Raf-1 kinase activity is necessary and sufficient for gene expression changes but not sufficient for cellular morphology changes associated with cardiac myocyte hypertrophy.

This publication has 38 references indexed in Scilit:

• Mitogen-activated protein kinases mediate changes in gene expression, but not cytoskeletal organization associated with cardiac muscle cell hypertrophy.
  The Journal of cell biology, 1994
• The Tyrosine Kinase Inhibitor, Genistein, Prevents α-Adrenergic-Induced Cardiac Muscle Cell Hypertrophy by Inhibiting Activation of the Ras-MAP Kinase Signaling Pathway
  Biochemical and Biophysical Research Communications, 1994
• Ras-dependent activation of MAP kinase pathway mediated by G-protein βγ subunits
  Nature, 1994
• Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro
  Cell, 1993
• The interaction of SV40 small tumor antigen with protein phosphatase 2A stimulates the map kinase pathway and induces cell proliferation
  Cell, 1993
• Protein kinase Cα activates RAF-1 by direct phosphorylation
  Nature, 1993
• Endothelin‐1, phorbol esters and phenylephrine stimulate MAP kinase activities in ventricular cardiomyocytes
  FEBS Letters, 1993
• Activation of the MAP kinase pathway by the protein kinase raf
  Cell, 1992
• Stimulation of p21ras upon T-cell activation
  Nature, 1990
• Phorbol esters induce immediate-early genes and activate cardiac gene transcription in neonatal rat myocardial cells
  Journal of Molecular and Cellular Cardiology, 1990