Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

ATR-dependent phosphorylation of FANCA on serine 1449 after DNA damage is important for FA pathway function.

Blood | Mar 5, 2009

Previous work has shown several proteins defective in Fanconi anemia (FA) are phosphorylated in a functionally critical manner. FANCA is phosphorylated after DNA damage and localized to chromatin, but the site and significance of this phosphorylation are unknown. Mass spectrometry of FANCA revealed one phosphopeptide, phosphorylated on serine 1449. Serine 1449 phosphorylation was induced after DNA damage but not during S phase, in contrast to other posttranslational modifications of FA proteins. Furthermore, the S1449A mutant failed to completely correct a variety of FA-associated phenotypes. The DNA damage response is coordinated by phosphorylation events initiated by apical kinases ATM (ataxia telangectasia mutated) and ATR (ATM and Rad3-related), and ATR is essential for proper FA pathway function. Serine 1449 is in a consensus ATM/ATR site, phosphorylation in vivo is dependent on ATR, and ATR phosphorylated FANCA on serine 1449 in vitro. Phosphorylation of FANCA on serine 1449 is a DNA damage-specific event that is downstream of ATR and is functionally important in the FA pathway.

Pubmed ID: 19109555 RIS Download

Mesh terms: Alkylating Agents | Ataxia Telangiectasia Mutated Proteins | Blotting, Western | Cell Cycle Proteins | DNA Damage | Electrophoresis, Polyacrylamide Gel | Fanconi Anemia | Fanconi Anemia Complementation Group A Protein | HeLa Cells | Humans | Immunoprecipitation | Mass Spectrometry | Mitomycin | Phosphorylation | Protein-Serine-Threonine Kinases | Serine

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: PHS HHS, Id: R01-063776

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.