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Type I IFN induces long-chain acyl-CoA synthetase 1 to generate a phosphatidic acid reservoir for lipotoxic saturated fatty acids.
J Lipid Res
December 2024
Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington, Seattle, WA; UW Medicine Diabetes Institute, University of Washington, Seattle, WA; Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA. Electronic address:
Long-chain acyl-CoA synthetase 1 (ACSL1) catalyzes the conversion of long-chain fatty acids to acyl-CoAs. ACSL1 is required for β-oxidation in tissues that rely on fatty acids as fuel, but no consensus exists on why ACSL1 is induced by inflammatory mediators in immune cells. We used a comprehensive and unbiased approach to investigate the role of ACSL1 induction by interferon type I (IFN-I) in myeloid cells in vitro and in a mouse model of IFN-I overproduction.
View Article and Find Full Text PDFElectron-Transferring Flavoprotein and Its Dehydrogenase Required for Fungal Pathogenicity in .
Int J Mol Sci
October 2024
State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University, Kunming 650091, China.
Article Synopsis
- Electron transfer flavoprotein (ETF) is crucial for fatty acid beta oxidation and amino acid metabolism, and its function is linked to the pathogenicity of some fungi that attack nematodes.
- Mutations in ETF and its dehydrogenase resulted in serious mitochondrial defects and disrupted fatty acid metabolism, severely affecting the fungi's ability to trap nematodes.
- Rich nutritional conditions can compensate for these mutations, allowing the fungi to regain trap formation and predatory activity, while the absence of certain genes leads to the accumulation of attractants that draw in nematodes.
Overexpression of the key metabolic protein Carnitine Palmitoyl Transferase 1A (CPT1A) in equine sarcoid.
J Equine Vet Sci
December 2024
Department of Veterinary Medicine and Animal Production, University of Naples Federico II, Via Delpino 80137, Naples, Italy.
The equine sarcoid is the most common skin neoplasia of fibroblastic origin in horses, characterized by an excessive accumulation of extracellular matrix produced by sarcoid fibroblasts under hypoxic condition. Neoplastic cells can adapt to hypoxia by using alternative energy sources, particularly those that arise from fatty acid oxidation (FAO). The Carnitine Palmitoyl Transferase 1A (CPT1A) belongs to Carnitine System (CS) and promotes the entrance of fatty acids into the mitochondria for β-oxidation.
View Article and Find Full Text PDFKnock-out of CD73 delays the onset of HR-negative breast cancer by reprogramming lipid metabolism and is associated with increased tumor mutational burden.
Mol Metab
November 2024
Laboratory of Cell Biology and Immunology, Institute of Medical Biotechnology and Experimental Oncology, Intercollegiate Faculty of Biotechnology University of Gdańsk and Medical University of Gdańsk, Medical University of Gdańsk, Poland. Electronic address:
Objective: CD73 (ecto-5'-nucleotidase, NT5E), a cell-surface enzyme converting 5'-AMP to adenosine, is crucial for cancer progression. However, its role in the tumorigenesis process remains mostly obscure. We aimed to demonstrate CD73's role in breast cancer (BC) tumorigenesis through metabolic rewiring of fatty acid metabolism, a process recently indicated to be regulated by BC major prognostic markers, hormone receptors (HR) for estrogen (ER), and progesterone (PR).
View Article and Find Full Text PDFEtomoxir repurposed as a promiscuous fatty acid mimetic chemoproteomic probe.
iScience
September 2024
Department of Physiology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Article Synopsis
- Etomoxir is a medicine that has been used for a long time to block a process called fatty acid β-oxidation in cells.
- Researchers found that etomoxir not only works on one specific protein called Cpt1 but also attaches to many other proteins involved in processing fatty acids in different parts of the cell.
- When they removed a protein called Pex5 that helps transport certain proteins into a part of the cell called the peroxisome, they discovered that etomoxir affected even more proteins, showing that it isn't a precise tool for studying fatty acid oxidation.
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