Biography and Research Information
OverviewAI-generated summary
Zheng‐Yu Wang's research focuses on xenotransplantation, specifically investigating methods to reduce immunological barriers between species. His work has involved the genetic modification of pigs to create models for transplantation studies. Publications detail the generation of pigs deficient in specific carbohydrate antigens, such as N-glycolylneuraminic acid and galactose α-1,3-galactose, which are known targets for immune rejection in xenotransplantation.
Further research includes the development of genetically modified pigs lacking Class I MHC, a key component of the immune system. Wang has also explored the potential of erythrocytes from genetically modified pigs for xenotransfusion applications. His research utilizes techniques such as CRISPR-Cas9 for gene editing and multiplexed single-guide RNA for efficient genetic modification. Collaborations within the University of Arkansas for Medical Sciences contribute to his research network.
Beyond xenotransplantation, Wang's publications also touch on other areas of molecular biology, including the role of NSUN2 as a glucose sensor in cancer and the regulation of cytokine gene expression in immune cells. His scholarship metrics include an h-index of 24, with 77 total publications and over 2,300 citations.
Metrics
- h-index: 24
- Publications: 77
- Citations: 2,317
Positions
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Research Associate Professor 2020–presentUniversity of Miami Miller School of Medicine Palm Beach Regional Campus Miami Transplant Institute, Department of Surgery ORCID
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Research Associate ProfessorUniversity of Arkansas for Medical Sciences ORCID
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Assistant Professor 2016–2020The University of Alabama at Birmingham School of Medicine Department of Surgery ORCID
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Research Assistant Professor 2010–2016Indiana University School of Medicine Department of Surgery ORCID
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Physician/Attending 1988–1997Liaoning Health Industry Group Fushun General Hospital Neurology ORCID
Selected Publications
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CD36-mediated endocytosis of proteolysis-targeting chimeras (2025)
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NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance (2023)
Collaboration Network
Top Collaborators
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- CD36-mediated endocytosis of proteolysis-targeting chimeras
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- CD36-mediated endocytosis of proteolysis-targeting chimeras
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- CD36-mediated endocytosis of proteolysis-targeting chimeras
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- CD36-mediated endocytosis of proteolysis-targeting chimeras
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- CD36-mediated endocytosis of proteolysis-targeting chimeras
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance
- CD36-mediated endocytosis of proteolysis-targeting chimeras
- CD36-mediated endocytosis of proteolysis-targeting chimeras
- CD36-mediated endocytosis of proteolysis-targeting chimeras
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