A5065547663- Endoplasmic Reticulum Stress and Disease
- Sirtuins and Resveratrol in Medicine
- Cholesterol and Lipid Metabolism
- Autophagy in Disease and Therapy
- Calcium signaling and nucleotide metabolism
- Diabetes and associated disorders
- Biochemical and Molecular Research
- Immune cells in cancer
- Epigenetics and DNA Methylation
- Receptor Mechanisms and Signaling
- Lipid metabolism and biosynthesis
- Child Nutrition and Water Access
- Lipid Membrane Structure and Behavior
- Tuberculosis Research and Epidemiology
- Genetics, Aging, and Longevity in Model Organisms
- Phagocytosis and Immune Regulation
- Cellular transport and secretion
- Caveolin-1 and cellular processes
University of Massachusetts Chan Medical School
2013-2023
University of Massachusetts Amherst
2015
Lipogenesis requires coordinated expression of genes for fatty acid, phospholipid, and triglyceride synthesis. Transcription factors, such as SREBP-1 (Sterol regulatory element binding protein), may be activated in response to feedback mechanisms linking gene activation levels metabolites the pathways. SREBPs can regulated membrane cholesterol we also found that low phosphatidylcholine (a methylated phospholipid) led SBP-1/SREBP-1 maturation C. elegans or mammalian models. To identify...
Tuberculosis, the disease caused by bacterium M. tuberculosis , remains one of top 10 causes death worldwide. Macrophages, first cells to encounter and critical for defense against infection, are hijacked as a protected growth niche. -infected macrophages undergo metabolic reprogramming where key mitochondrial pathways modulated, but mechanisms driving this shift is unknown.
Diabetes mellitus increases risk for tuberculosis disease and adverse outcomes. Most people with both conditions have type 2 diabetes, but it is unknown if 1 diabetes identical effects on susceptibility. Here we show that male mice receiving a high-fat diet streptozotocin to model higher mortality, more lung pathology, bacterial burden following Mycobacterium infection compared treated or alone. Type elevated plasma glycerol, which preferred carbon source M. tuberculosis. Infection studies...
Infection response and other immunity-linked genes (ILGs) were first named in Caenorhabditis elegans-based expression after pathogen challenge, but many are also up-regulated when lipid metabolism is perturbed. Why attack metabolic changes both increase ILGs unclear. We find that activated phosphatidylcholine (PC) levels change membranes of secretory organelles C. elegans. RNAi targeting the ADP-ribosylation factor arf-1, which disrupts Golgi function, activates ILGs. Low PC limits ARF-1...
The sterol regulatory element‐binding protein (SREBP‐1a, ‐1c, and 2) family of transcription factors control genes involved in cholesterol, fatty acid, triacylglycerol biosynthesis. Misregulation these can contribute to development the metabolic syndrome. Although cholesterol regulation SREBP's has been well characterized, by nutritional cues is less defined. Previously, we identified an additional level SREBP‐1 whereby proteolytic maturation controlled levels intracellular...
Abstract Immunity-linked genes (ILGs) are activated by pathogens but also may respond to imbalances in lipids. Why pathogen attack and metabolic changes both impact ILG activation is unclear. We find that ILGs when membrane phosphatidylcholine ratios change secretory organelles C. elegans . RNAi targeting of the ADP-ribosylation factor ARF-1, which disrupts Golgi, activates expression, suggesting this stress response could occur outside ER. Our data argue upregulation a coordinated...