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Article

XPG stabilizes TFIIH, allowing transactivation of nuclear receptors: implications for Cockayne syndrome in XP-G/CS patients.

Molecular cell - 27 Apr 2007

Ito Shinsuke, Kuraoka Isao, Chymkowitch Pierre, Compe Emmanuel, Takedachi Arato, Ishigami Chie, Coin Frédéric, Egly Jean-Marc, Tanaka Kiyoji

Abstract excerpt

Mutations in the human XPG gene give rise to an inherited photosensitive disorder, xeroderma pigmentosum (XP) associated with Cockayne syndrome (XP-G/CS). The clinical features of CS in XP-G/CS patients are difficult to explain on the basis of a defect in nucleotide excision repair (NER). We found that XPG forms a stable complex with TFIIH, which is active in transcription and NER. Mutations in XPG found in...

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Identifiers

PMID: 17466625
DOI: 10.1016/j.molcel.2007.03.013

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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XPG stabilizes TFIIH, allowing transactivation of nuclear receptors: implications for Cockayne syndrome in XP-G/CS patients.PMID 17466625Read ↗

Hot topics in DNA repair: the molecular basis for different disease states caused by mutations in TFIIH and XPG.Semantic proximity Read ↗

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New insights into the combined Cockayne/xeroderma pigmentosum complex: human XPG protein can function in transcription factor stability.Semantic proximity Read ↗

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Mutations in XPB and XPD helicases found in xeroderma pigmentosum patients impair the transcription function of TFIIH.Semantic proximity Read ↗

The Role of TFIIH Complex in Nucleotide Excision RepairSemantic proximity Read ↗

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TFIIH: from transcription to clinicSemantic proximity Read ↗

Repair protein persistence at DNA lesions characterizes XPF defect with Cockayne syndrome features.Semantic proximity Read ↗

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