Curated Information

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Curated Information Page

PubMed Id: 11520785

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.

Somervaille TC, Linch DC, Khwaja A (2001) Growth factor withdrawal from primary human erythroid progenitors induces apoptosis through a pathway involving glycogen synthase kinase-3 and Bax. Blood 98, 1374-81 11520785

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.

S21-p - GSK3A (human)

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Orthologous residues

GSK3A (human): S21‑p, GSK3A (mouse): S21‑p, GSK3A (rat): S21‑p, GSK3A (cow): S21‑p

Characterization

Methods used to characterize site in vivo: phospho-antibody

Relevant cell lines - cell types - tissues: erythroblast-spleen

Cellular systems studied: primary cells

Species studied: human

Upstream Regulation

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Manipulated Protein	Referenced Protein	Effect	Notes
Epo				increase
SCF				increase

Downstream Regulation

Effect of modification (function): enzymatic activity, inhibited

S9-p - GSK3B (human)

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