A5103218090- DNA Repair Mechanisms
- Glycosylation and Glycoproteins Research
- Metallic Glasses and Amorphous Alloys
- Aluminum Alloy Microstructure Properties
- Phase-change materials and chalcogenides
- CRISPR and Genetic Engineering
- Metallurgical and Alloy Processes
- High Entropy Alloys Studies
- Cell death mechanisms and regulation
- Cytomegalovirus and herpesvirus research
- RNA regulation and disease
- Ubiquitin and proteasome pathways
- Magnesium Alloys: Properties and Applications
Beijing Institute of Genomics
2024-2025
Chinese Academy of Sciences
2022-2025
Shanghai Center For Bioinformation Technology
2024-2025
University of Chinese Academy of Sciences
2024-2025
DNA-RNA hybrids triggered by double-strand breaks (DSBs) are crucial intermediates during DSB repair, and their timely resolution requires numbers of RNA helicases, including DEAD box 1 (DDX1). However, how these helicases recruited to DSB-induced in time remains largely unclear. Here, we revealed that squamous cell carcinoma antigen recognized T cells 3 (SART3) promotes DDX1 binding at DSBs for optimal homologous recombination (HR) repair. SART3 itself associates with PAR chains accumulates...
Transcription cofactor vestigial-like 3 (VGLL3), as a master regulator of female-biased autoimmunity, also functions in tumor development, while the underlying mechanisms remain largely elusive. Here, we report that VGLL3 plays an important role DNA damage response (DDR). can be recruited to sites PARylation-dependent manner. depletion impairs accumulation RNF8 and RAD51 at damage, leading reduced homologous recombination efficiency increased cellular sensitivity chemotherapeutic drugs....
RAD18, an important ubiquitin E3 ligase, plays a dual role in translesion DNA synthesis (TLS) and homologous recombination (HR) repair. However, whether how the regulatory mechanism of O-linked N-acetylglucosamine (O-GlcNAc) modification governing RAD18 its function during these processes remains unknown. Here, we report that human can undergo O-GlcNAcylation at Ser130/Ser164/Thr468, which is for optimal accumulation damage sites. Mechanistically, abrogation limits CDC7-dependent Ser434...