Biography and Research Information
OverviewAI-generated summary
Gang Li's research has explored diverse areas within the biological and medical sciences. His work includes investigations into immune response mechanisms, such as the role of lymphocytes in compensating for DNA repair deficiencies, as evidenced by his 2008 publication on V(D)J recombination. Li has also examined the molecular mechanisms of disease progression and treatment, including the role of exosomal microRNAs in promoting epithelial-to-mesenchymal transition and chemoresistance in gastric cancer cells, detailed in a 2018 publication. His research interests extend to therapeutic strategies, such as the engineering of neutrophil-based biomotors for nanodrug delivery and thrombolytic therapy, as described in a 2022 publication.
Further contributions include studies on the protective effects of compounds like acacetin against sepsis-induced acute lung injury through anti-inflammatory and antioxidative activities, and research on antihypertensive treatments for patients with COVID-19 and hypertension. Li's scholarly output is substantial, with a high-impact researcher designation, reflected in 364 total publications and over 5,000 citations, alongside an h-index of 38. His recent activity indicates ongoing engagement in research.
Metrics
- h-index: 38
- Publications: 364
- Citations: 5,080
Positions
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Ph.DXiamen University Xiamen Cardiovascular Hospital ORCID
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Ph.DUniversity of Arkansas for Medical Sciences ORCID
Selected Publications
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Single cell in vivo analysis of type I IFN and NK cell-mediated control of B cell infection densities during acute gammaherpesvirus infection (2026)
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Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment (2025)
Collaboration Network
Top Collaborators
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Single cell in vivo analysis of type I IFN and NK cell-mediated control of B cell infection densities during acute gammaherpesvirus infection
- Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture
- Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture
- Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture
- Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture
- Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture
- Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture
- Murine Gammaherpesvirus 68 Pathogenesis Is Independent of Caspase-1 and Caspase-11 in Mice and Impairs Interleukin-1β Production upon Extrinsic Stimulation in Culture
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
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