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Functional analysis of the novel mitochondrial tRNA and tRNA variants associated with type 2 diabetes mellitus.
World J Diabetes
August 2024
Central Laboratory, Hangzhou First People's Hospital, Hangzhou 310006, Zhejiang Province, China.
Article Synopsis
- Mutations in mitochondrial tRNA genes are linked to type 2 diabetes mellitus (T2DM), with a focus on novel variants found in a Chinese family.
- A study aimed to evaluate the genetic and biochemical impacts of these variants using specially created cell lines, comparing them to healthy controls.
- Results showed that one variant led to significant mitochondrial dysfunction and increased oxidative stress, while the other did not appear to affect mitochondrial function significantly.
Knocking out central metabolism genes to identify new targets and alternating substrates to improve lipid synthesis in .
Front Bioeng Biotechnol
January 2023
Department of Chemical, Biochemical and Environmental Engineering, University of MD, Baltimore County, Baltimore, MD, United States.
Systematic gene knockout studies may offer us novel insights on cell metabolism and physiology. Specifically, the lipid accumulation mechanism at the molecular or cellular level is yet to be determined in the oleaginous yeast . Herein, we established ten engineered strains with the knockout of important genes involving in central carbon metabolism, NADPH generation, and fatty acid biosynthetic pathways.
View Article and Find Full Text PDFMitochondrial C3a Receptor Activation in Oxidatively Stressed Epithelial Cells Reduces Mitochondrial Respiration and Metabolism.
Front Immunol
September 2021
Department of Ophthalmology, Medical University of South Carolina, Charleston, SC, United States.
Complement component 3 fragment C3a is an anaphylatoxin involved in promoting cellular responses important in immune response and host defense. Its receptor (C3a receptor, C3aR) is distributed on the plasma membrane; however, lysosomal localization in immune cells has been reported. Oxidative stress increases intracellular reactive oxygen species (ROS), and ROS activate complement signaling in immune cells and metabolic reprogramming.
View Article and Find Full Text PDFA Mitochondrial DNA Variant Elevates the Risk of Gallstone Disease by Altering Mitochondrial Function.
Cell Mol Gastroenterol Hepatol
March 2022
State Key Laboratory of Genetic Engineering, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, China; Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, China; Research Unit of Dissecting the Population Genetics and Developing New Technologies for Treatment and Prevention of Skin Phenotypes and Dermatological Diseases (2019RU058), Chinese Academy of Medical Sciences, Shanghai, China; Taizhou Institute of Health Sciences, Fudan University, Taizhou, China. Electronic address:
Background And Aims: Gallstone disease (cholelithiasis) is a cholesterol-related metabolic disorders with strong familial predisposition. Mitochondrial DNA (mtDNA) variants accumulated during human evolution are associated with some metabolic disorders related to modified mitochondrial function. The mechanistic links between mtDNA variants and gallstone formation need further exploration.
View Article and Find Full Text PDFCybrid technology.
Methods Cell Biol
December 2020
Department of Neurology, University of Miami School of Medicine, Miami, FL, United States. Electronic address:
The study of the mitochondrial DNA (mtDNA) has been hampered by the lack of methods to genetically manipulate the mitochondrial genome in living animal cells. This limitation has been partially alleviated by the ability to transfer mitochondria (and their mtDNAs) from one cell into another, as long as they are from the same species. This is done by isolating mtDNA-containing cytoplasts and fusing these to cells lacking mtDNA.
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