BAIT

PARK2

PRKN
Parkinson disease (autosomal recessive, juvenile) 2, parkin
GO Process (48)
GO Function (21)
GO Component (21)

Gene Ontology Biological Process

Mus musculus
PREY

ABL1

AI325092, Abl, E430008G22Rik, c-Abl, RP23-65P13.3
c-abl oncogene 1, non-receptor tyrosine kinase
GO Process (57)
GO Function (18)
GO Component (16)

Gene Ontology Biological Process

Mus musculus

Affinity Capture-Western

An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner identified by Western blot with a specific polyclonal antibody or second epitope tag. This category is also used if an interacting protein is visualized directly by dye stain or radioactivity. Note that this differs from any co-purification experiment involving affinity capture in that the co-purification experiment involves at least one extra purification step to get rid of potential contaminating proteins.

Publication

Phosphorylation by the c-Abl protein tyrosine kinase inhibits parkin's ubiquitination and protective function.

Ko HS, Lee Y, Shin JH, Karuppagounder SS, Gadad BS, Koleske AJ, Pletnikova O, Troncoso JC, Dawson VL, Dawson TM

Mutations in PARK2/Parkin, which encodes a ubiquitin E3 ligase, cause autosomal recessive Parkinson disease (PD). Here we show that the nonreceptor tyrosine kinase c-Abl phosphorylates tyrosine 143 of parkin, inhibiting parkin's ubiquitin E3 ligase activity and protective function. c-Abl is activated by dopaminergic stress and by dopaminergic neurotoxins, 1-methyl-4-phenylpyridinium (MPP(+)) in vitro and in vivo by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), leading to ... [more]

Proc. Natl. Acad. Sci. U.S.A. Sep. 21, 2010; 107(38);16691-6 [Pubmed: 20823226]

Throughput

  • Low Throughput

Curated By

  • BioGRID