Curated Information
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Home > Curated Information Page > PubMed Id: 15064744
Schwindling SL, Noll A, Montenarh M, Götz C (2004) Mutation of a CK2 phosphorylation site in cdc25C impairs importin alpha/beta binding and results in cytoplasmic retention. Oncogene 23, 4155-65 15064744
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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T236-p - CDC25C (human)
Modsite: VEKFkDNtIPDkVKK SwissProt Entrez-Gene
Orthologous residues
CDC25C (human): T236‑p, CDC25C iso3 (human): T193‑p, CDC25C (mouse): , CDC25C (frog): E307‑p
Characterization
Methods used to characterize site in vivo [32P] bio-synthetic labeling, mutation of modification site, peptide sequencing
Relevant cell lines - cell types - tissues:  HeLa (cervical)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE CK2A1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CK2A1 (human) pharmacological inhibitor of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
emodin decrease
Downstream Regulation
Effect of modification (function):  intracellular localization, molecular association, regulation
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
KPNB3 (human) Disrupts co-immunoprecipitation, electrophoretic visualization