Curated Information

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PubMed Id: 15574412

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.

Information from this record has been curated, but not yet edited in PhosphoSitePlus^® and may be incomplete.

Liberman Z, Eldar-Finkelman H (2005) Serine 332 phosphorylation of insulin receptor substrate-1 by glycogen synthase kinase-3 attenuates insulin signaling. J Biol Chem 280, 4422-8 15574412

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.

T308-p - Akt1 (rat)

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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: CHO (fibroblast) [InsR (human)]

Cellular systems studied: cell lines

Species studied: hamster

Upstream Regulation

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Manipulated Protein	Referenced Protein	Effect	Notes
insulin				increase

S473-p - Akt1 (rat)

▲

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

Relevant cell lines - cell types - tissues: CHO (fibroblast) [InsR (human)]

Cellular systems studied: cell lines

Species studied: hamster

Upstream Regulation

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Manipulated Protein	Referenced Protein	Effect	Notes
insulin				increase

S332-p - IRS1 (rat)

▲

Orthologous residues

IRS1 (human): S337‑p, IRS1 (mouse): S332‑p, IRS1 (rat): S332‑p

Characterization

Methods used to characterize site in vivo: mutation of modification site, phospho-antibody, western blotting

Relevant cell lines - cell types - tissues: 293 (epithelial), CHO (fibroblast) [InsR (human)]

Cellular systems studied: cell lines

Species studied: hamster, human

Enzymes shown to modify site in vitro:

Type	Enzyme
KINASE	GSK3B (human)

Upstream Regulation

Potential in vivo enzymes for site:

Type	Enzyme	Evidence	Notes
KINASE	GSK3B (human)	pharmacological inhibitor of upstream enzyme, phospho-antibody, transfection of wild-type enzyme, pharmacological activator of upstream enzyme

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Manipulated Protein	Referenced Protein	Effect	Notes
lithium				decrease
insulin				no change compared to control

Downstream Regulation

Effect of modification (function): phosphorylation

Comments: decreases tyrosine phosphorylation of IRS-1 and Akt1 phosphorylation upon insulin stimulation

S336-p - IRS1 (rat)

▲

Orthologous residues

IRS1 (human): S341‑p, IRS1 (mouse): S336‑p, IRS1 (rat): S336‑p

Characterization

Methods used to characterize site in vivo: mutation of modification site

Relevant cell lines - cell types - tissues: 293 (epithelial), CHO (fibroblast) [InsR (human)]

Cellular systems studied: cell lines

Species studied: hamster, human

Downstream Regulation

Effect of modification (function): phosphorylation

Comments: decreases tyrosine phosphorylation of IRS-1 and Akt1 phosphorylation upon insulin stimulation; primes S332 for phosphorylation by GSK3B

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