Curated Information
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Curated Information Page
PubMed Id: 19109555 
Collins NB, et al. (2009) ATR-dependent phosphorylation of FANCA on serine 1449 after DNA damage is important for FA pathway function. Blood 113, 2181-90 19109555
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, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
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S1449-p - FANCA (human)
Orthologous residues
FANCA (human): S1449‑p, FANCA (mouse): Y1433‑p
 Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  Fanconi's anaemia
 Relevant cell lines - cell types - tissues:  DK0064, GM01389D, GM6914 (fibroblast), HeLa (cervical)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE ATR (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ATR (human) phospho-motif antibody, genetic knockout/knockin of upstream enzyme, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
MMC increase
okadaic acid increase
wortmannin decrease
SB28078 no change compared to control
Downstream Regulation
 Effect of modification (function):  molecular association, regulation, ubiquitination
 Effect of modification (process):  chromatin organization, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
DNA Induces co-immunoprecipitation
 Comments:  level of monoubiquitinated FANCD2 was decreased in FANCA S1449A mutant

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