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• W2307793323 abstract "The transcription-coupled repair pathway (TC-NER) plays a vital role in removing transcription-blocking DNA lesions, particularly UV-induced damage. Clinical symptoms of the two TC-NER-deficiency syndromes, Cockayne syndrome (CS) and UV-hypersensitivity syndrome (UVSS) are dissimilar and the underlying molecular mechanism causing this difference in disease pathology is not yet clearly understood. UV-stimulated scaffold protein A (UVSSA) has been identified recently as a new causal gene for UVSS. Here we describe a functional homolog of the human UVSSA gene in the nematode Caenorhabditis elegans, uvs-1 (UVSSA-like-1). Mutations in uvs-1 render the animals hypersensitive to UV-B irradiation and transcription-blocking lesion-inducing illudin-M, similar to mutations in TC-NER deficient mutants. Moreover, we demonstrate that TC-NER factors including UVS-1 are required for the survival of the adult animals after UV-treatment." @default.
• W2307793323 created "2016-06-24" @default.
• W2307793323 creator A5062040602 @default.
• W2307793323 creator A5067353582 @default.
• W2307793323 date "2016-05-01" @default.
• W2307793323 modified "2023-09-26" @default.
• W2307793323 title "A C. elegans homolog for the UV-hypersensitivity syndrome disease gene UVSSA" @default.
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• W2307793323 doi "https://doi.org/10.1016/j.dnarep.2016.03.008" @default.
• W2307793323 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4886821" @default.
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