Curated Information

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PubMed Id: 16141217

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.

Katsanakis KD, Pillay TS (2005) Cross-talk between the two divergent insulin signaling pathways is revealed by the protein kinase B (Akt)-mediated phosphorylation of adapter protein APS on serine 588. J Biol Chem 280, 37827-32 16141217

S588-p - APS (rat)

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Orthologous residues

APS (human): S598‑p, APS (mouse): S588‑p, APS (rat): S588‑p

Characterization

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

Relevant cell lines - cell types - tissues: 3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout], CHO (fibroblast) [EphB1 (human), transfection]

Cellular systems studied: cell lines

Species studied: hamster

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)	pharmacological inhibitor of upstream enzyme, antisense inhibition of upstream enzyme

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Effect
insulin		increase
LY294002	insulin	inhibit treatment-induced increase
deguelin	insulin	inhibit treatment-induced increase

Downstream Regulation

Effect of modification (function): intracellular localization

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