Curated Information

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PubMed Id: 11955452

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.

Keriel A, et al. (2002) XPD mutations prevent TFIIH-dependent transactivation by nuclear receptors and phosphorylation of RARalpha. Cell 109, 125-35 11955452

S77-p - RARA (human)

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Orthologous residues

RARA (human): S77‑p, RARA (mouse): S77‑p, RARA (rat): S74‑p

Characterization

Methods used to characterize site in vivo: [32P] bio-synthetic labeling, mutation of modification site

Relevant cell lines - cell types - tissues: HeLa (cervical), TTd1VI (fibroblast), XP6BE (fibroblast)

Cellular systems studied: cell lines

Species studied: human

Enzymes shown to modify site in vitro:

Type	Enzyme
KINASE	CDK7 (human)

Upstream Regulation

Potential in vivo enzymes for site:

Type	Enzyme	Evidence	Notes
KINASE	CDK7 (human)	transfection of inactive enzyme, transfection of wild-type enzyme

Downstream Regulation

Effect of modification (function): activation

Associated Diseases

Diseases:	Alterations:	Comments:
Xeroderma pigmentosum	mutation of site

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