Muscle ring finger protein-1 inhibits PKCε activation and prevents cardiomyocyte hypertrophy
R Arya, V Kedar, JR Hwang, H McDonough… - Journal of Cell …, 2004 - rupress.org
R Arya, V Kedar, JR Hwang, H McDonough, HH Li, J Taylor, C Patterson
Journal of Cell Biology, 2004•rupress.orgM stimulated interaction, MURF1 blocks PKCε translocation to focal adhesions, which is a
critical event in the hypertrophic signaling cascade. MURF1 inhibits focal adhesion
formation, and the activity of downstream effector ERK1/2 is also inhibited in the presence of
MURF1. MURF1 inhibits phenylephrine-induced (but not IGF-1–induced) increases in cell
size. These findings establish that MURF1 is a key regulator of the PKC-dependent
hypertrophic response and can blunt cardiomyocyte hypertrophy, which may have important …
critical event in the hypertrophic signaling cascade. MURF1 inhibits focal adhesion
formation, and the activity of downstream effector ERK1/2 is also inhibited in the presence of
MURF1. MURF1 inhibits phenylephrine-induced (but not IGF-1–induced) increases in cell
size. These findings establish that MURF1 is a key regulator of the PKC-dependent
hypertrophic response and can blunt cardiomyocyte hypertrophy, which may have important …
M stimulated interaction, MURF1 blocks PKCε translocation to focal adhesions, which is a critical event in the hypertrophic signaling cascade. MURF1 inhibits focal adhesion formation, and the activity of downstream effector ERK1/2 is also inhibited in the presence of MURF1. MURF1 inhibits phenylephrine-induced (but not IGF-1–induced) increases in cell size. These findings establish that MURF1 is a key regulator of the PKC-dependent hypertrophic response and can blunt cardiomyocyte hypertrophy, which may have important implications in the pathophysiology of clinical cardiac hypertrophy.
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