The complexity in regulation of MEF2D by chaperone-mediated autophagy.
Chaperone-mediated autophagy (CMA) targets specific cytoplasmic proteins for degradation by lysosomes and has been implicated to play a role in neurodegeneration. Our recent studies identify neuronal survival factor MEF2D as a direct substrate of CMA and show that dysregulation of this process may contribute to the pathogenesis of Parkinson disease. One interesting finding presented in our study is the apparent loss of DNA binding capacity by the accumulated MEF2D following inhibition of CMA. The possibilities and implication of this finding are discussed.
Yang
Qian
Q
Department of Pharmacology and Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Mao
Zixu
Z
D001343:Autophagy / Q000502:physiology*; D006801:Humans; D026161:MADS Domain Proteins / Q000378:metabolism*; D064326:MEF2 Transcription Factors; D018832:Molecular Chaperones / Q000378:metabolism*; D018006:Myogenic Regulatory Factors / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism; D010300:Parkinson Disease / Q000503:physiopathology
D026161:MADS Domain Proteins; D064326:MEF2 Transcription Factors; C578043:MEF2D protein, human; D018832:Molecular Chaperones; D018006:Myogenic Regulatory Factors