Search

Your search keyword '"Tang, Zizhi"' showing total 17 results
Start Over Author "Tang, Zizhi"
17 results on '"Tang, Zizhi"'

2. Hepatitis B virus infection disrupts homologous recombination in hepatocellular carcinoma by stabilizing resection inhibitor ADRM1

Author

Zeng, Ming, Tang, Zizhi, Ren, Laifeng, Wang, Haibin, Wang, Xiaojun, Zhu, Wenyuan, Mao, Xiaobing, Li, Zeyang, Mo, Xianming, Chen, Jun, Han, Junhong, Kong, Daochun, Ji, Jianguo, Carr, Antony M., and Liu, Cong

Subjects
R and D Systems -- International economic relations, Computer software industry -- International economic relations, Chromatin -- Health aspects -- Genetic aspects, Biotechnology -- Genetic aspects -- Health aspects, Ubiquitin -- Genetic aspects -- Health aspects, Ligases -- Health aspects -- Genetic aspects, Hepatitis B -- Development and progression -- Genetic aspects, Hepatitis B virus -- Genetic aspects -- Development and progression, Hepatoma -- Development and progression -- Genetic aspects, Surgery -- Health aspects, Health care industry
Abstract

Many cancers harbor homologous recombination defects (HRDs). A HRD is a therapeutic target that is being successfully utilized in treatment of breast/ovarian cancer via synthetic lethality. However, canonical HRD caused by BRCAness mutations do not prevail in liver cancer. Here we report a subtype of HRD caused by the perturbation of a proteasome variant (CDW19S) in hepatitis B virus-bearing (HBV-bearing) cells. This amalgamate protein complex contained the 19S proteasome decorated with [CRL4.sup.WDR70] ubiquitin ligase, and assembled at broken chromatin in a [PSMD4.sup.Rpn10]-and ATM-MDC1-RNF8-dependent manner. CDW19S promoted DNA end processing via segregated modules that promote nuclease activities of MRE11 and EXO1. Contrarily, a proteasomal component, [ADRM1.sup.Rpn13], inhibited resection and was removed by [CRL4WDR.sup.70]-catalyzed ubiquitination upon commitment of extensive resection. HBx interfered with [ADRM1.sup.Rpn13] degradation, leading to the imposition of [ADRM1.sup.Rpn13]- dependent resection barrier and consequent viral HRD subtype distinguishable from that caused by BRCA1 defect. Finally, we demonstrated that viral HRD in HBV-associated hepatocellular carcinoma can be exploited to restrict tumor progression. Our work clarifies the underlying mechanism of a virus-induced HRD subtype., Introduction Long-term liver infection with hepatitis B virus (HBV) predisposes carriers to hepatocellular carcinoma (1). Therapy for late-stage HBV-associated hepatocellular carcinoma remains a major challenge, with poor therapy responses and [...]

Published
2023
Full Text
View/download PDF

6. Mechanistic basis for targeting homologous recombination defective liver cancer via synthetic lethality

Author

Zeng, Ming, primary, Tang, Zizhi, additional, Ren, Laifeng, additional, Wang, Haibin, additional, Wang, Xiaojun, additional, Zhu, Wenyuan, additional, Mao, Xiaobing, additional, Li, Zeyang, additional, Mo, Xianming, additional, Chen, Jun, additional, Han, Junhong, additional, Kong, Daochun, additional, Ji, Jianguo, additional, Carr, Antony M., additional, and Liu, Cong, additional

Published
2022
Full Text
View/download PDF

13. The Antiresection Activity of the X Protein Encoded by Hepatitis Virus B

Author

Ren, Laifeng, primary, Zeng, Ming, additional, Tang, Zizhi, additional, Li, Mingyuan, additional, Wang, Xiaojun, additional, Xu, Yang, additional, Weng, Yuding, additional, Wang, Xiaobo, additional, Wang, Huan, additional, Guo, Liandi, additional, Zuo, Bing, additional, Wang, Xin, additional, Wang, Si, additional, Lou, Jiangyan, additional, Tang, Yaxiong, additional, Mu, Dezhi, additional, Zheng, Ning, additional, Wu, Xianhui, additional, Han, Junhong, additional, Carr, Antony M., additional, Jeggo, Penelope, additional, and Liu, Cong, additional

Published
2019
Full Text
View/download PDF

14. HBx affects CUL4-DDB1 function in both positive and negative manners

Author

Tang Zizhi, Xin Wang, Xiaobo Wang, Laifeng Ren, Ming Zeng, Yaxiong Tang, Si Wang, Cong Liu, Huaidong Hu, Liandi Guo, Mingyuan Li, Yuding Weng, and Chongjie Zhang

Subjects
Hepatitis B virus, Protein-Arginine N-Methyltransferases, viruses, Biophysics, Biology, medicine.disease_cause, Virus Replication, Biochemistry, Cell Line, DDB1, Ubiquitin, Gene expression, medicine, Humans, Viral Regulatory and Accessory Proteins, Molecular Biology, DNA Primers, Base Sequence, Reverse Transcriptase Polymerase Chain Reaction, Ubiquitination, RNA, Cell Biology, Cullin Proteins, Virology, digestive system diseases, Ubiquitin ligase, DNA-Binding Proteins, Repressor Proteins, HBx, Viral replication, biology.protein, Trans-Activators
Abstract

Hepatitis B virus (HBV) infection is a major public health problem by affecting 350 million people worldwide. The mechanisms that regulate HBV gene expression and viral replication remain poorly understood. HBx is known as the central regulator for HBV replication and is associated with the CUL4–DDB1 ubiquitin ligase through H-box motif. Here, we show that blocking the activity of DDB1 by RNA interfering inhibited viral production and gene expression of HBV, and direct association of HBx with DDB1 promoted viral activities, indicating that DDB1 function is required for viral production. On the other hand, HBx interfered with DDB1-dependent polyubiquitination of PRMT1, arginine methyltransferase 1, suggesting that HBx can also block the function of a subset of CUL4–DDB1 E3 ligases. Thus, we conclude that HBx regulates the function of DDB1 in both positive and negative manners in the context of distinct CUL4–DDB1 complexes and plays different roles in HBV replication cycle.

Published
2014

16. HBx affects CUL4–DDB1 function in both positive and negative manners

Author

Guo, Liandi, primary, Wang, Xiaobo, additional, Ren, Laifeng, additional, Zeng, Ming, additional, Wang, Si, additional, Weng, Yuding, additional, Tang, Zizhi, additional, Wang, Xin, additional, Tang, Yaxiong, additional, Hu, Huaidong, additional, Li, Mingyuan, additional, Zhang, Chongjie, additional, and Liu, Cong, additional

Published
2014
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results