A5008232066- Endoplasmic Reticulum Stress and Disease
- Adipose Tissue and Metabolism
- Genetics, Aging, and Longevity in Model Organisms
- Adipokines, Inflammation, and Metabolic Diseases
- Genomics, phytochemicals, and oxidative stress
- Autophagy in Disease and Therapy
- RNA regulation and disease
- Lipid metabolism and biosynthesis
Weill Cornell Medicine
2024
Cornell University
2015-2024
Transcriptional networks that govern secretory cell specialization, including instructing cells to develop a unique cytoarchitecture, amass extensive protein synthesis machinery, and be embodied respond endoplasmic reticulum (ER) stress, remain largely uncharacterized. In this study, we discovered the transcription factor MIST1 (Bhlha15), previously shown essential for cytoskeletal organization activity, also functions as potent ER stress-inducible transcriptional regulator. Genome-wide DNA...
The unfolded protein response (UPR) regulates endoplasmic reticulum (ER) homeostasis and protects cells from ER stress. IRE1α is a central regulator of the UPR that activates transcription factor XBP1s through an unconventional splicing mechanism using its endoribonuclease activity. also cleaves certain mRNAs containing XBP1-like secondary structures to promote degradation these mRNAs, process known as regulated IRE1α-dependent decay (RIDD). We show here mRNA CReP/Ppp1r15b, regulatory...
Activation of thermogenic brown adipose tissue (BAT) and inducible beige (BeAT) is triggered by environmental or metabolic stimuli, including cold ambient temperatures nutrient stress. Thioesterase superfamily member 1 (Them1), a long-chain fatty acyl-CoA thioesterase that enriched in BAT, suppresses acute cold-induced thermogenesis. Here, we demonstrate Them1 expression was induced BAT BeAT the carbohydrate response element binding protein (ChREBP) to chronic exposure activation integrated...