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Efficacy and safety of pharmacological treatments in inclusion body myositis: a systematic review.
RMD Open
January 2025
Department of Neuromuscular Diseases, University College London, London, UK
Objective: To identify the best evidence on the efficacy of treatment interventions for inclusion body myositis (IBM) and to describe their safety.
Methods: Systematic review of randomised controlled trials (RCTs) of pharmacological treatments of adults with IBM, conducted according to the Cochrane Handbook, updating a previous Cochrane review. The search strategy was run on Cochrane Neuromuscular Disease Group Specialized Register, CENTRAL, MEDLINE and EMBASE, ClinicalTrials.
Chronic CRYPTOCHROME deficiency enhances cell-intrinsic antiviral defences.
Philos Trans R Soc Lond B Biol Sci
January 2025
Department of Infectious Disease, Imperial College London, London SW7 2AZ, UK.
The within-host environment changes over circadian time and influences the replication and severity of viruses. Genetic knockout of the circadian transcription factors CRYPTOCHROME 1 and CRYPTOCHROME 2 (/; CKO) leads to altered protein homeostasis and chronic activation of the integrated stress response (ISR). The adaptive ISR signalling pathways help restore cellular homeostasis by downregulating protein synthesis in response to endoplasmic reticulum overloading or viral infections.
View Article and Find Full Text PDFMitochondrial fatty acid oxidation regulates monocytic type I interferon signaling via histone acetylation.
Sci Adv
January 2025
Laboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Although lipid-derived acetyl-coenzyme A (CoA) is a major carbon source for histone acetylation, the contribution of fatty acid β-oxidation (FAO) to this process remains poorly characterized. To investigate this, we generated mitochondrial acetyl-CoA acetyltransferase 1 (ACAT1, distal FAO enzyme) knockout macrophages. C-carbon tracing confirmed reduced FA-derived carbon incorporation into histone H3, and RNA sequencing identified diminished interferon-stimulated gene expression in the absence of ACAT1.
View Article and Find Full Text PDFImplications of Raftlin in different diseases: from molecular biology to diagnostic value.
Biomark Med
January 2025
Department of Clinical Laboratory, Gansu Provincial Clinical Research Center for Laboratory Medicine, Lanzhou, China.
Raftlin (raft-linking) protein is an essential component of the lipid raft structure and plays a crucial role in B and T cell signaling pathways. It facilitates B cell receptor (BCR) signaling by promoting calcium mobilization and tyrosine phosphorylation in the cells while colocalizing with BCR on the cell membrane. Interestingly, Raftlin is internalized in lipopolysaccharide-stimulated T cells by colocalization with Toll-like receptor 4 (TLR4), wherein it exerts a similar role as in B cells.
View Article and Find Full Text PDFGenetic deficiency or pharmacological inhibition of cGAS-STING signalling suppresses kidney inflammation and fibrosis.
Br J Pharmacol
January 2025
Division of Nephrology, Department of Medicine, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
Background And Purpose: Chronic kidney disease (CKD) is characterised by inflammation, which can lead to tubular atrophy and fibrosis. The molecular mechanisms are not well understood. In this study, we investigated the functional role of the cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signalling in renal inflammation and fibrosis.
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