Tamamori Mimi | Department Of Biochemical Genetics Medical Research Instisute Graduate School Of Tokyo Medical And D

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著作論文

CYCLIN D1 AND CDK4 INDUCE HYPERTROPHY THROUGH PHOSPHORYLATION OF RNA POLYMERASE II C-TERMINAL DOMAIN IN NEONATAL RAT CARDIOMYOCYTES
IS157 Endothelin-1 Antagonizes Nitric Oxide-induced Bax Expression, Caspase-3 Activation and Subsequent Apoptosis of Neonatal Rat Cardiomyocytes
IS042 G1 Cyclin-Dependent Kinase Activity is Required for the Development of Cardiomyocyte Hypertrophy
ATF3 Inhibits Doxorubicin-induced Apoptosis in Cardiac Myocytes
Role and Relation of p70 S6 and Extracellular Signal-Regulated Kinases in the Phenotypic Changes of Hypertrophy of Cardiac Myocytes
G_1 Cyclins are Involved in the Mechanism of Cardiac Myocyte Hypertrophy Induced by Angiotensin II
IS028 Cyclin A Mediated p53-Independent Apoptosis in Cardiomyocytes Under Hypoxic Conditions
Overexpression of ATF3 Inhibits Doxorubicin-Induced Apoptosis through Downregulation of p53 Transcription in Cardiac Myocytes
Endogenous Nitric Oxide Inhibits Hypoxia-Reoxygenation-lnduced Myocardial Apoptosis with the Modulation of Cyclin A-Associated Kinase Activity
Cyclin A / cdk2 kinase activity regulates apoptosis of cardiomyocytes induced by doxorubicin
Nitric Oxide Inhibits Ischemia-Reperfusion-induced Myocardial Apoptosis by Suppression of Cyclin A-associated Kinase Activity
Transcriptional Represser ATF3 Protects Human Umbilical Vein Endothelial Cells from TNF-α-Induced Apoptosis through Downregulation of p53 Transcription

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