Curated Information

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Curated Information Page

PubMed Id: 12086603

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.

Taniguchi T, et al. (2002) Convergence of the fanconi anemia and ataxia telangiectasia signaling pathways. Cell 109, 459-72 12086603

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.

S222-p - FANCD2 (human)

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Orthologous residues

FANCD2 (human): S222‑p, FANCD2 iso2 (human): S222‑p, FANCD2 (mouse): S220‑p, FANCD2 (chicken): S225‑p

Characterization

Methods used to characterize site in vivo: mass spectrometry, mutation of modification site, phospho-antibody, western blotting

Disease tissue studied: ataxia-telangiectasia

Relevant cell lines - cell types - tissues: AT22IJE-T (fibroblast), FA-D2 (fibroblast), GM01526 (fibroblast), HeLa (cervical)

Cellular systems studied: cell lines

Species studied: human

Comments: PD7 lymphoblasts, PD20F

Enzymes shown to modify site in vitro:

Type	Enzyme
KINASE	ATM (human)

Upstream Regulation

Treatments, proteins and their effect on site modification:

Treatments	Referenced Treatments	Manipulated Protein	Referenced Protein	Effect	Notes
ionizing radiation				increase
ionizing radiation				no change compared to control	ATM-deficient AT cells

Downstream Regulation

Effect of modification (process): cell cycle regulation

Comments: Phosphorylation of FANCD2 on S222 is required for the IR-inducible S phase checkpoint but not the G1/S or G2/M checkpoints

S1404-p - FANCD2 (human)

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