Curated Information
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Home > Curated Information Page > PubMed Id: 16962287
Lessmann E, et al. (2007) Oxysterol-binding protein-related protein (ORP) 9 is a PDK-2 substrate and regulates Akt phosphorylation. Cell Signal 19, 384-92 16962287
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
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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 phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  293 (epithelial)
Cellular systems studied:  cell lines
Species studied:  human
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
siRNA OSBPL9 (human) no change compared to control

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 phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  293 (epithelial), B lymphocyte-spleen, mast-bone marrow
Cellular systems studied:  cell lines, primary cultured cells
Species studied:  human, mouse
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
DNP increase
wortmannin DNP inhibit treatment-induced increase
bisindolylmaleimide DNP inhibit treatment-induced increase
Go_6976 DNP inhibit treatment-induced increase
LY294002 decrease
wortmannin decrease
rapamycin no change compared to control
okadaic_acid no change compared to control
siRNA OSBPL9 (human) increase
siRNA siRNA mTOR (human) OSBPL9 (human) inhibit treatment-induced increase
siRNA mTOR (human) no change compared to control

S287-p - OSBPL9 (human)
Modsite: PNTVPEFsYSSsEDE SwissProt Entrez-Gene
Orthologous residues
OSBPL9 (human): S287‑p, OSBPL9 (mouse): S287‑p, OSBPL9 (rat): S274‑p
Characterization
Methods used to characterize site in vivo electrophoretic mobility shift, mutation of modification site, phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  293 (epithelial), B lymphocyte-spleen, COS (fibroblast), mast-bone marrow
Cellular systems studied:  cell lines, primary cultured cells
Species studied:  green monkey, human, mouse
Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKCB (mouse)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKCB (mouse) phospho-antibody, modification site within consensus motif, co-immunoprecipitation, pharmacological inhibitor of upstream enzyme, pharmacological activator of upstream enzyme, genetic knockout/knockin of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
DNP increase
wortmannin DNP no effect upon treatment-induced increase
bisindolylmaleimide DNP inhibit treatment-induced increase
Go_6976 DNP inhibit treatment-induced increase
LY294002 no change compared to control
wortmannin no change compared to control
phorbol_ester increase
bisindolylmaleimide increase
Go_6976 no change compared to control
rapamycin no change compared to control
okadaic_acid no change compared to control
siRNA mTOR (human) decrease
anti-IgM increase
wortmannin anti-IgM augment treatment-induced increase
Go_6976 anti-IgM inhibit treatment-induced increase

T412-p - p70S6K (human)
Modsite: NQVFLGFtyVAPsVL SwissProt Entrez-Gene
Orthologous residues
p70S6K (human): T412‑p, p70S6K iso2 (human): T389‑p, p70S6K (mouse): T412‑p, p70S6K (rat): T412‑p, p70S6K iso2 (rat): T389‑p, p70S6K (fruit fly): T398‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  293 (epithelial)
Cellular systems studied:  cell lines
Species studied:  human
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
siRNA OSBPL9 (human) no change compared to control

S738-p - PRKD1 (human)
Modsite: ARIIGEksFRRsVVG SwissProt Entrez-Gene
Orthologous residues
PRKD1 (human): S738‑p, PRKD1 (mouse): S744‑p, PRKD1 (rat): S744‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  293 (epithelial), B lymphocyte-spleen, mast-bone marrow
Cellular systems studied:  cell lines, primary cultured cells
Species studied:  human, mouse
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anti-IgM increase
wortmannin anti-IgM inhibit treatment-induced increase
Go_6976 anti-IgM inhibit treatment-induced increase

S742-p - PRKD1 (human)
Modsite: GEksFRRsVVGtPAy SwissProt Entrez-Gene
Orthologous residues
PRKD1 (human): S742‑p, PRKD1 (mouse): S748‑p, PRKD1 (rat): S748‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  293 (epithelial), B lymphocyte-spleen, mast-bone marrow
Cellular systems studied:  cell lines, primary cultured cells
Species studied:  human, mouse
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anti-IgM increase
wortmannin anti-IgM inhibit treatment-induced increase
Go_6976 anti-IgM inhibit treatment-induced increase