A5005875123- Cell death mechanisms and regulation
- Inflammasome and immune disorders
- Mitochondrial Function and Pathology
- Immune Response and Inflammation
- Respiratory Support and Mechanisms
- interferon and immune responses
- Endoplasmic Reticulum Stress and Disease
- ATP Synthase and ATPases Research
- RNA Research and Splicing
- Exercise and Physiological Responses
- Metabolism and Genetic Disorders
- RNA regulation and disease
- Heme Oxygenase-1 and Carbon Monoxide
- Animal Nutrition and Physiology
- Lipid metabolism and biosynthesis
- Phagocytosis and Immune Regulation
- Toxoplasma gondii Research Studies
- Genetic Neurodegenerative Diseases
- Malaria Research and Control
- Neonatal Respiratory Health Research
- Physiological and biochemical adaptations
- Intensive Care Unit Cognitive Disorders
- Photosynthetic Processes and Mechanisms
- Fish Ecology and Management Studies
- Chronic Obstructive Pulmonary Disease (COPD) Research
Enzo Life Sciences (United States)
2024
University of California, Davis
2014-2021
McGill University
2004-2014
Mitochondrial function is integrated with cellular status through the regulation of opposing mitochondrial fusion and division events. Here we uncover a link between dynamics lipid metabolism by examining role carrier homologue 2 (MTCH2). MTCH2 modified outer membrane protein implicated in intrinsic cell death vivo fatty acid metabolism. Our data indicate that selective effector starvation-induced hyperfusion, cytoprotective response to nutrient deprivation. We find stimulates manner...
Sepsis-induced diaphragmatic force loss and failure are associated with an increased exposure of the muscle to proinflammatory mediators.Our objectives were test hypothesis that force-inhibiting mediators may arise in large part from diaphragm itself evaluate roles mechanical stress, free radicals, nuclear factor (NF)-kappaB transcription pathway endotoxin (LPS)-induced responses diaphragm.Murine limb cells exposed LPS vitro vivo. Proinflammatory gene expression was measured using RNase...
Pathogen sensing by the inflammasome activates inflammatory caspases that mediate inflammation and cell death. Caspase-12 antagonizes NF-κB is associated with susceptibility to bacterial sepsis. A single-nucleotide polymorphism (T(125)C) in human Casp12 restricts its expression Africa, Southeast Asia, South America. Here, we investigated role of caspase-12 control parasite replication pathogenesis malaria report dampened clearance blood-stage modulated cerebral malaria. This response was...
Dephosphorylation of pSer51 the α subunit translation initiation factor 2 (eIF2α P ) terminates signaling in integrated stress response (ISR). A trimeric mammalian holophosphatase comprised a protein phosphatase 1 (PP1) catalytic subunit, conserved C-terminally located ~70 amino acid core substrate-specific regulatory (PPP1R15A/GADD34 or PPP1R15B/CReP) and G-actin (an essential cofactor) efficiently dephosphorylate eIF2α vitro. Unlike their viral invertebrate counterparts, with whom they...
Abstract Introduction Respiratory muscle weakness is common in sepsis patients. Proinflammatory mediators produced during have been implicated diaphragmatic contractile dysfunction, but the role of chemokines has not explored. This study addressed monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), pathogenesis inflammation and endotoxemia. Methods Mice were treated follows ( n = 6 per group): (a) saline, (b) endotoxin (25 μg/g IP), (c) + anti-MCP-1 antibody, (d) isotype control...
Mitochondria are double‐membrane organelles that generate most of the energy used by cells and play key roles in cellular growth, death differentiation. Continuous remodeling redistribution mitochondrial membrane structure critical for integrating organelle physiology with needs. Cardiolipin (CL) is a diphosphotidyl lipid found almost exclusively bacteria inner eukaryotes. CL distribution within membranes important determining structure, regulating bioenergetic processes, recruiting factors...
Abstract Dephosphorylation of pSer51 the α subunit translation initiation factor 2 (eIF2α P ) terminates signalling in integrated stress response (ISR). A trimeric mammalian holophosphatase comprised a PP1 catalytic subunit, conserved C-terminally located ∼70 amino acid core substrate-specific regulatory (PPP1R15A/GADD34 or PPP1R15B/CReP) and G-actin (an essential co-factor) efficiently dephosphorylate eIF2α vitro. Unlike their viral invertebrate counterparts, with whom they share 70 residue...