Curated Information
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Lu W, et al. (2015) SKP2 inactivation suppresses prostate tumorigenesis by mediating JARID1B ubiquitination. Oncotarget 6, 771-88 25596733
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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K242-ub - JARID1B (human)
Modsite: RAEAMNIkIEPEETT SwissProt Entrez-Gene
Orthologous residues
JARID1B (human): K242‑ub, JARID1B iso2 (human): K278‑ub, JARID1B (mouse): K242‑ub, JARID1B (rat): K242‑ub
Characterization
Methods used to characterize site in vivo immunoassay, immunoprecipitation, mutation of modification site, western blotting
Disease tissue studied:  prostate cancer
Relevant cell lines - cell types - tissues:  HEK293T (epithelial), PC3 (prostate cell)
Cellular systems studied:  cell lines
Species studied:  human
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
UBIQUITIN LIGASE TRAF6 (human) microscopy-colocalization, inhibition of upstream enzyme, transfection of inactive enzyme, co-immunoprecipitation, modification site within consensus motif, transfection of wild-type enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
SKP2 (human) decrease
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced, intracellular localization
Effect of modification (process):  carcinogenesis, inhibited
Comments:  decreases H3K4Me3 methylation, induces senescence