Curated Information
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Curated Information Page
PubMed Id: 19176382 
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.
Cai Y, et al. (2009) GGAP2/PIKE-a directly activates both the Akt and nuclear factor-kappaB pathways and promotes prostate cancer progression. Cancer Res 69, 819-27 19176382
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S629-p - CENTG1 iso2 (human)
Orthologous residues
CENTG1 (human): S985‑p, CENTG1 iso2 (human): S629‑p, CENTG1 (mouse): S979‑p, CENTG1 (rat): S979‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mutation of modification site, western blotting
 Disease tissue studied:  prostate cancer
 Relevant cell lines - cell types - tissues:  DU 145 (prostate cell), LNCaP (prostate cell), PC3 (prostate cell), PNT1A (prostate cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 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, activation of upstream enzyme
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, molecular association, regulation
 Effect of modification (process):  cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
NFkB-p105 (human) Induces activity, induced transcription, altered co-immunoprecipitation
 Comments:  enhances proliferation , foci formation, and tumor progression in prostate cancer cells


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