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Your search keyword '"Wei, Wenming"' showing total 8 results
Start Over Author "Wei, Wenming" Publisher springer science and business media llc
8 results on '"Wei, Wenming"'

2. Identifying novel chemical-related susceptibility genes for five psychiatric disorders through integrating genome-wide association study and tissue-specific 3′aQTL annotation datasets

Author

Shi, Sirong, primary, Zhang, Huijie, additional, Chu, Xiaoge, additional, Cai, Qingqing, additional, He, Dan, additional, Qin, Xiaoyue, additional, Wei, Wenming, additional, Zhang, Na, additional, Zhao, Yijing, additional, Jia, Yumeng, additional, Zhang, Feng, additional, and Wen, Yan, additional

Published
2024
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3. Association between electronic device use and health status among a middle-aged and elderly population: a cross-sectional analysis in the UK Biobank

Author

Wei, Wenming, primary, Liu, Huan, additional, Cheng, Bolun, additional, Qin, Xiaoyue, additional, He, Dan, additional, Zhang, Na, additional, Zhao, Yijing, additional, Cai, Qingqing, additional, Shi, Sirong, additional, Chu, Xiaoge, additional, Wen, Yan, additional, Jia, Yumeng, additional, and Zhang, Feng, additional

Published
2023
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4. SHLD1 is dispensable for 53BP1-dependent V(D)J recombination but critical for productive class switch recombination

Author

Vincendeau, Estelle, primary, Wei, Wenming, additional, Zhang, Xuefei, additional, Planchais, Cyril, additional, Yu, Wei, additional, Lenden-Hasse, Hélène, additional, Cokelaer, Thomas, additional, Pipoli da Fonseca, Juliana, additional, Mouquet, Hugo, additional, Adams, David J., additional, Alt, Frederick W., additional, Jackson, Stephen P., additional, Balmus, Gabriel, additional, Lescale, Chloé, additional, and Deriano, Ludovic, additional

Published
2022
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7. Shieldin complex promotes DNA end-joining and counters homologous recombination in BRCA1-null cells

Author

Dev, Harveer, primary, Chiang, Ting-Wei Will, additional, Lescale, Chloe, additional, de Krijger, Inge, additional, Martin, Alistair G., additional, Pilger, Domenic, additional, Coates, Julia, additional, Sczaniecka-Clift, Matylda, additional, Wei, Wenming, additional, Ostermaier, Matthias, additional, Herzog, Mareike, additional, Lam, Jonathan, additional, Shea, Abigail, additional, Demir, Mukerrem, additional, Wu, Qian, additional, Yang, Fengtang, additional, Fu, Beiyuan, additional, Lai, Zhongwu, additional, Balmus, Gabriel, additional, Belotserkovskaya, Rimma, additional, Serra, Violeta, additional, O’Connor, Mark J., additional, Bruna, Alejandra, additional, Beli, Petra, additional, Pellegrini, Luca, additional, Caldas, Carlos, additional, Deriano, Ludovic, additional, Jacobs, Jacqueline J. L., additional, Galanty, Yaron, additional, and Jackson, Stephen P., additional

Published
2018
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8. Shieldin complex promotes DNA end-joining and counters homologous recombination in BRCA1-null cells

Author

Dev, Harveer, Chiang, Ting-Wei Will, Lescale, Chloe, De Krijger, Inge, Martin, Alistair G, Pilger, Domenic, Coates, Julia, Sczaniecka-Clift, Matylda, Wei, Wenming, Ostermaier, Matthias, Herzog, Mareike, Lam, Jonathan, Shea, Abigail, Demir, Mukerrem, Wu, Qian, Yang, Fengtang, Fu, Beiyuan, Lai, Zhongwu, Balmus, Gabriel, Belotserkovskaya, Rimma, Serra, Violeta, O'Connor, Mark J, Bruna, Alejandra, Beli, Petra, Pellegrini, Luca, Caldas, Carlos, Deriano, Ludovic, Jacobs, Jacqueline JL, Galanty, Yaron, and Jackson, Stephen P

Subjects
DNA End-Joining Repair, Telomere-Binding Proteins, Bone Neoplasms, Breast Neoplasms, Cell Cycle Proteins, Poly(ADP-ribose) Polymerase Inhibitors, Mice, Cell Line, Tumor, Animals, Humans, DNA Breaks, Double-Stranded, skin and connective tissue diseases, Ovarian Neoplasms, Osteosarcoma, Dose-Response Relationship, Drug, BRCA1 Protein, Proteins, Recombinational DNA Repair, Xenograft Model Antitumor Assays, 3. Good health, DNA-Binding Proteins, HEK293 Cells, Drug Resistance, Neoplasm, Multiprotein Complexes, Mad2 Proteins, Female, Cisplatin, Tumor Suppressor p53-Binding Protein 1
Abstract

BRCA1 deficiencies cause breast, ovarian, prostate and other cancers, and render tumours hypersensitive to poly(ADP-ribose) polymerase (PARP) inhibitors. To understand the resistance mechanisms, we conducted whole-genome CRISPR-Cas9 synthetic-viability/resistance screens in BRCA1-deficient breast cancer cells treated with PARP inhibitors. We identified two previously uncharacterized proteins, C20orf196 and FAM35A, whose inactivation confers strong PARP-inhibitor resistance. Mechanistically, we show that C20orf196 and FAM35A form a complex, 'Shieldin' (SHLD1/2), with FAM35A interacting with single-stranded DNA through its C-terminal oligonucleotide/oligosaccharide-binding fold region. We establish that Shieldin acts as the downstream effector of 53BP1/RIF1/MAD2L2 to promote DNA double-strand break (DSB) end-joining by restricting DSB resection and to counteract homologous recombination by antagonizing BRCA2/RAD51 loading in BRCA1-deficient cells. Notably, Shieldin inactivation further sensitizes BRCA1-deficient cells to cisplatin, suggesting how defining the SHLD1/2 status of BRCA1-deficient tumours might aid patient stratification and yield new treatment opportunities. Highlighting this potential, we document reduced SHLD1/2 expression in human breast cancers displaying intrinsic or acquired PARP-inhibitor resistance.

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