A truncated fragment of p35, the Cdk5 kinase regulatory protein (TFP5), inhibits specifically hyperactive Cdk5/p25 activity and rescues the Alzheimer’s disease and Parkinson’s disease phenotype in model mice. To account for the selective inhibition of Cdk5/p25 activity, the p10 N-terminal domain of p35, absent in p25, spares Cdk5/p35.
The interaction of Munc 18 (p67) with the p10 domain of p35 protects in vivo Cdk5/p35 activity from inhibition by TFP5, a peptide derived from p35
N. Amin,Yali Zheng,Binukumar Bk,V. Shukla,Susan Skuntz,P. Grant,J. Steiner,M. Bhaskar,H. Pant
Published 2016 in Molecular Biology of the Cell
ABSTRACT
PUBLICATION RECORD
- Publication year
2016
- Venue
Molecular Biology of the Cell
- Publication date
2016-11-01
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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