A5084831413- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- Immunotherapy and Immune Responses
- Immune cells in cancer
- CAR-T cell therapy research
- PI3K/AKT/mTOR signaling in cancer
- Cancer Immunotherapy and Biomarkers
- Genomics, phytochemicals, and oxidative stress
- Single-cell and spatial transcriptomics
- Skin Protection and Aging
- NF-κB Signaling Pathways
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Immune Response and Inflammation
- Diabetes and associated disorders
- interferon and immune responses
- Pancreatic function and diabetes
- RNA Research and Splicing
- Bioinformatics and Genomic Networks
- melanin and skin pigmentation
- CRISPR and Genetic Engineering
- Cancer, Hypoxia, and Metabolism
- COVID-19 Clinical Research Studies
- Peroxisome Proliferator-Activated Receptors
- Inflammasome and immune disorders
- Acute Myeloid Leukemia Research
St. Jude Children's Research Hospital
2016-2025
Wenzhou Medical University
2013-2024
Zhejiang Taizhou Hospital
2018-2024
University of Tennessee Health Science Center
2014-2015
Ducks Unlimited
2013-2014
Washington University in St. Louis
2012
Yale University
2004-2010
Howard Hughes Medical Institute
2006-2007
University of Rochester
1999-2001
University of Toronto
1995
Upon antigen stimulation, the bioenergetic demands of T cells increase dramatically over resting state. Although a role for metabolic switch to glycolysis has been suggested support increased anabolic activities and facilitate cell growth proliferation, whether cellular metabolism controls lineage choices remains poorly understood. We report that glycolytic pathway is actively regulated during differentiation inflammatory TH17 Foxp3-expressing regulatory (Treg cells) fate determination. but...
Engagement of Toll-like receptors (TLRs) on macrophages leads to activation the mitogen-activated protein kinases (MAPKs), which contribute innate immune responses. MAPK activity is regulated negatively by phosphatases (MKPs). MKP-1, founding member this family dual-specificity phosphatases, has been implicated in regulating lipopolysaccharide (LPS) responses, but its role TLR-mediated responses vivo not defined. Here, we show that mice deficient MKP-1 were highly susceptible endotoxic shock...
The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) central regulator spontaneous cell death. Absence TAK1 in macrophages induced without requiring toll-like (TLR) priming subsequent activating signals, suggesting distinctive role for maintaining homeostasis. Autocrine tumor necrosis factor...