Facilitation of STK19 in transcription coupled nuclear excision repair (TC-NER): Mechanisms, interactions, and genome stability

No abstract is available for this paper.

• Publication year

  2026

• Venue

  Human Gene

• Publication date

  2026-02-01

• Fields of study

  Not labeled

• Identifiers
  DOI 10.1016/j.humgen.2026.201537
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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• STK19 is a DNA/RNA-binding protein critical for DNA damage repair and cell proliferation

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• Lesion recognition by XPC, TFIIH and XPA in DNA excision repair

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• Regulation of the RNAPII Pool Is Integral to the DNA Damage Response

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• Inhibition of UVSSA ubiquitination suppresses transcription‐coupled nucleotide excision repair deficiency caused by dissociation from USP7

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• Amplification of unscheduled DNA synthesis signal enables fluorescence-based single cell quantification of transcription-coupled nucleotide excision repair

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• The molecular basis of CRL4DDB2/CSA ubiquitin ligase architecture, targeting, and activation.

  2011cited by this paper
• Transcription-coupled repair and apoptosis provide specific protection against transcription-associated mutagenesis by ultraviolet light

  2010cited by this paper
• Proteins of nucleotide and base excision repair pathways interact in mitochondria to protect from loss of subcutaneous fat, a hallmark of aging

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• UV-induced association of the CSB remodeling protein with chromatin requires ATP-dependent relief of N-terminal autorepression.

  2010cited by this paper
• Distinct ubiquitin ligases act sequentially for RNA polymerase II polyubiquitylation

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• A UV-sensitive syndrome patient with a specific CSA mutation reveals separable roles for CSA in response to UV and oxidative DNA damage

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• Persistent transcription-blocking DNA lesions trigger somatic growth attenuation associated with longevity

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• Transcription-coupled DNA repair: two decades of progress and surprises

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• Isolation of XAB2 Complex Involved in Pre-mRNA Splicing, Transcription, and Transcription-coupled Repair*

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  2008cited by this paper
• Damage-induced ubiquitylation of human RNA polymerase II by the ubiquitin ligase Nedd4, but not Cockayne syndrome proteins or BRCA1.

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• Transcriptional bypass of bulky DNA lesions causes new mutant RNA transcripts in human cells

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• Genome maintenance mechanisms are critical for preventing cancer as well as other aging-associated diseases.

  2007cited by this paper
• CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome.

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• Retinal Degeneration and Ionizing Radiation Hypersensitivity in a Mouse Model for Cockayne Syndrome

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• UV-sensitive syndrome.

  2005cited by this paper
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  2005cited by this paper
• Transcription arrest at DNA damage sites.

  2005cited by this paper
• DNA damage stabilizes interaction of CSB with the transcription elongation machinery

  2004cited by this paper
• Blockage of RNA polymerase II at a cyclobutane pyrimidine dimer and 6-4 photoproduct.

  2004cited by this paper
• Complete absence of Cockayne syndrome group B gene product gives rise to UV-sensitive syndrome but not Cockayne syndrome.

  2004cited by this paper
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• Sequential assembly of the nucleotide excision repair factors in vivo.

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• TFIIH with Inactive XPD Helicase Functions in Transcription Initiation but Is Defective in DNA Repair*

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• XAB2, a Novel Tetratricopeptide Repeat Protein Involved in Transcription-coupled DNA Repair and Transcription*

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• The Oxidative DNA Lesion 8,5′-(S)-Cyclo-2′-deoxyadenosine Is Repaired by the Nucleotide Excision Repair Pathway and Blocks Gene Expression in Mammalian Cells*

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• Xeroderma pigmentosum p48 gene enhances global genomic repair and suppresses UV-induced mutagenesis.

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• Structural Characterization of RNA Polymerase II Complexes Arrested by a Cyclobutane Pyrimidine Dimer in the Transcribed Strand of Template DNA*

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• Expression of the p48 xeroderma pigmentosum gene is p53-dependent and is involved in global genomic repair.

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• DNA-binding polarity of human replication protein A positions nucleases in nucleotide excision repair.

  1998cited by this paper
• Functional Analysis of Human Replication Protein A in Nucleotide Excision Repair*

  1998cited by this paper
• The G11 Gene Located in the Major Histocompatibility Complex Encodes a Novel Nuclear Serine/Threonine Protein Kinase*

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• Xeroderma pigmentosum group C protein complex is the initiator of global genome nucleotide excision repair.

  1998cited by this paper
• Human Transcription-Repair Coupling Factor CSB/ERCC6 Is a DNA-stimulated ATPase but Is Not a Helicase and Does Not Disrupt the Ternary Transcription Complex of Stalled RNA Polymerase II*

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• No citing papers are available for this paper.