Curated Information
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Home > Curated Information Page > PubMed Id: 16467851
Braiman A, Barda-Saad M, Sommers CL, Samelson LE (2006) Recruitment and activation of PLCgamma1 in T cells: a new insight into old domains. EMBO J 25, 774-84 16467851
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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Y783-p - PLCG1 (cow)
Modsite: EGRNPGFyVEANPMP SwissProt Entrez-Gene
Orthologous residues
PLCG1 (human): Y783‑p, PLCG1 iso2 (human): Y783‑p, PLCG1 (mouse): Y783‑p, PLCG1 (rat): Y783‑p, PLCG1 (cow): Y783‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  Jurkat (T lymphocyte)
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
anti-CD3 increase The loss of function mutations in either of the three SH domains strongly inhibits phosphorylation of Y783 as compared with wild-type. SH3*-YFP and SH2C*-YFP are recruited to the LAT-nucleated signaling complex, Y783 phosphorylation in these mutants is inhibited more severely than that in SH2N*-YFP, which is not recruited to the signaling complex.