Curated Information
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Curated Information Page
PubMed Id: 15364919 
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.
Li Y, et al. (2004) Protein kinase C Theta inhibits insulin signaling by phosphorylating IRS1 at Ser(1101). J Biol Chem 279, 45304-7 15364919
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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S1101-p - IRS1 (human) ▲
Orthologous residues
IRS1 (human): S1101‑p, IRS1 (mouse): S1097‑p, IRS1 (rat): S1100‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  CHO (fibroblast) [InsR (human)], CHO (fibroblast) [IRS1 (human)], CHO (fibroblast) [PKCT (mouse)]
 Cellular systems studied:  cell lines
 Species studied:  hamster
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE PKCT (mouse)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKCT (mouse) transfection of inactive enzyme, transfection of constitutively active enzyme Overexpression of constitutively active PKC-theta attenuates the insulin-induced tyrosine phosphorylation of co-transfected wild-type IRS-1, but not S1101A IRS1.
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
Downstream Regulation
 Effect of modification (function):  inhibition

S1149-p - IRS2 (human) ▲
Orthologous residues
IRS2 (human): S1149‑p, IRS2 (mouse): S1138‑p, IRS2 (rat): S1141‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  CHO (fibroblast) [InsR (human)], CHO (fibroblast) [IRS2 (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

S1097-p - IRS1 (mouse) ▲
Orthologous residues
IRS1 (human): S1101‑p, IRS1 (mouse): S1097‑p, IRS1 (rat): S1100‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast) [SHP-2 (mouse), homozygous knockout], C2C12 (myoblast)
 Cellular systems studied:  cell lines
 Species studied:  mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKCT (mouse) genetic knockout/knockin of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
bisindolylmaleimide insulin inhibit treatment-induced increase
wortmannin insulin no effect upon treatment-induced increase
U0126 insulin no effect upon treatment-induced increase
phorbol ester increase
arachidonic acid increase
oleic acid increase
TNF increase
IGF-1 increase
Downstream Regulation
 Effect of modification (function):  inhibition


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