Deletion of Akt1 causes heart defects and abnormal cardiomyocyte proliferation

Developmental Biology

Volumn 347, Issue 2, 2010, Pages 384-391

  Chang, Zai ^a   Zhang, Qin ^a   Feng, Qiuting ^a   Xu, Jie ^a   Teng, Teng ^a   Luan, Qing ^a   Shan, Congjia ^a   Hu, Yali ^a   Hemmings, Brian A ^b   Gao, Xiang ^a   Yang, Zhongzhou ^a  

^a NANJING UNIVERSITY   (China)

^b FRIEDRICH MIESCHER INSTITUTE FOR BIOMEDICAL RESEARCH   (Switzerland)

Author keywords

Akt PKB knockout; Heart defects; P38 MAPK

Indexed keywords

MITOGEN ACTIVATED PROTEIN KINASE P38; 3 PHOSPHOINOSITIDE DEPENDENT PROTEIN KINASE; AKT1 PROTEIN, MOUSE; MITOGEN ACTIVATED PROTEIN KINASE 14; PDPK1 PROTEIN, MOUSE; PROTEIN KINASE B; PROTEIN SERINE THREONINE KINASE;

AKT1 GENE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL PROLIFERATION; CONGENITAL HEART MALFORMATION; CONTROLLED STUDY; DEVELOPMENTAL DISORDER; ECHOCARDIOGRAPHY; EMBRYO; EMBRYO DEVELOPMENT; ENZYME ACTIVATION; ENZYME INHIBITION; GENE; GENE DELETION; HEART DEVELOPMENT; HEART MUSCLE CELL; HETEROZYGOTE; HISTOPATHOLOGY; MORTALITY; MOUSE; NONHUMAN; P38ALPHA GENE; PERINATAL PERIOD; PRIORITY JOURNAL; ANIMAL; DEFICIENCY; ECHOGRAPHY; EMBRYOLOGY; ENZYMOLOGY; FEMALE; GENETICS; KNOCKOUT MOUSE; MALE; METABOLISM; NEWBORN; PATHOLOGY; PREGNANCY; SIGNAL TRANSDUCTION;

MUS;

3-PHOSPHOINOSITIDE-DEPENDENT PROTEIN KINASES; ANIMALS; ANIMALS, NEWBORN; CELL PROLIFERATION; FEMALE; HEART DEFECTS, CONGENITAL; HETEROZYGOTE; MALE; MAP KINASE SIGNALING SYSTEM; MICE; MICE, KNOCKOUT; MITOGEN-ACTIVATED PROTEIN KINASE 14; MYOCYTES, CARDIAC; PREGNANCY; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION;

EID: 77957889287     PISSN: 00121606     EISSN: 1095564X     Source Type: Journal    
DOI: 10.1016/j.ydbio.2010.08.033     Document Type: Article

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