A Direct HDAC4-MAP Kinase Crosstalk Activates Muscle Atrophy Program

Prolonged deficits in neural input activate pathological muscle remodeling, leading to atrophy. In denervated muscle, activation of the atrophy program requires HDAC4, a potent repressor of the master muscle transcription factor MEF2. However, the signaling mechanism that connects HDAC4, a protein d...

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Veröffentlicht in:	Molecular cell 2012-07, Vol.47 (1), p.122-132
Hauptverfasser:	Choi, Moon-Chang, Cohen, Todd J., Barrientos, Tomasa, Wang, Bin, Li, Ming, Simmons, Bryan J., Yang, Jeong Soo, Cox, Gregory A., Zhao, Yingming, Yao, Tso-Pang
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetylation Animals Blotting, Western Cell Line HEK293 Cells Histone Deacetylases - genetics Histone Deacetylases - metabolism Humans MAP Kinase Kinase Kinase 2 - genetics MAP Kinase Kinase Kinase 2 - metabolism MAP Kinase Signaling System Mice Mice, Inbred C57BL Mice, Transgenic mitogen-activated protein kinase Molecular Sequence Data Muscle Denervation Muscle, Skeletal - innervation Muscle, Skeletal - metabolism muscles muscular atrophy Muscular Atrophy - genetics Muscular Atrophy - metabolism Phosphorylation Protein Binding repressor proteins RNA Interference Transcription Factor AP-1 - genetics Transcription Factor AP-1 - metabolism
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