Malonyl-CoA, a product of acetyl-CoA carboxylase is a metabolic intermediate in lipogenic tissues that include liver and adipose tissue, where it is involved in the de novo fatty acid synthesis and elongation. Malonyl-CoA decarboxylase (MLYCD, E.C.4.1.1.9), a 55-kDa enzyme catalyses the conversion of malonyl-CoA to acetyl-CoA and carbon dioxide, thus providing a route for disposal of malonyl-CoA from mitochondria and peroxisomes, whereas in the cytosol, the malonyl-CoA pool is regulated by the balance of MLYCD and acetyl-CoA carboxylase activities. So far, 34 cases with different MLYCD gene defects comprising point mutations, stop codons, and frameshift mutations have been reported in the literature. Here, we describe the follow-up of a patient affected by malonic aciduria upon neonatal onset. Molecular analysis showed novel homozygous mutations in the MLYCD gene. Our findings expand the number of reported cases and add a novel variant to the repertoire of MLYCD mutations.
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http://dx.doi.org/10.1017/S104795112100113X | DOI Listing |
Animals (Basel)
March 2025
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
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View Article and Find Full Text PDFJ Immunol
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Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA, United States.
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View Article and Find Full Text PDFElife
March 2025
Department of Physiology and Biophysics, Stony Brook University, Stony Brook, New York, United States.
Most human pancreatic ductal adenocarcinoma (PDAC) are not infiltrated with cytotoxic T cells and are highly resistant to immunotherapy. Over 90% of PDAC have oncogenic KRAS mutations, and phosphoinositide 3-kinases (PI3Ks) are direct effectors of KRAS. Our previous study demonstrated that ablation of in KPC (; ; ) pancreatic cancer cells induced host T cells to infiltrate and completely eliminate the tumors in a syngeneic orthotopic implantation mouse model.
View Article and Find Full Text PDFFASEB J
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Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture and Rural Affairs) and Key Laboratory of Mariculture (Ministry of Education), Ocean University of China, Qingdao, People's Republic of China.
As an important kinase that maintains metabolic homeostasis, salt-induced kinase 2 (SIK2) inhibits adipogenesis in adipocytes and regulates mammalian glucose metabolism. Excessive lipid accumulation can lead to an inflammatory response, and SIK2 also controls the expression of inflammatory cytokines. However, the precise mechanisms and interconnections through which SIK2 modulates these processes remain incompletely understood.
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