Curated Information
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Bone KM, et al. (2015) NPM-ALK mediates phosphorylation of MSH2 at tyrosine 238, creating a functional deficiency in MSH2 and the loss of mismatch repair. Blood Cancer J 5, e311 25978431
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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Y238-p - MSH2 (human)
Modsite: DFSTkDIyQDLNRLL SwissProt Entrez-Gene
Orthologous residues
MSH2 (human): Y238‑p, MSH2 iso2 (human): Y172‑p, MSH2 (mouse): Y238‑p, MSH2 (rat): Y238‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  lymphoma, anaplastic large cell lymphoma, T cell lymphoma
Relevant cell lines - cell types - tissues:  293 (epithelial), Karpas-299 (T lymphocyte), SUP-M2 (T lymphocyte)
Cellular systems studied:  cell lines
Species studied:  human
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE NPM-ALK (human) co-immunoprecipitation, transfection of wild-type enzyme
Downstream Regulation
Effect of modification (function):  molecular association, regulation
Effect of modification (process):  apoptosis, inhibited
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
MSH6 (human) Disrupts co-immunoprecipitation
Comments:  Enforced expression of MSH2 Y238F induces spontaneous apoptosis