Xiaobing Mao

ORCID: 0009-0008-8166-9748
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About
Contact & Profiles
Research Areas
  • DNA Repair Mechanisms
  • Genomics and Chromatin Dynamics
  • Epigenetics and DNA Methylation
  • PARP inhibition in cancer therapy
  • Cancer Cells and Metastasis
  • Cell death mechanisms and regulation
  • Autophagy in Disease and Therapy
  • Mechanisms of cancer metastasis
  • Adenosine and Purinergic Signaling
  • Endoplasmic Reticulum Stress and Disease
  • Barrier Structure and Function Studies
  • Cytomegalovirus and herpesvirus research

Sichuan University
2021-2024

State Key Laboratory of Biotherapy
2021-2024

Abstract Chemoresistance has long been the bottleneck of ovarian cancer (OC) prognosis. It shown that mitochondria play a crucial role in cell response to chemotherapy and dysregulated mitochondrial dynamics is intricately linked with diseases like OC, but underlying mechanisms remain equivocal. Here, we demonstrate new mechanism where CRL4 CUL4A/DDB1 manipulates OC chemoresistance by regulating mitophagy. depletion enhanced fission upregulating AMPKα Thr172 MFF Ser172/Ser146...

10.1038/s41392-022-01253-y article EN cc-by Signal Transduction and Targeted Therapy 2022-12-09

H2BK120ub1 triggers several prominent downstream histone modification pathways and changes in chromatin structure, therefore involving it into multiple critical cellular processes including DNA transcription damage repair. Although has been reported that is mediated by RNF20/40 CRL4 WDR70 , less known about the underlying regulation mechanism for WDR70. By using a series of biochemical cell-based studies, we find promotes interacting with complex, deposition H3K79me2 POLE3 loci highly...

10.1126/sciadv.adh2358 article EN cc-by-nc Science Advances 2023-09-08

Many cancers harbor homologous recombination defects (HRDs). A HRD is a therapeutic target that being successfully utilized in treatment of breast/ovarian cancer via synthetic lethality. However, canonical caused by BRCAness mutations do not prevail liver cancer. Here we report subtype the perturbation proteasome variant (CDW19S) hepatitis B virus-bearing (HBV-bearing) cells. This amalgamate protein complex contained 19S decorated with CRL4WDR70 ubiquitin ligase, and assembled at broken...

10.1172/jci171533 article EN cc-by Journal of Clinical Investigation 2023-10-10

Abstract Genomic instability is one of the hallmarks cancer. While loss histone demethylase KDM6A increases risk tumorigenesis, its specific role in maintaining genomic stability remains poorly understood. Here, we propose a mechanism which maintains independently on activity. This occurs through interaction with SND1, resulting establishment protective chromatin state that prevents replication fork collapse by recruiting RPA and Ku70 to nascent DNA strand. Notably, KDM6A–SND1 up-regulated...

10.1093/nar/gkae487 article EN cc-by Nucleic Acids Research 2024-06-08

Abstract Many cancers harbour homologous recombination defects (HRD). The identification of PARP inhibitors as synthetic lethal with HRD has led to new therapeutic strategies for cancers. Here we report a subtype that is caused by the perturbation previously uncharacterised proteasome variant, CDW19S, in hepatitis virus B (HBV) positive hepatocellular carcinoma (HBVHCC). CDW19S contains 19S complex decorated Cullin 4 ubiquitin ligase (CRL4 WDR70 ) assembled at broken chromatin and regulates...

10.1101/2022.07.21.500952 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2022-07-22
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