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...

Cijeli opis

Spremljeno u:
Bibliografski detalji
Glavni autori: Choi, Moon-Chang, Cohen, Todd J., Barrientos, Tomasa, Wang, Bin, Li, Ming, Simmons, Bryan J., Yang, Jeong Soo, Cox, Gregory A., Zhao, Ying-Ming, Yao, Tso-Pang
Format: Artigo
Jezik:Inglês
Izdano: 2012
Teme:
Article
Online pristup:https://ncbi.nlm.nih.gov/pmc/articles/PMC3398192/
https://ncbi.nlm.nih.gov/pubmed/22658415
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.molcel.2012.04.025
Oznake: Dodaj oznaku
Bez oznaka, Budi prvi tko označuje ovaj zapis!

Similar Items