A5020025290- interferon and immune responses
- Mitochondrial Function and Pathology
- Immune Cell Function and Interaction
- Ubiquitin and proteasome pathways
- Neuroinflammation and Neurodegeneration Mechanisms
- Endoplasmic Reticulum Stress and Disease
- Inflammasome and immune disorders
- Protein Kinase Regulation and GTPase Signaling
- Melanoma and MAPK Pathways
- Chemical Synthesis and Analysis
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Allergic Rhinitis and Sensitization
- Epigenetics and DNA Methylation
- Cancer, Hypoxia, and Metabolism
- Genetics, Bioinformatics, and Biomedical Research
- Viral Infections and Vectors
- Click Chemistry and Applications
- Cancer Genomics and Diagnostics
- Microbial Metabolic Engineering and Bioproduction
- Toxoplasma gondii Research Studies
Novartis (United States)
2023-2024
Bryan College
2021-2023
Texas A&M University
2018-2023
Texas A&M Health Science Center
2018-2021
Yale University
2012-2013
Mitochondrial DNA (mtDNA) is a potent agonist of the innate immune system; however, exact immunostimulatory features mtDNA and kinetics detection by cytosolic nucleic acid sensors remain poorly defined. Here, we show that mitochondrial genome instability promotes Z-form accumulation. Z-DNA binding protein 1 (ZBP1) stabilizes nucleates complex containing cGAS, RIPK1, RIPK3 to sustain STAT1 phosphorylation type I interferon (IFN-I) signaling. Elevated mtDNA, ZBP1 expression, IFN-I signaling...
Mitochondrial dysfunction is a key driver of inflammatory responses in human disease. However, it remains unclear whether alterations mitochondria-innate immune cross-talk contribute to the pathobiology mitochondrial disorders and aging. Using polymerase gamma (POLG) mutator model DNA instability, we report that aberrant activation type I interferon (IFN-I) innate axis potentiates immunometabolic dysfunction, reduces health span, accelerates aging mice. Mechanistically, elevated IFN-I...
Mitochondria are central key players in cell metabolism, and mitochondrial DNA (mtDNA) instability has been linked to metabolic changes that contribute tumorigenesis increased expression of pro-tumorigenic genes. Here, we use melanoma lines metastatic tumors evaluate the effect mtDNA alterations packaging factor, TFAM, on energetic metabolism nuclear gene changes. We report a positive correlation between copy number, glucose consumption, ATP production lines. Gene analysis reveals...
WDR5 is a critical chromatin cofactor of MYC. interacts with MYC through the WBM pocket and hypothesized to anchor its WIN site. Blocking interaction impairs recruitment target genes disrupts oncogenic function in cancer development, thus providing promising strategy for treatment MYC-dysregulated cancers. Here, we describe discovery novel antagonists containing 1-phenyl dihydropyridazinone 3-carboxamide core that was identified from high-throughput screening subsequent structure-based...
Gamma-interferon-inducible lysosomal thiol reductase (GILT) is known to reduce disulfide bonds present in proteins internalized by antigen presenting cells, facilitating optimal processing and presentation of peptides on Major Histocompatibility Complex class II molecules, as well the subsequent activation CD4-positive T lymphocytes. Here, we show that GILT required for II-restricted immunodominant epitopes from major house dust mite allergen Der p 1. In absence GILT, cell responses 1 are...
SUMMARY Mitochondrial DNA (mtDNA) is a potent agonist of the innate immune system; however, exact immunostimulatory features mtDNA and kinetics detection by cytosolic nucleic acid sensors remain poorly defined. Here, we show that mitochondrial genome instability leads to Z-form accumulation. Z-DNA Binding Protein 1 (ZBP1) stabilizes nucleates complex containing cGAS, RIPK1, RIPK3 sustain STAT1 phosphorylation type I interferon (IFN-I) signaling. Increased Z-DNA, ZBP1 expression, IFN-I...
Abstract Mitochondrial dysfunction is a key driver of inflammatory responses in human disease. However, it remains unclear whether alterations mitochondria-innate immune crosstalk contribute to the pathobiology mitochondrial disorders and aging. Using polymerase gamma (POLG) mutator model DNA (mtDNA) instability, we report that aberrant activation type I interferon (IFN-I) innate axis potentiates immunometabolic dysfunction, reduces healthspan, accelerates aging mice. Mechanistically,...
Abstract Gulf War Illness (GWI) is a chronic, multi-symptom disorder affecting approximately 30 percent of the nearly 700,000 veterans 1991 Persian War. Recent studies have revealed that GWI-related chemical (GWIC) exposure promotes immune activation and metabolic rewiring, which correlate with neurocognitive impairments other symptoms GWI. However, molecular mechanisms signaling pathways linking GWIC to inflammation, alterations, neurological remain unclear. Mitochondrial dysfunction has...