Curated Information
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Home > Curated Information Page > PubMed Id: 20220133
Gutierrez GJ, et al. (2010) JNK-mediated phosphorylation of Cdc25C regulates cell cycle entry and G(2)/M DNA damage checkpoint. J Biol Chem 285, 14217-28 20220133
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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S168-p - CDC25C (human)
Modsite: SEMKyLGsPIttVPK SwissProt Entrez-Gene
Orthologous residues
CDC25C (human): S168‑p, CDC25C iso3 (human): S125‑p, CDC25C (mouse): S192‑p, CDC25C (frog): S205‑p
Methods used to characterize site in vivo immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  brain cancer, glioblastoma, glioma, melanoma skin cancer
Relevant cell lines - cell types - tissues:  A375 (melanocyte), HeLa (cervical), U87MG (glial)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE JNK2 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JNK1 (human) genetic knockout/knockin of upstream enzyme
KINASE JNK2 (human) genetic knockout/knockin of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase
JNK_inhibitor_VII UV inhibit treatment-induced increase
Downstream Regulation
Effect of modification (function):  enzymatic activity, inhibited
Effect of modification (process):  cell cycle regulation