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PubMed Id: 11855836

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.

Otsuki T, et al. (2002) Phosphorylation of Fanconi anemia protein, FANCA, is regulated by Akt kinase. Biochem Biophys Res Commun 291, 628-34 11855836

S1149-p - FANCA (human)

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Orthologous residues

FANCA (human): S1149‑p, FANCA (mouse): A1142‑p

Characterization

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

Disease tissue studied: leukemia, acute myelogenous leukemia, liver cancer, squamous cell carcinoma of the liver

Relevant cell lines - cell types - tissues: 293 (epithelial), HSC (squamous), UT-7 (myeloid)

Enzymes shown to modify site in vitro:

Type	Enzyme
KINASE	Akt1 (human)

Upstream Regulation

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Manipulated Protein	Referenced Protein	Effect	Notes
		Akt1 (human)		increase	Dominant negative
		Akt1 (human)		decrease	constitutively active

Downstream Regulation

Effect of modification (function): molecular association, regulation

Comments: Complementation assays showed similar results for WT-FANCA and S1149A mutant.

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