Curated Information
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Home > Curated Information Page > PubMed Id: 24670654
Liu P, et al. (2014) Cell-cycle-regulated activation of Akt kinase by phosphorylation at its carboxyl terminus. Nature 508, 541-5 24670654
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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T308-p - Akt1 (human)
Modsite: kDGAtMKtFCGtPEy SwissProt Entrez-Gene
Orthologous residues
Akt1 (human): T308‑p, Akt1 iso2 (human): T246‑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 immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  glioblastoma multiforme, glioma, breast cancer
Relevant cell lines - cell types - tissues:  fibroblast-foreskin, HeLa (cervical), MCF-7 (breast cell), MEF (fibroblast), T47D (breast cell), T98G (glial)
Cellular systems studied:  cell lines, primary cells
Species studied:  human, mouse

S473-p - Akt1 (human)
Modsite: RPHFPQFsysAsGtA SwissProt Entrez-Gene
Orthologous residues
Akt1 (human): S473‑p, Akt1 iso2 (human): S411‑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 immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  glioblastoma multiforme, glioma, breast cancer
Relevant cell lines - cell types - tissues:  fibroblast-foreskin, HeLa (cervical), MCF-7 (breast cell), MEF (fibroblast), T47D (breast cell), T98G (glial)
Cellular systems studied:  cell lines, primary cells
Species studied:  human, mouse
Enzymes shown to modify site in vitro
Type Enzyme
KINASE mTOR (human)
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced, molecular association, regulation, phosphorylation
Effect of modification (process):  apoptosis, inhibited, carcinogenesis, induced, cell cycle regulation, cell growth, induced
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Sin1 (human) Induces co-immunoprecipitation
Comments:  primed for phosphorylation of S473

S477-p - Akt1 (human)
Modsite: PQFsysAsGtA____ SwissProt Entrez-Gene
Orthologous residues
Akt1 (human): S477‑p, Akt1 iso2 (human): S415‑p, Akt1 (mouse): S477‑p, Akt1 (rat): S477‑p, Akt1 (fruit fly): T603‑p, Akt1 (cow): S477‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  glioblastoma multiforme, glioma, breast cancer
Relevant cell lines - cell types - tissues:  fibroblast-foreskin, HeLa (cervical), MCF-7 (breast cell), MEF (fibroblast), T47D (breast cell), T98G (glial)
Cellular systems studied:  cell lines, primary cells
Species studied:  human, mouse
Enzymes shown to modify site in vitro
Type Enzyme
KINASE CDK2 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK2 (human) phospho-antibody, genetic knockout/knockin of upstream enzyme, modification site within consensus motif, inhibition of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
5-methoxypsoralen decrease
seliciclib decrease
CVT-313 decrease
mimosine decrease
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced, molecular association, regulation, phosphorylation
Effect of modification (process):  apoptosis, inhibited, carcinogenesis, induced, cell cycle regulation, cell growth, induced
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Sin1 (human) Induces co-immunoprecipitation
Comments:  primed for phosphorylation of S473

T479-p - Akt1 (human)
Modsite: FsysAsGtA______ SwissProt Entrez-Gene
Orthologous residues
Akt1 (human): T479‑p, Akt1 iso2 (human): T417‑p, Akt1 (mouse): T479‑p, Akt1 (rat): T479‑p, Akt1 (fruit fly): T605‑p, Akt1 (cow): T479‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  glioblastoma multiforme, glioma, breast cancer
Relevant cell lines - cell types - tissues:  fibroblast-foreskin, HeLa (cervical), MCF-7 (breast cell), MEF (fibroblast), T47D (breast cell), T98G (glial)
Cellular systems studied:  cell lines, primary cells
Species studied:  human, mouse
Enzymes shown to modify site in vitro
Type Enzyme
KINASE CDK2 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK2 (human) phospho-antibody, genetic knockout/knockin of upstream enzyme, modification site within consensus motif, inhibition of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
5-methoxypsoralen decrease
seliciclib decrease
CVT-313 decrease
mimosine decrease
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced, molecular association, regulation, phosphorylation
Effect of modification (process):  apoptosis, inhibited, carcinogenesis, induced, cell cycle regulation, cell growth, induced
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Sin1 (human) Induces co-immunoprecipitation
Comments:  primed for phosphorylation of S473