Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function

Nature

Volumn 478, Issue 7367, 2011, Pages 114-118

  McDermott Roe, Chris ^a   Ye, Junmei ^b   Ahmed, Rizwan ^a   Sun, Xi Ming ^a   Serafín, Anna ^c   Ware, James ^a   Bottolo, Leonardo ^a   Muckett, Phil ^a   Cañas, Xavier ^c   Zhang, Jisheng ^b   Rowe, Glenn C ^d   Buchan, Rachel ^a   Lu, Han ^a   Braithwaite, Adam ^a   Mancini, Massimiliano ^e   Hauton, David ^f   Martí, Ramon ^g   Garcí Arumí, Elena ^g   Hubner, Norbert ^h,i   Jacob, Howard ^j   Serikawa, Tadao ^k   Zidek, Vaclav ^l   Papousek, Frantisek ^l   Kolar, Frantisek ^l   Cardona, Maria ^b   Ruiz Meana, Marisol ^g   García Dorado, David ^g   Comella, Joan X ^m,n   Felkin, Leanne E ^o   Barton, Paul J R ^o,p   Arany, Zoltan ^d   Pravenec, Michal ^l   Petretto, Enrico ^a,o   Sanchis, Daniel ^b   Cook, Stuart A ^a,p   more..

^a HAMMERSMITH HOSPITAL   (United Kingdom)

^b UNIVERSITY OF LLEIDA   (Spain)

^c Platform of Applied Research on Laboratory Animal   (Spain)

^d BETH ISRAEL DEACONESS MEDICAL CENTER   (United States)

^e SAPIENZA UNIVERSITY OF ROME   (Italy)

^f UNIVERSITY OF BIRMINGHAM   (United Kingdom)

^g HOSPITAL UNIVERSITARI VALL D HEBRON   (Spain)

^h MAX DELBRÜCK CENTER FOR MOLECULAR MEDICINE   (Germany)

ⁱ CHARITÉ UNIVERSITÄTSMEDIZIN BERLIN   (Germany)

^j MEDICAL COLLEGE OF WISCONSIN   (United States)

^k KYOTO UNIVERSITY   (Japan)

^l INSTITUTE OF PHYSIOLOGY   (Czech Republic)

^m CENTRO DE INVESTIGACIÓN BIOMÉDICA EN RED SOBRE ENFERMEDADES NEURODEGENERATIVAS CIBERNED   (Spain)

ⁿ INSTITUT DE NEUROCIÈNCIES   (Spain)

^o IMPERIAL COLLEGE LONDON   (United Kingdom)

^p ROYAL BROMPTON AND HAREFIELD NHS FOUNDATION TRUST   (United Kingdom)

more..

Author keywords

[No Author keywords available]

Indexed keywords

ENDONUCLEASE G; ESTROGEN RELATED RECEPTOR ALPHA; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA COACTIVATOR 1ALPHA; REACTIVE OXYGEN METABOLITE;

APOPTOSIS; BIOMARKER; CARDIOLOGY; CARDIOVASCULAR DISEASE; CHROMOSOME; ENZYME ACTIVITY; GENETIC ANALYSIS; GENOME; INHIBITION; MORTALITY; MUTATION; RISK FACTOR;

APOPTOSIS; ARTICLE; BIOGENESIS; CELL DEGENERATION; CELL FUNCTION; CELL SIZE; DISORDERS OF MITOCHONDRIAL FUNCTIONS; GENE DELETION; GENE IDENTIFICATION; GENE LOCUS; GENE REGULATORY NETWORK; GENETIC ASSOCIATION; HEART FUNCTION; HEART MITOCHONDRION; HEART MUSCLE CELL; HEART VENTRICLE HYPERTROPHY; HUMAN; LOSS OF FUNCTION MUTATION; MITOCHONDRIAL GENOME; NONHUMAN; PRIORITY JOURNAL; QUANTITATIVE TRAIT LOCUS; STEATOSIS;

ANIMALS; APOPTOSIS; BODY WEIGHT; CARDIOMEGALY; CELL RESPIRATION; CHROMOSOMES, MAMMALIAN; CROSSES, GENETIC; ENDODEOXYRIBONUCLEASES; FEMALE; GENE EXPRESSION REGULATION; GENES, MITOCHONDRIAL; HYPERTROPHY, LEFT VENTRICULAR; LIPID METABOLISM; MALE; MITOCHONDRIA; ORGAN SIZE; QUANTITATIVE TRAIT LOCI; RATS; RATS, INBRED STRAINS; REACTIVE OXYGEN SPECIES; RECEPTORS, ESTROGEN; RNA-BINDING PROTEINS; TRANSCRIPTION FACTORS;

RATTUS;

EID: 80053897262     PISSN: 00280836     EISSN: 14764687     Source Type: Journal    
DOI: 10.1038/nature10490     Document Type: Article

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