Curated Information
Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
PhosphoSitePlus
HomeAbout PhosphoSiteUsing PhosphoSiteCuration ProcessContact
NIH-logos NIGMS Logo NIAAA Logo NCI Logo NIH Logo
Curated Information Page
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
Download Sites

S1149-p - FANCA (human)
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.


Home  |  Curator Login With enhanced literature mining using Linguamatics I2E I2E Logo Produced by 3rd Millennium  |  Design by Digizyme
©2003-2013 Cell Signaling Technology, Inc.