Curated Information
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PubMed Id: 20333297 
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.
Mahajan K, et al. (2010) Ack1 mediated AKT/PKB tyrosine 176 phosphorylation regulates its activation. PLoS One 5, e9646 20333297
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
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Y284-p - Ack (human) ▲
Orthologous residues
Ack (human): Y284‑p, Ack iso3 (human): Y347‑p, Ack (mouse): Y284‑p, Ack iso2 (mouse): Y284‑p, Ack (rat): Y284‑p
Associated Diseases
Diseases: Alterations: Comments:
breast cancer hyperphosphorylation

Y176-p - Akt1 (human) ▲
Orthologous residues
Akt1 (human): Y176‑p, Akt1 (mouse): Y176‑p, Akt1 (rat): Y176‑p, Akt1 (fruit fly): Y292‑p, Akt1 (cow): Y176‑p
Characterization
 Methods used to characterize site in vivo:  mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  293T (epithelial), breast, MCF-7 (breast cell), RWPE1 (prostate cell)
 Cellular systems studied:  cell lines, tissue
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
heregulin increase
insulin increase
LY294002 heregulin no effect upon treatment-induced increase
Ack (human) increase Ack1 siRNA decreases
PIK3CA (human) no change compared to control PIK3CA siRNA- no change
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, intracellular localization
 Effect of modification (process):  cell cycle regulation, transcription, altered
 Comments:  membrane localization
Associated Diseases
Diseases: Alterations: Comments:
breast cancer hyperphosphorylation

S473-p - Akt1 (human) ▲
Orthologous residues
Akt1 (human): S473‑p, Akt1 (mouse): S473‑p, Akt1 (rat): S473‑p, Akt1 (fruit fly): S586‑p, Akt1 (cow): S473‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  breast cancer
 Relevant cell lines - cell types - tissues:  breast, MCF-7 (breast cell), RWPE1 (prostate cell)
 Cellular systems studied:  cell lines, tissue
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
heregulin increase
insulin increase
LY294002 heregulin inhibit treatment-induced increase
Ack (human) increase Ack siRNA decreases
PIK3CA (human) increase PI3CA siRNA decreases

Y284-p - Ack (mouse) ▲
Orthologous residues
Ack (human): Y284‑p, Ack iso3 (human): Y347‑p, Ack (mouse): Y284‑p, Ack iso2 (mouse): Y284‑p, Ack (rat): Y284‑p

Y176-p - Akt1 (mouse) ▲
Orthologous residues
Akt1 (human): Y176‑p, Akt1 (mouse): Y176‑p, Akt1 (rat): Y176‑p, Akt1 (fruit fly): Y292‑p, Akt1 (cow): Y176‑p
Characterization
 Methods used to characterize site in vivo:  flow cytometry, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  MEF (fibroblast) [Akt1 (mouse), heterozygous knockout], MEF (fibroblast) [Akt2 (mouse), homozygous knockout], prostate
 Cellular systems studied:  cell lines, primary cells
 Species studied:  mouse
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE Ack (mouse)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Ack (mouse) mutation in upstream enzyme recognition motif, siRNA inhibition of enzyme, co-immunoprecipitation
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, intracellular localization
 Effect of modification (process):  cell cycle regulation, transcription, altered
 Comments:  membrane localization
Associated Diseases
Diseases: Alterations: Comments:
prostate cancer hyperphosphorylation murine prostatic intraepithelial neoplasia (mPINs)

T308-p - Akt1 (mouse) ▲
Orthologous residues
Akt1 (human): T308‑p, Akt1 (mouse): T308‑p, Akt1 (rat): T308‑p, Akt1 (fruit fly): T423‑p, Akt1 (cow): T308‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  prostate
 Cellular systems studied:  cell lines
 Species studied:  mouse

S473-p - Akt1 (mouse) ▲
Orthologous residues
Akt1 (human): S473‑p, Akt1 (mouse): S473‑p, Akt1 (rat): S473‑p, Akt1 (fruit fly): S586‑p, Akt1 (cow): S473‑p
Characterization
 Methods used to characterize site in vivo:  flow cytometry, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  MEF (fibroblast) [Akt1 (mouse), heterozygous knockout], MEF (fibroblast) [Akt2 (mouse), homozygous knockout], prostate
 Cellular systems studied:  cell lines, primary cells
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
LY294002 EGF inhibit treatment-induced increase


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