Curated Information
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Curated Information Page
PubMed Id: 18354084 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
Maddika S, et al. (2008) Akt-mediated phosphorylation of CDK2 regulates its dual role in cell cycle progression and apoptosis. J Cell Sci 121, 979-88 18354084
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T39-p - CDK2 (human)
Orthologous residues
CDK2 (human): T39‑p, CDK2 (mouse): T39‑p, CDK2 (rat): T39‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mutation of modification site
 Relevant cell lines - cell types - tissues:  293T (epithelial), 3T3 (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) co-immunoprecipitation, phospho-motif antibody
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
serum starvation decrease
serum serum starvation inhibit treatment-induced decrease
EGF serum starvation inhibit treatment-induced decrease
EGF, rapamycin serum starvation inhibit treatment-induced decrease
EGF, wortmannin serum starvation no effect upon treatment-induced decrease
EGF, Akt-I-1 serum starvation no effect upon treatment-induced decrease
methotrexate increase
roscovitine methotrexate inhibit treatment-induced increase
wortmannin methotrexate inhibit treatment-induced increase
docetaxel increase
roscovitine docetaxel inhibit treatment-induced increase
wortmannin docetaxel inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Effect of modification (process):  apoptosis, induced, cell cycle regulation
 Comments:  contributes to the cell death induced by methotrexate and docetaxel


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