesRyzP_L0H3nrBm_j7SLiWUkYzSN6vUVLaJQwVrt4qtxEillGMS4yFtkUpSNqqayKnxirq018fOBPR7zszJ3YR2cjaPMDVWvkaOq7gxei6dWvfglDCOLyx_dD-_7_dnZ9M_86qqV3IXilHwpCsNg0rdhr2qhf7dfwwf7t0gje7AAECY32YKUJj64oK05jP0zRh60LccsulX-s0Ni5vwEGQgLJ |
| CODEN | NATUAS |
| CitedBy_id | crossref_primary_10_1161_HYPERTENSIONAHA_111_00814 crossref_primary_10_1038_ncomms12061 crossref_primary_10_1186_s13059_021_02397_w crossref_primary_10_1126_science_aaf4777 crossref_primary_10_1016_j_devcel_2011_12_021 crossref_primary_10_7554_eLife_69916 crossref_primary_10_1016_j_redox_2018_02_021 crossref_primary_10_1161_CIRCGENETICS_115_001067 crossref_primary_10_1007_s10495_023_01835_3 crossref_primary_10_1093_hmg_ddae031 crossref_primary_10_1016_j_bbrc_2017_09_149 crossref_primary_10_1021_ac501726s crossref_primary_10_1016_j_cjca_2015_10_021 crossref_primary_10_1016_j_freeradbiomed_2014_04_016 crossref_primary_10_1161_CIRCRESAHA_112_269084 crossref_primary_10_3389_fphar_2021_739615 crossref_primary_10_1161_RES_0b013e318249dcc8 crossref_primary_10_1371_journal_pone_0164951 crossref_primary_10_1039_D2MO00004K crossref_primary_10_1097_HJH_0000000000001613 crossref_primary_10_1038_nrg3575 crossref_primary_10_1016_j_bbadis_2014_11_009 crossref_primary_10_1007_s43032_022_00953_8 crossref_primary_10_1002_2211_5463_13572 crossref_primary_10_1126_science_aav4011 crossref_primary_10_1016_j_cels_2017_01_005 crossref_primary_10_1089_ars_2013_5438 crossref_primary_10_33549_physiolres_934740 crossref_primary_10_1134_S0006297916020103 crossref_primary_10_1152_physiolgenomics_00083_2011 crossref_primary_10_1111_jcmm_16665 crossref_primary_10_1038_emboj_2013_238 crossref_primary_10_1134_S0006297912130032 crossref_primary_10_1016_j_redox_2020_101736 crossref_primary_10_1242_dmm_009787 crossref_primary_10_1016_j_yjmcc_2014_10_003 crossref_primary_10_3109_10799893_2014_959592 crossref_primary_10_1016_j_tcm_2012_07_003 crossref_primary_10_1371_journal_pone_0131411 crossref_primary_10_1111_febs_16113 crossref_primary_10_1007_s00395_016_0537_6 crossref_primary_10_3390_cells11060974 crossref_primary_10_1186_s12929_020_00673_8 crossref_primary_10_1038_s41467_020_20780_2 crossref_primary_10_1038_s41598_023_27590_8 crossref_primary_10_1242_dmm_026716 crossref_primary_10_1371_journal_pgen_1004813 crossref_primary_10_1038_onc_2012_348 crossref_primary_10_1097_HCO_0000000000000160 crossref_primary_10_1186_s13395_015_0059_1 crossref_primary_10_1096_fj_15_276360 crossref_primary_10_1152_physiolgenomics_00009_2014 crossref_primary_10_3389_fonc_2021_689063 crossref_primary_10_1016_j_jbc_2021_100825 crossref_primary_10_1002_jcp_25851 crossref_primary_10_1038_s41467_023_41757_x crossref_primary_10_1042_CS20220242 crossref_primary_10_1134_S0026893316020175 crossref_primary_10_1016_j_bbabio_2020_148158 crossref_primary_10_1093_bib_bbt007 crossref_primary_10_1161_CIRCGENETICS_113_000732 crossref_primary_10_33549_physiolres_932622 crossref_primary_10_1242_dmm_026104 crossref_primary_10_1093_ajh_hpt156 crossref_primary_10_1007_s10565_022_09735_z crossref_primary_10_1016_j_tibs_2020_07_002 crossref_primary_10_1016_j_celrep_2016_05_090 crossref_primary_10_1128_JVI_02306_13 crossref_primary_10_1016_j_ydbio_2017_06_028 crossref_primary_10_1101_gr_169029_113 crossref_primary_10_18632_oncotarget_24822 crossref_primary_10_15252_msb_20145117 crossref_primary_10_1016_j_bbadis_2017_08_022 crossref_primary_10_1242_dmm_027789 crossref_primary_10_3390_jcm12052063 crossref_primary_10_1016_j_bbrc_2017_10_119 crossref_primary_10_3390_ijms241914752 crossref_primary_10_1016_j_isci_2018_03_005 crossref_primary_10_7554_eLife_91004 crossref_primary_10_1093_cvr_cvs303 crossref_primary_10_3389_fcvm_2021_822969 crossref_primary_10_1038_s41526_021_00171_7 crossref_primary_10_1002_cmdc_201300129 crossref_primary_10_1161_HYPERTENSIONAHA_117_09242 crossref_primary_10_1007_s12265_013_9504_x crossref_primary_10_1152_ajpcell_00227_2014 crossref_primary_10_1016_j_bbrc_2014_08_047 crossref_primary_10_1093_eurjhf_hfs121 crossref_primary_10_1016_j_cell_2013_06_040 crossref_primary_10_1016_j_stemcr_2019_07_004 crossref_primary_10_1038_s41598_019_52724_2 crossref_primary_10_1016_j_yjmcc_2012_06_008 crossref_primary_10_3109_10641963_2014_943405 crossref_primary_10_1155_2012_936486 crossref_primary_10_1371_journal_pone_0113642 crossref_primary_10_1042_CS20220832 crossref_primary_10_1152_ajpheart_00631_2012 crossref_primary_10_1111_nph_15972 crossref_primary_10_1097_HJH_0000000000001155 crossref_primary_10_3389_fimmu_2021_629922 crossref_primary_10_1038_s41420_017_0005_6 crossref_primary_10_1093_bfgp_elt030 crossref_primary_10_1042_CS20191320 crossref_primary_10_18632_aging_102647 crossref_primary_10_1042_CS20210648 crossref_primary_10_1016_j_biocel_2024_106539 crossref_primary_10_1073_pnas_1315587110 crossref_primary_10_1016_j_expneurol_2013_03_028 crossref_primary_10_1371_journal_pone_0170458 crossref_primary_10_1371_journal_pone_0294187 crossref_primary_10_3389_fcvm_2022_821317 crossref_primary_10_1242_dmm_048090 crossref_primary_10_18632_oncotarget_15693 |
| Cites_doi | 10.1172/JCI0214571 10.1172/JCI27794 10.1016/j.molcel.2006.12.021 10.1038/sj.emboj.7600461 10.1038/nature09386 10.1038/5089 10.1056/NEJMra072139 10.1161/01.CIR.102.4.470 10.1161/CIRCRESAHA.110.232306 10.1038/labinvest.3700523 10.2202/1544-6115.1128 10.7326/0003-4819-144-7-200604040-00011 10.1038/sj.cdd.4401787 10.1016/0888-7543(95)80058-T 10.1016/j.cmet.2007.03.007 10.1161/01.ATV.0000079509.20542.C9 10.1291/hypres.28.273 10.1126/science.7688144 10.1074/jbc.M601025200 10.1161/01.HYP.30.5.1025 10.1074/jbc.M808319200 10.1093/hmg/ddp327 10.1038/35083620 10.1038/ng.134 10.1128/MCB.25.1.294-302.2005 10.1038/ncpcardio0943 10.1136/hrt.2005.068270 10.1016/S0092-8674(00)80611-X 10.1001/jama.2009.978-a 10.1002/9780470725207.ch5 |
| ContentType | Journal Article |
| Copyright | Springer Nature Limited 2011 2015 INIST-CNRS COPYRIGHT 2011 Nature Publishing Group Copyright Nature Publishing Group Oct 6, 2011 |
| Copyright_xml | – notice: Springer Nature Limited 2011 – notice: 2015 INIST-CNRS – notice: COPYRIGHT 2011 Nature Publishing Group – notice: Copyright Nature Publishing Group Oct 6, 2011 |
| DBID | IQODW CGR CUY CVF ECM EIF NPM AAYXX CITATION ATWCN 3V. 7QG 7QL 7QP 7QR 7RV 7SN 7SS 7ST 7T5 7TG 7TK 7TM 7TO 7U9 7X2 7X7 7XB 88A 88E 88G 88I 8AF 8AO 8C1 8FD 8FE 8FG 8FH 8FI 8FJ 8FK 8G5 ABJCF ABUWG AFKRA ARAPS ATCPS AZQEC BBNVY BEC BENPR BGLVJ BHPHI BKSAR C1K CCPQU D1I DWQXO FR3 FYUFA GHDGH GNUQQ GUQSH H94 HCIFZ K9. KB. KB0 KL. L6V LK8 M0K M0S M1P M2M M2O M2P M7N M7P M7S MBDVC NAPCQ P5Z P62 P64 PATMY PCBAR PDBOC PQEST PQQKQ PQUKI PSYQQ PTHSS PYCSY Q9U R05 RC3 S0X SOI 7X8 5PM |
| DOI | 10.1038/nature10490 |
| DatabaseName | Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef Gale In Context: Middle School ProQuest Central (Corporate) Animal Behavior Abstracts Bacteriology Abstracts (Microbiology B) Calcium & Calcified Tissue Abstracts Chemoreception Abstracts ProQuest Nursing and Allied Health Journals Ecology Abstracts Entomology Abstracts (Full archive) Environment Abstracts Immunology Abstracts Meteorological & Geoastrophysical Abstracts Neurosciences Abstracts Nucleic Acids Abstracts Oncogenes and Growth Factors Abstracts Virology and AIDS Abstracts Agricultural Science Collection ProQuest Health & Medical Collection ProQuest Central (purchase pre-March 2016) Biology Database (Alumni Edition) Medical Database (Alumni Edition) Psychology Database (Alumni) Science Database (Alumni Edition) STEM Database ProQuest Pharma Collection ProQuest Public Health Database Technology Research Database ProQuest SciTech Collection ProQuest Technology Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) Research Library (Alumni Edition) Materials Science & Engineering Collection ProQuest Central (Alumni) ProQuest Central UK/Ireland Advanced Technologies & Aerospace Database (1962 - current) ProQuest Agriculture & Environmental Science Database ProQuest Central Essentials Biological Science Collection eLibrary AUTh Library subscriptions: ProQuest Central Technology Collection ProQuest Natural Science Collection Earth, Atmospheric & Aquatic Science Collection Environmental Sciences and Pollution Management ProQuest One Community College ProQuest Materials Science Collection ProQuest Central Engineering Research Database Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student Research Library Prep AIDS and Cancer Research Abstracts SciTech Premium Collection (Proquest) (PQ_SDU_P3) ProQuest Health & Medical Complete (Alumni) ProQuest Materials Science Database Nursing & Allied Health Database (Alumni Edition) Meteorological & Geoastrophysical Abstracts - Academic ProQuest Engineering Collection Biological Sciences Agriculture Science Database Health & Medical Collection (Alumni Edition) PML(ProQuest Medical Library) Psychology Database (ProQuest) ProQuest research library ProQuest Science Journals Algology Mycology and Protozoology Abstracts (Microbiology C) Biological Science Database ProQuest Engineering Database Research Library (Corporate) Nursing & Allied Health Premium ProQuest Advanced Technologies & Aerospace Database ProQuest Advanced Technologies & Aerospace Collection Biotechnology and BioEngineering Abstracts Environmental Science Database ProQuest Earth, Atmospheric & Aquatic Science Database Materials Science Collection ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition ProQuest One Psychology Engineering Collection Environmental Science Collection ProQuest Central Basic University of Michigan Genetics Abstracts SIRS Editorial Environment Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) |
| DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef Agricultural Science Database ProQuest One Psychology Research Library Prep ProQuest Central Student Oncogenes and Growth Factors Abstracts ProQuest Advanced Technologies & Aerospace Collection ProQuest Central Essentials Nucleic Acids Abstracts elibrary ProQuest AP Science SciTech Premium Collection Environmental Sciences and Pollution Management Health Research Premium Collection Meteorological & Geoastrophysical Abstracts Natural Science Collection Biological Science Collection Chemoreception Abstracts ProQuest Medical Library (Alumni) Engineering Collection Advanced Technologies & Aerospace Collection Engineering Database Virology and AIDS Abstracts ProQuest Science Journals (Alumni Edition) ProQuest Biological Science Collection ProQuest One Academic Eastern Edition Earth, Atmospheric & Aquatic Science Database Agricultural Science Collection ProQuest Hospital Collection ProQuest Technology Collection Health Research Premium Collection (Alumni) Biological Science Database Ecology Abstracts Neurosciences Abstracts ProQuest Hospital Collection (Alumni) Biotechnology and BioEngineering Abstracts Environmental Science Collection Entomology Abstracts Nursing & Allied Health Premium ProQuest Health & Medical Complete ProQuest One Academic UKI Edition Environmental Science Database ProQuest Nursing & Allied Health Source (Alumni) Engineering Research Database ProQuest One Academic Calcium & Calcified Tissue Abstracts Meteorological & Geoastrophysical Abstracts - Academic University of Michigan Technology Collection Technology Research Database SIRS Editorial Materials Science Collection ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College Research Library (Alumni Edition) ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Biology Journals (Alumni Edition) ProQuest Central Earth, Atmospheric & Aquatic Science Collection Genetics Abstracts ProQuest Engineering Collection Health and Medicine Complete (Alumni Edition) ProQuest Central Korea Bacteriology Abstracts (Microbiology B) Algology Mycology and Protozoology Abstracts (Microbiology C) Agricultural & Environmental Science Collection AIDS and Cancer Research Abstracts Materials Science Database ProQuest Research Library ProQuest Materials Science Collection ProQuest Public Health ProQuest Central Basic ProQuest Science Journals ProQuest Nursing & Allied Health Source ProQuest Psychology Journals (Alumni) ProQuest SciTech Collection Advanced Technologies & Aerospace Database ProQuest Medical Library ProQuest Psychology Journals Animal Behavior Abstracts Materials Science & Engineering Collection Immunology Abstracts Environment Abstracts ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | Agricultural Science Database MEDLINE - Academic MEDLINE |
| Database_xml | – sequence: 1 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: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 3 dbid: 8FG name: ProQuest Technology Collection url: https://search.proquest.com/technologycollection1 sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Sciences (General) Physics |
| EISSN | 1476-4687 |
| EndPage | 118 |
| ExternalDocumentID | 2490125091 A270042887 10_1038_nature10490 21979051 24569712 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GeographicLocations | United States United Kingdom |
| GeographicLocations_xml | – name: United Kingdom – name: United States |
| GrantInformation_xml | – fundername: Medical Research Council grantid: MC_U120097112 – fundername: British Heart Foundation grantid: SP/10/10/28431 – fundername: Wellcome Trust grantid: 087183 – fundername: Medical Research Council grantid: MC_U120085815 – fundername: Wellcome Trust : grantid: 087183 || WT |
| GroupedDBID | --- --Z -DZ -ET -~X .55 .CO .HR .XZ 00M 07C 08P 0R~ 0WA 123 186 1OL 1VR 29M 2KS 2XV 39C 3V. 4.4 41X 53G 5RE 6TJ 70F 7RV 7X2 7X7 7XC 85S 88A 88E 88I 8AF 8AO 8C1 8CJ 8FE 8FG 8FH 8FI 8FJ 8G5 8R4 8R5 8WZ 97F 97L A6W A7Z A8Z AAEEF AAHBH AAHTB AAIKC AAKAB AAKAS AAMNW AASDW AAYEP ABAWZ ABDBF ABFSI ABIVO ABJCF ABJNI ABLJU ABOCM ABPEJ ABPPZ ABUWG ABVXF ABWJO ABZEH ACBEA ACBWK ACGFO ACGFS ACGOD ACIWK ACKOT ACMJI ACNCT ACPRK ACWUS ADBBV ADFRT ADUKH ADYSU ADZCM AENEX AFFNX AFKRA AFLOW AFRAH AFRQD AFSHS AGAYW AGCDD AGEZK AGHSJ AGHTU AGNAY AGSOS AHMBA AHSBF AIDAL AIDUJ AIYXT ALFFA ALIPV ALMA_UNASSIGNED_HOLDINGS AMTXH APEBS ARAPS ARMCB ARTTT ASPBG ATCPS ATWCN AVWKF AXYYD AZFZN AZQEC B-7 B0M BBNVY BCR BCU BDKGC BEC BENPR BGLVJ BHPHI BIN BKEYQ BKKNO BKSAR BLC BPHCQ BVXVI CCPQU CJ0 CS3 D1I D1J D1K DO4 DU5 DWQXO E.- E.L EAD EAP EAS EAZ EBC EBD EBO EBS ECC EE. EJD EMB EMF EMH EMK EMOBN EPL EPS ESE ESN ESTFP ESX EX3 EXGXG F20 F5P FEDTE FQGFK FSGXE FYUFA GNUQQ GUQSH HCIFZ HMCUK HVGLF HZ~ I-F IAO ICQ IEA IEP IGS IH2 IHR INH INR IOF IPY ISR ITC K6- KB. KOO L-9 L6V L7B LK5 LK8 LSO M0K M0L M1P M2M M2O M2P M7P M7R M7S N9A NAPCQ NEJ NEPJS O9- OBC OES OHH OHT OMK OVD P-O P2P P62 PATMY PCBAR PDBOC PEA PM3 PQQKQ PROAC PSQYO PSYQQ PTHSS PYCSY Q2X R05 RND RNS RNT RNTTT RXW S0X SC5 SHXYY SIXXV SJFOW SJN SNYQT SV3 TAE TAOOD TBHMF TDRGL TEORI TH9 TN5 TSG TUS TWZ U5U UIG UKHRP UKR UMD UQL VQA VVN WH7 WOW X7M XIH XKW XZL Y6R YAE YCJ YFH YNT YOC YQT YR2 YXB YZZ ZCA ZE2 ZKB ~02 ~7V ~88 ~8M ~G0 ~KM .-4 .GJ 08R 0B8 1CY 1VW 354 3EH 3O- 41~ 42X 4R4 663 68V 79B 9M8 AADEA AADWK AAEXX AAGJQ AAJMP AAJWC AAJYS AAPBV AAUGY AAVBQ AAYJO AAYOK AAZLF ABEEJ ABEFU ABGFU ABGIJ ABPTK ABTAH ACBMV ACBNA ACBRV ACBTR ACBYP ACIGE ACTDY ACTTH ACVWB ADFPY ADMDM ADQMX ADRHT ADZGE AEDAW AEFTE AETEA AFDAS AFFDN AFHKK AFMIJ AFNRJ AGGBP AHGBK AJDOV AJUXI AMRJV BES BKOMP DB5 FA8 FAC G8K HG6 I-U IQODW J5H MVM N4W PV9 QS- R4F RHI SKT TUD U1R UAO UBY UHB USG VOH X7L XFK XOL YJ6 YQI YQJ YV5 YXA YYP YYQ ZA5 ZCG ZGI ZHY ZKG ZY4 AAYZH CGR CUY CVF ECM EIF NPM AAYXX CITATION NXXTH AGPPL AHPSJ AEQTP 7QG 7QL 7QP 7QR 7SN 7SS 7ST 7T5 7TG 7TK 7TM 7TO 7U9 7XB 8FD 8FK C1K FR3 H94 K9. KL. M7N MBDVC P64 PQEST PQUKI Q9U RC3 SOI 7X8 5PM |
| ID | FETCH-LOGICAL-c676t-89a8987967775155e8b2c1facfeb41644acadc95f915ccccd0a912ff952123813 |
| IEDL.DBID | 7X7 |
| ISSN | 0028-0836 1476-4687 |
| IngestDate | Tue Sep 17 21:12:56 EDT 2024 Sat Oct 26 04:55:05 EDT 2024 Thu Oct 10 20:59:32 EDT 2024 Thu Feb 22 23:49:56 EST 2024 Fri Feb 02 04:54:26 EST 2024 Tue Dec 12 21:18:09 EST 2023 Fri Feb 02 04:03:07 EST 2024 Thu Aug 01 19:54:55 EDT 2024 Thu Aug 01 20:02:57 EDT 2024 Thu Sep 26 19:05:08 EDT 2024 Sat Nov 02 12:29:15 EDT 2024 Sun Oct 29 17:08:39 EDT 2023 Fri Oct 11 20:46:31 EDT 2024 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 7367 |
| Keywords | Hypertrophic cardiomyopathy Cardiovascular disease Mitochondria Pathogenesis Myocardial disease Heart disease |
| Language | English |
| License | CC BY 4.0 Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c676t-89a8987967775155e8b2c1facfeb41644acadc95f915ccccd0a912ff952123813 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://pubmed.ncbi.nlm.nih.gov/PMC3189541 |
| PMID | 21979051 |
| PQID | 899251873 |
| PQPubID | 40569 |
| PageCount | 5 |
| ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_3189541 proquest_miscellaneous_896830841 proquest_journals_899251873 gale_infotracmisc_A270042887 gale_infotracgeneralonefile_A270042887 gale_infotraccpiq_270042887 gale_infotracacademiconefile_A270042887 gale_incontextgauss_ISR_A270042887 gale_incontextgauss_ATWCN_A270042887 crossref_primary_10_1038_nature10490 pubmed_primary_21979051 pascalfrancis_primary_24569712 springer_journals_10_1038_nature10490 |
| PublicationCentury | 2000 |
| PublicationDate | 2011-10-06 |
| PublicationDateYYYYMMDD | 2011-10-06 |
| PublicationDate_xml | – month: 10 year: 2011 text: 2011-10-06 day: 06 |
| PublicationDecade | 2010 |
| PublicationPlace | London |
| PublicationPlace_xml | – name: London – name: England |
| PublicationSubtitle | International weekly journal of science |
| PublicationTitle | Nature (London) |
| PublicationTitleAbbrev | Nature |
| PublicationTitleAlternate | Nature |
| PublicationYear | 2011 |
| Publisher | Nature Publishing Group UK Nature Publishing Group |
| Publisher_xml | – name: Nature Publishing Group UK – name: Nature Publishing Group |
| References | Spiegelman (CR24) 2007; 287 Tiranti (CR26) 1995; 25 Dai (CR21) 2011; 108 Lewis (CR29) 2007; 87 Wu (CR10) 1999; 98 Petretto (CR7) 2008; 40 Li, Luo, Wang (CR8) 2001; 412 Siegel (CR14) 2003; 23 Wang (CR28) 1999; 21 Irvine (CR17) 2005; 25 Hill, Olson (CR12) 2008; 358 Inomata (CR13) 2005; 28 Heinig (CR6) 2010; 467 Vasan (CR3) 2009; 302 Wong, Marwick (CR5) 2007; 4 Arad (CR20) 2002; 109 David, Sasaki, Yu, Dawson, Dawson (CR16) 2006; 13 Bahi (CR19) 2006; 281 Dufour (CR9) 2007; 5 Lorell, Carabello (CR2) 2000; 102 Zhang, Horvath (CR23) 2005; 4 Post, Larson, Myers, Galderisi, Levy (CR1) 1997; 30 Vahsen (CR30) 2004; 23 Seddon, Looi, Shah (CR22) 2007; 93 Rothfuss (CR27) 2009; 18 Finck, Kelly (CR11) 2006; 116 Temme (CR18) 2009; 284 McGavock, Victor, Unger, Szczepaniak (CR4) 2006; 144 Cote, Ruiz-Carrillo (CR25) 1993; 261 Büttner (CR15) 2007; 25 22302752 - Circ Res. 2012 Feb 3;110(3):378-80 N Vahsen (BFnature10490_CR30) 2004; 23 BM Spiegelman (BFnature10490_CR24) 2007; 287 AK Siegel (BFnature10490_CR14) 2003; 23 H Inomata (BFnature10490_CR13) 2005; 28 RA Irvine (BFnature10490_CR17) 2005; 25 BH Lorell (BFnature10490_CR2) 2000; 102 KK David (BFnature10490_CR16) 2006; 13 C Temme (BFnature10490_CR18) 2009; 284 O Rothfuss (BFnature10490_CR27) 2009; 18 V Tiranti (BFnature10490_CR26) 1995; 25 LY Li (BFnature10490_CR8) 2001; 412 E Petretto (BFnature10490_CR7) 2008; 40 M Heinig (BFnature10490_CR6) 2010; 467 M Arad (BFnature10490_CR20) 2002; 109 M Seddon (BFnature10490_CR22) 2007; 93 C Wong (BFnature10490_CR5) 2007; 4 J Wang (BFnature10490_CR28) 1999; 21 WS Post (BFnature10490_CR1) 1997; 30 Z Wu (BFnature10490_CR10) 1999; 98 JA Hill (BFnature10490_CR12) 2008; 358 B Zhang (BFnature10490_CR23) 2005; 4 BN Finck (BFnature10490_CR11) 2006; 116 S Büttner (BFnature10490_CR15) 2007; 25 W Lewis (BFnature10490_CR29) 2007; 87 J Cote (BFnature10490_CR25) 1993; 261 JM McGavock (BFnature10490_CR4) 2006; 144 RS Vasan (BFnature10490_CR3) 2009; 302 DF Dai (BFnature10490_CR21) 2011; 108 N Bahi (BFnature10490_CR19) 2006; 281 CR Dufour (BFnature10490_CR9) 2007; 5 |
| References_xml | – volume: 109 start-page: 357 year: 2002 end-page: 362 ident: CR20 article-title: Constitutively active AMP kinase mutations cause glycogen storage disease mimicking hypertrophic cardiomyopathy publication-title: J. Clin. Invest. doi: 10.1172/JCI0214571 contributor: fullname: Arad – volume: 116 start-page: 615 year: 2006 end-page: 622 ident: CR11 article-title: PGC-1 coactivators: inducible regulators of energy metabolism in health and disease publication-title: J. Clin. Invest. doi: 10.1172/JCI27794 contributor: fullname: Kelly – volume: 25 start-page: 233 year: 2007 end-page: 246 ident: CR15 article-title: Endonuclease G regulates budding yeast life and death publication-title: Mol. Cell doi: 10.1016/j.molcel.2006.12.021 contributor: fullname: Büttner – volume: 23 start-page: 4679 year: 2004 end-page: 4689 ident: CR30 article-title: AIF deficiency compromises oxidative phosphorylation publication-title: EMBO J. doi: 10.1038/sj.emboj.7600461 contributor: fullname: Vahsen – volume: 467 start-page: 460 year: 2010 end-page: 464 ident: CR6 article-title: A -acting locus regulates an anti-viral expression network and type 1 diabetes risk publication-title: Nature doi: 10.1038/nature09386 contributor: fullname: Heinig – volume: 21 start-page: 133 year: 1999 end-page: 137 ident: CR28 article-title: Dilated cardiomyopathy and atrioventricular conduction blocks induced by heart-specific inactivation of mitochondrial DNA gene expression publication-title: Nature Genet. doi: 10.1038/5089 contributor: fullname: Wang – volume: 358 start-page: 1370 year: 2008 end-page: 1380 ident: CR12 article-title: Cardiac plasticity publication-title: N. Engl. J. Med. doi: 10.1056/NEJMra072139 contributor: fullname: Olson – volume: 102 start-page: 470 year: 2000 end-page: 479 ident: CR2 article-title: Left ventricular hypertrophy: pathogenesis, detection, and prognosis publication-title: Circulation doi: 10.1161/01.CIR.102.4.470 contributor: fullname: Carabello – volume: 108 start-page: 837 year: 2011 end-page: 846 ident: CR21 article-title: Mitochondrial oxidative stress mediates angiotensin II-induced cardiac hypertrophy and Gαq overexpression-induced heart failure publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.110.232306 contributor: fullname: Dai – volume: 87 start-page: 326 year: 2007 end-page: 335 ident: CR29 article-title: Decreased mtDNA, oxidative stress, cardiomyopathy, and death from transgenic cardiac targeted human mutant polymerase γ publication-title: Lab. Invest. doi: 10.1038/labinvest.3700523 contributor: fullname: Lewis – volume: 4 start-page: 17 year: 2005 ident: CR23 article-title: A general framework for weighted gene co-expression network analysis publication-title: Stat. Appl. Genet. Mol. Biol. doi: 10.2202/1544-6115.1128 contributor: fullname: Horvath – volume: 144 start-page: 517 year: 2006 end-page: 524 ident: CR4 article-title: Adiposity of the heart, revisited publication-title: Ann. Intern. Med. doi: 10.7326/0003-4819-144-7-200604040-00011 contributor: fullname: Szczepaniak – volume: 13 start-page: 1147 year: 2006 end-page: 1155 ident: CR16 article-title: EndoG is dispensable in embryogenesis and apoptosis publication-title: Cell Death Differ. doi: 10.1038/sj.cdd.4401787 contributor: fullname: Dawson – volume: 287 start-page: 60 year: 2007 end-page: 69 ident: CR24 article-title: Transcriptional control of mitochondrial energy metabolism through the PGC1 coactivators publication-title: Novartis Found. Symp. contributor: fullname: Spiegelman – volume: 25 start-page: 559 year: 1995 end-page: 564 ident: CR26 article-title: Chromosomal localization of mitochondrial transcription factor A (TCF6), single-stranded DNA-binding protein (SSBP), and endonuclease G (ENDOG), three human housekeeping genes involved in mitochondrial biogenesis publication-title: Genomics doi: 10.1016/0888-7543(95)80058-T contributor: fullname: Tiranti – volume: 5 start-page: 345 year: 2007 end-page: 356 ident: CR9 article-title: Genome-wide orchestration of cardiac functions by the orphan nuclear receptors ERRα and γ publication-title: Cell Metab. doi: 10.1016/j.cmet.2007.03.007 contributor: fullname: Dufour – volume: 23 start-page: 1211 year: 2003 end-page: 1217 ident: CR14 article-title: Genetic loci contribute to the progression of vascular and cardiac hypertrophy in salt-sensitive spontaneous hypertension publication-title: Arterioscler. Thromb. Vasc. Biol. doi: 10.1161/01.ATV.0000079509.20542.C9 contributor: fullname: Siegel – volume: 28 start-page: 273 year: 2005 end-page: 281 ident: CR13 article-title: Identification of quantitative trait loci for cardiac hypertrophy in two different strains of the spontaneously hypertensive rat publication-title: Hypertens. Res. doi: 10.1291/hypres.28.273 contributor: fullname: Inomata – volume: 261 start-page: 765 year: 1993 end-page: 769 ident: CR25 article-title: Primers for mitochondrial DNA replication generated by endonuclease G publication-title: Science doi: 10.1126/science.7688144 contributor: fullname: Ruiz-Carrillo – volume: 281 start-page: 22943 year: 2006 end-page: 22952 ident: CR19 article-title: Switch from caspase-dependent to caspase-independent death during heart development: essential role of endonuclease G in ischemia-induced DNA processing of differentiated cardiomyocytes publication-title: J. Biol. Chem. doi: 10.1074/jbc.M601025200 contributor: fullname: Bahi – volume: 30 start-page: 1025 year: 1997 end-page: 1028 ident: CR1 article-title: Heritability of left ventricular mass: the Framingham Heart Study publication-title: Hypertension doi: 10.1161/01.HYP.30.5.1025 contributor: fullname: Levy – volume: 284 start-page: 8337 year: 2009 end-page: 8348 ident: CR18 article-title: The gene encodes a high affinity inhibitor for endonuclease G publication-title: J. Biol. Chem. doi: 10.1074/jbc.M808319200 contributor: fullname: Temme – volume: 18 start-page: 3832 year: 2009 end-page: 3850 ident: CR27 article-title: Parkin protects mitochondrial genome integrity and supports mitochondrial DNA repair publication-title: Hum. Mol. Genet. doi: 10.1093/hmg/ddp327 contributor: fullname: Rothfuss – volume: 412 start-page: 95 year: 2001 end-page: 99 ident: CR8 article-title: Endonuclease G is an apoptotic DNase when released from mitochondria publication-title: Nature doi: 10.1038/35083620 contributor: fullname: Wang – volume: 40 start-page: 546 year: 2008 end-page: 552 ident: CR7 article-title: Integrated genomic approaches implicate osteoglycin (Ogn) in the regulation of left ventricular mass publication-title: Nature Genet. doi: 10.1038/ng.134 contributor: fullname: Petretto – volume: 25 start-page: 294 year: 2005 end-page: 302 ident: CR17 article-title: Generation and characterization of endonuclease G null mice publication-title: Mol. Cell. Biol. doi: 10.1128/MCB.25.1.294-302.2005 contributor: fullname: Irvine – volume: 4 start-page: 436 year: 2007 end-page: 443 ident: CR5 article-title: Obesity cardiomyopathy: pathogenesis and pathophysiology publication-title: Nature Clin. Pract. Cardiovasc. Med. doi: 10.1038/ncpcardio0943 contributor: fullname: Marwick – volume: 93 start-page: 903 year: 2007 end-page: 907 ident: CR22 article-title: Oxidative stress and redox signalling in cardiac hypertrophy and heart failure publication-title: Heart doi: 10.1136/hrt.2005.068270 contributor: fullname: Shah – volume: 98 start-page: 115 year: 1999 end-page: 124 ident: CR10 article-title: Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator PGC-1 publication-title: Cell doi: 10.1016/S0092-8674(00)80611-X contributor: fullname: Wu – volume: 302 start-page: 168 year: 2009 end-page: 178 ident: CR3 article-title: Genetic variants associated with cardiac structure and function: a meta-analysis and replication of genome-wide association data publication-title: J. Am. Med. Assoc. doi: 10.1001/jama.2009.978-a contributor: fullname: Vasan – volume: 93 start-page: 903 year: 2007 ident: BFnature10490_CR22 publication-title: Heart doi: 10.1136/hrt.2005.068270 contributor: fullname: M Seddon – volume: 28 start-page: 273 year: 2005 ident: BFnature10490_CR13 publication-title: Hypertens. Res. doi: 10.1291/hypres.28.273 contributor: fullname: H Inomata – volume: 25 start-page: 294 year: 2005 ident: BFnature10490_CR17 publication-title: Mol. Cell. Biol. doi: 10.1128/MCB.25.1.294-302.2005 contributor: fullname: RA Irvine – volume: 25 start-page: 233 year: 2007 ident: BFnature10490_CR15 publication-title: Mol. Cell doi: 10.1016/j.molcel.2006.12.021 contributor: fullname: S Büttner – volume: 109 start-page: 357 year: 2002 ident: BFnature10490_CR20 publication-title: J. Clin. Invest. doi: 10.1172/JCI0214571 contributor: fullname: M Arad – volume: 116 start-page: 615 year: 2006 ident: BFnature10490_CR11 publication-title: J. Clin. Invest. doi: 10.1172/JCI27794 contributor: fullname: BN Finck – volume: 284 start-page: 8337 year: 2009 ident: BFnature10490_CR18 publication-title: J. Biol. Chem. doi: 10.1074/jbc.M808319200 contributor: fullname: C Temme – volume: 18 start-page: 3832 year: 2009 ident: BFnature10490_CR27 publication-title: Hum. Mol. Genet. doi: 10.1093/hmg/ddp327 contributor: fullname: O Rothfuss – volume: 287 start-page: 60 year: 2007 ident: BFnature10490_CR24 publication-title: Novartis Found. Symp. doi: 10.1002/9780470725207.ch5 contributor: fullname: BM Spiegelman – volume: 23 start-page: 1211 year: 2003 ident: BFnature10490_CR14 publication-title: Arterioscler. Thromb. Vasc. Biol. doi: 10.1161/01.ATV.0000079509.20542.C9 contributor: fullname: AK Siegel – volume: 102 start-page: 470 year: 2000 ident: BFnature10490_CR2 publication-title: Circulation doi: 10.1161/01.CIR.102.4.470 contributor: fullname: BH Lorell – volume: 25 start-page: 559 year: 1995 ident: BFnature10490_CR26 publication-title: Genomics doi: 10.1016/0888-7543(95)80058-T contributor: fullname: V Tiranti – volume: 13 start-page: 1147 year: 2006 ident: BFnature10490_CR16 publication-title: Cell Death Differ. doi: 10.1038/sj.cdd.4401787 contributor: fullname: KK David – volume: 21 start-page: 133 year: 1999 ident: BFnature10490_CR28 publication-title: Nature Genet. doi: 10.1038/5089 contributor: fullname: J Wang – volume: 23 start-page: 4679 year: 2004 ident: BFnature10490_CR30 publication-title: EMBO J. doi: 10.1038/sj.emboj.7600461 contributor: fullname: N Vahsen – volume: 4 start-page: 17 year: 2005 ident: BFnature10490_CR23 publication-title: Stat. Appl. Genet. Mol. Biol. doi: 10.2202/1544-6115.1128 contributor: fullname: B Zhang – volume: 281 start-page: 22943 year: 2006 ident: BFnature10490_CR19 publication-title: J. Biol. Chem. doi: 10.1074/jbc.M601025200 contributor: fullname: N Bahi – volume: 4 start-page: 436 year: 2007 ident: BFnature10490_CR5 publication-title: Nature Clin. Pract. Cardiovasc. Med. doi: 10.1038/ncpcardio0943 contributor: fullname: C Wong – volume: 358 start-page: 1370 year: 2008 ident: BFnature10490_CR12 publication-title: N. Engl. J. Med. doi: 10.1056/NEJMra072139 contributor: fullname: JA Hill – volume: 87 start-page: 326 year: 2007 ident: BFnature10490_CR29 publication-title: Lab. Invest. doi: 10.1038/labinvest.3700523 contributor: fullname: W Lewis – volume: 40 start-page: 546 year: 2008 ident: BFnature10490_CR7 publication-title: Nature Genet. doi: 10.1038/ng.134 contributor: fullname: E Petretto – volume: 302 start-page: 168 year: 2009 ident: BFnature10490_CR3 publication-title: J. Am. Med. Assoc. doi: 10.1001/jama.2009.978-a contributor: fullname: RS Vasan – volume: 144 start-page: 517 year: 2006 ident: BFnature10490_CR4 publication-title: Ann. Intern. Med. doi: 10.7326/0003-4819-144-7-200604040-00011 contributor: fullname: JM McGavock – volume: 261 start-page: 765 year: 1993 ident: BFnature10490_CR25 publication-title: Science doi: 10.1126/science.7688144 contributor: fullname: J Cote – volume: 412 start-page: 95 year: 2001 ident: BFnature10490_CR8 publication-title: Nature doi: 10.1038/35083620 contributor: fullname: LY Li – volume: 108 start-page: 837 year: 2011 ident: BFnature10490_CR21 publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.110.232306 contributor: fullname: DF Dai – volume: 467 start-page: 460 year: 2010 ident: BFnature10490_CR6 publication-title: Nature doi: 10.1038/nature09386 contributor: fullname: M Heinig – volume: 98 start-page: 115 year: 1999 ident: BFnature10490_CR10 publication-title: Cell doi: 10.1016/S0092-8674(00)80611-X contributor: fullname: Z Wu – volume: 30 start-page: 1025 year: 1997 ident: BFnature10490_CR1 publication-title: Hypertension doi: 10.1161/01.HYP.30.5.1025 contributor: fullname: WS Post – volume: 5 start-page: 345 year: 2007 ident: BFnature10490_CR9 publication-title: Cell Metab. doi: 10.1016/j.cmet.2007.03.007 contributor: fullname: CR Dufour |
| SSID | ssj0005174 |
| Score | 2.4562547 |
| Snippet | Endonuclease G and heart disease
Elevated left ventricular mass, a highly heritable trait, is an important risk factor for heart failure and death. Stuart Cook... Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have... Left ventricular mass (LVM) is a highly heritable trait (1) and an independent risk factor for all-cause mortality (2). So far, genomewide association studies... Left ventricular mass (LVM) is a highly heritable trait 1 and an independent risk factor for all-cause mortality 2 . To date, genome-wide association studies... |
| SourceID | pubmedcentral proquest gale crossref pubmed pascalfrancis springer |
| SourceType | Open Access Repository Aggregation Database Index Database Publisher |
| StartPage | 114 |
| SubjectTerms | 631/443/319/333 631/443/592/1540 631/80/304 692/699/317 Animals Apoptosis Biological and medical sciences Biomarkers Blood Blood pressure Body Weight - genetics Cardiology. Vascular system Cardiomegaly - enzymology Cardiomegaly - genetics Cardiomegaly - pathology Cardiomegaly - physiopathology Cardiomyocytes Cardiovascular diseases Cell Respiration Chromosomes, Mammalian - genetics Crosses, Genetic Diagnosis Endodeoxyribonucleases - deficiency Endodeoxyribonucleases - genetics Endodeoxyribonucleases - metabolism ERRalpha Estrogen-Related Receptor Female Gene Expression Regulation Genes, Mitochondrial - genetics Genetic aspects Genetic factors Genetics Genomes Heart Heart enlargement Humanities and Social Sciences Hypertrophy, Left Ventricular - enzymology Hypertrophy, Left Ventricular - genetics Hypertrophy, Left Ventricular - pathology Hypertrophy, Left Ventricular - physiopathology Kinases letter Lipid Metabolism Male Medical sciences Mitochondria Mitochondria - genetics Mitochondria - metabolism Mitochondria - pathology multidisciplinary Myocarditis. Cardiomyopathies Nucleases Organ Size - genetics Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Physiological aspects Quantitative Trait Loci - genetics Rats Rats, Inbred Strains Reactive Oxygen Species - metabolism Receptors, Estrogen - metabolism Risk factors RNA-Binding Proteins - metabolism Rodents Science Science (multidisciplinary) Studies Transcription Factors - metabolism |
| Title | Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function |
| URI | https://link.springer.com/article/10.1038/nature10490 https://www.ncbi.nlm.nih.gov/pubmed/21979051 https://www.proquest.com/docview/899251873 https://www.proquest.com/docview/896830841 https://pubmed.ncbi.nlm.nih.gov/PMC3189541 |
| Volume | 478 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3db9MwELdgExISQmzACBuVhcbXQ7Q4X7afUKnaDSQqNDatb5Fjx1slSLqm5e_nLnHbZVTkIS93tizf-c72nX9HyDEingih8cY9Nn6sZOKLxBif5WGUClVI0zyk_T5Ozy7jb5Nk4nJzapdWubKJjaE2lcY78hM4F4ArFjz6PLv1sWgUBlddBY2HZJeFQYpKzSd8k-FxD4TZPc8LInHSomYyDHt1HJIzy09mqoYpsm1ti22bz39zKO8FUhv_NHpGnrqNJe23mrBHHhTlPnnUJHjqep_suUVc048OafrTc3I1xFoeiGgMvoye0mlNFS2rP8UvajZpMrSyVDeKpOkNHFvni3kFwqGqNPQ3GAQwoKVBPaboJFHQL8jlaHgxOPNdpQVfpzxd-EIqIQWXKecca74UIg81s0rbIocdWxwrrYyWiZUs0fCZQEkWWiubl7-CRS_JTlmVxStCtYW2ykSJSqFdbqU0XOpI6tAEkQ20R45X053NWkCNrAmERyK7IxVgQ1FkCFFRYg7MtVrWdda_uBqMsz5Gy-HcJLhH3m5j-_rzvMP0wTHZCmSllXt5AANG8KsO52GHU8-mt9kd6vsO9boV17ZujjqMsGJ1h9zr6Nd6HjAILTkLYRgrhcucSamz9QLwCF1TsWfMkiuLaoksqYgCETOPHLTauemayQaKzSO8o7drBoQZ71LK6U0DNw5WXybY57uVhm8GtUVyr_87-EPyOFxlUaZHZGcxXxZvYFu3yHvN4oW_GDD8j057ZPfLcPzj_C8U9U_P |
| link.rule.ids | 230,315,783,787,888,12069,12236,12778,21401,27937,27938,31732,31733,33279,33280,33386,33387,33757,33758,43323,43592,43613,43818,74080,74349,74370,74637 |
| linkProvider | ProQuest |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3db9MwELegEwIJITa-wsaw0IDxEC3ftp9QmTo62Co0Om1vlmPHWyVIuqbl78eXOO08KvJ6Z8vyne_s3N3vENoDxBNKJfxxT5SfCJb6NFXKD_MozqgomGoKaU9H2fA8-XaZXtrcnNqmVXY2sTHUqpLwj_zAvAuMK6Yk_jy98aFpFARXbQeN-2gDkKpoD218GYx-nK1yPO7AMNsCvSCmBy1uZgiBL8clWcP8eCpqs0m67W6x7vr5bxblnVBq46GOnqIn9mqJ-60ubKJ7RbmFHjQpnrLeQpv2GNd432JNf3qGLgbQzQMwjY03w1_xpMYCl9Wf4hdWq0QZXGksG1WS-No8XGfzWWXEg0Wp8G9jEowJLRVoMgY3CaJ-js6PBuPDoW97LfgyI9ncp0xQRgnLCCHQ9aWgeSRDLaQucnNnSxIhhZIs1SxMpflUIFgYac2a2l8axi9Qr6zK4hXCUpuxQsWpyMy4XDOmCJMxk5EKYh1ID-11282nLaQGb0LhMeW3pGLYQBQcQCpKyIK5Eou65v3xxeGI9yFebl5OlHjo3Tq2459nDtNHy6QrIyspbO2BWTDAXzmc2w6nnE5u-C3qB4d61Ypr3TQ7DqM5s9Ih7zr6tdwHCEMzEkZmGZ3CcWtUar48Ah7CSyrMDHlyZVEtgCWjcUCT0EMvW-1cTR2yBozNQ8TR2yUDAI27lHJy3QCOG7vPUpjzfafhq0Wtkdzr_y7-LXo4HJ-e8JPj0fdt9CjqciqzHdSbzxbFG3PJm-e79ij_BV5nUNg |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3rb9MwELdgCISEEBuvsDEsNGB8iJp37E-oKisbjwrBpu2b5djxVgmSrmn5-7lz3EdGRb7e2bJ8Lzt3_h0hB4h4wpjCP-6J9hPJU5-lWvthEcUZkyXX9iHtt1F2fJZ8vkgvHKRQ48oqFz7ROmpdK_xH3oN7AYRilsc946oivn8cfphc-9hAChOtrpvGbXIHgmKCCs4Ga9UeNwCZ3VO9IGa9FkEzxBRYJzg5F_1gIhvYLtP2udh0EP23nvJGUtXGquEj8tAdMmm_1YptcqusdshdW-ypmh2y7Qy6oYcOdfr9Y3J-hH09EN0Y4hr9RMcNlbSq_5S_qF6VzNDaUGWVStEruMJOZ9MaBEVlpelvcA7gTCuNOk0xYKLQn5Cz4dHp4Nh3XRd8leXZzGdcMs5ynuV5jv1fSlZEKjRSmbKA01uSSCW14qnhYarg04HkYWQMt6-AWRg_JVtVXZXPCVUGxkodpzKDcYXhXOdcxVxFOohNoDxysNhuMWnBNYRNisdMrEkF2FAUAuEqKpT8pZw3jeifng9Goo-Zc7hDsdwjrzexnfz80WF655hMDbJS0r1CgAUjEFaHc7fDqSbja7FGfduhXrbi2jTNXocRrFd1yPsd_VruAyakeR5GsIyFwgnnXhqxNAaP0CUVZ8aKuaqs58iSsThgSeiRZ612rqYOuYVl80je0dslA0KOdynV-MpCj0ME4CnO-Wah4atFbZDci_8u_hW5BzYsvp6MvuyS-9GiuDLbI1uz6bx8Cae9WbFv7fgvTplTcg |
| 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=Endonuclease+G+is+a+novel+determinant+of+cardiac+hypertrophy+and+mitochondrial+function&rft.jtitle=Nature+%28London%29&rft.au=McDermott-Roe%2C+Chris&rft.au=Ye%2C+Junmei&rft.au=Ahmed%2C+Rizwan&rft.au=Sun%2C+Xi-Ming&rft.date=2011-10-06&rft.issn=1476-4687&rft.eissn=1476-4687&rft.volume=478&rft.issue=7367&rft.spage=114&rft_id=info:doi/10.1038%2Fnature10490&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0028-0836&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0028-0836&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0028-0836&client=summon |