Renier Velez-Cruz, Ph.D.
Affiliations: | 2005 | Vanderbilt University, Nashville, TN |
Area:
BiochemistryGoogle:
"Renier Velez-Cruz"Mean distance: (not calculated yet)
Parents
Sign in to add mentor| Neil Osheroff | grad student | 2005 | Vanderbilt | |
| (DNA lesions as cellular poisons of topoisomerase IIalpha.) | ||||
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Publications
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| Sadek M, Sheth A, Zimmerman G, et al. (2022) The role of SWI/SNF chromatin remodelers in the repair of DNA double strand breaks and cancer therapy. Frontiers in Cell and Developmental Biology. 10: 1071786 |
| Hays E, Nettleton E, Carter C, et al. (2020) The SWI/SNF ATPase BRG1 stimulates DNA end resection and homologous recombination by reducing nucleosome density at DNA double strand breaks and by promoting the recruitment of the CtIP nuclease. Cell Cycle (Georgetown, Tex.). 1-19 |
| Manickavinayaham S, Velez-Cruz R, Biswas AK, et al. (2020) The E2F1 transcription factor and RB tumor suppressor moonlight as DNA repair factors. Cell Cycle (Georgetown, Tex.). 1-10 |
| Manickavinayaham S, Vélez-Cruz R, Biswas AK, et al. (2019) E2F1 acetylation directs p300/CBP-mediated histone acetylation at DNA double-strand breaks to facilitate repair. Nature Communications. 10: 4951 |
| Vélez-Cruz R, Manickavinayaham S, Biswas AK, et al. (2016) RB localizes to DNA double-strand breaks and promotes DNA end resection and homologous recombination through the recruitment of BRG1. Genes & Development. 30: 2500-2512 |
| Vélez-Cruz R, Zadorin AS, Coin F, et al. (2013) Sirt1 suppresses RNA synthesis after UV irradiation in combined xeroderma pigmentosum group D/Cockayne syndrome (XP-D/CS) cells. Proceedings of the National Academy of Sciences of the United States of America. 110: E212-20 |
| Vélez-Cruz R, Johnson DG. (2012) E2F1 and p53 transcription factors as accessory factors for nucleotide excision repair. International Journal of Molecular Sciences. 13: 13554-68 |
| Le May N, Mota-Fernandes D, Vélez-Cruz R, et al. (2010) NER factors are recruited to active promoters and facilitate chromatin modification for transcription in the absence of exogenous genotoxic attack. Molecular Cell. 38: 54-66 |