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CSA-FLAG UV Treatment - TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A

ABSTRACT: SILAC comparison between CSA interactome before and after UV treatment.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Fibroblast

DISEASE(S): Cockayne Syndrome

SUBMITTER: Jeroen Demmers

LAB HEAD: Jeroen Demmers

PROVIDER: PXD008863 | Pride | 2018-10-19

REPOSITORIES: Pride

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			Action	DRS
	1310_AlexPines_01.raw	Raw
	1310_AlexPines_02.raw	Raw
	1310_AlexPines_03.raw	Raw
	1310_AlexPines_04.raw	Raw
	1310_AlexPines_05.raw	Raw

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TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A.

Pines Alex A Dijk Madelon M Makowski Matthew M Meulenbroek Elisabeth M EM Vrouwe Mischa G MG van der Weegen Yana Y Baltissen Marijke M French Pim J PJ van Royen Martin E ME Luijsterburg Martijn S MS Mullenders Leon H LH Vermeulen Michiel M Vermeulen Wim W Pannu Navraj S NS van Attikum Haico H

Nature communications 20180312 1

Transcription-blocking DNA lesions are removed by transcription-coupled nucleotide excision repair (TC-NER) to preserve cell viability. TC-NER is triggered by the stalling of RNA polymerase II at DNA lesions, leading to the recruitment of TC-NER-specific factors such as the CSA-DDB1-CUL4A-RBX1 cullin-RING ubiquitin ligase complex (CRL<sup>CSA</sup>). Despite its vital role in TC-NER, little is known about the regulation of the CRL<sup>CSA</sup> complex during TC-NER. Using conventional and cross ...[more]

PMID: 29531219

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