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Publication : MOXI Is a Mitochondrial Micropeptide That Enhances Fatty Acid β-Oxidation.

First Author  Makarewich CA Year  2018
Journal  Cell Rep Volume  23
Issue  13 Pages  3701-3709
PubMed ID  29949755 Mgi Jnum  J:271253
Mgi Id  MGI:6278482 Doi  10.1016/j.celrep.2018.05.058
Citation  Makarewich CA, et al. (2018) MOXI Is a Mitochondrial Micropeptide That Enhances Fatty Acid beta-Oxidation. Cell Rep 23(13):3701-3709
abstractText  Micropeptide regulator of beta-oxidation (MOXI) is a conserved muscle-enriched protein encoded by an RNA transcript misannotated as non-coding. MOXI localizes to the inner mitochondrial membrane where it associates with the mitochondrial trifunctional protein, an enzyme complex that plays a critical role in fatty acid beta-oxidation. Isolated heart and skeletal muscle mitochondria from MOXI knockout mice exhibit a diminished ability to metabolize fatty acids, while transgenic MOXI overexpression leads to enhanced beta-oxidation. Additionally, hearts from MOXI knockout mice preferentially oxidize carbohydrates over fatty acids in an isolated perfused heart system compared to wild-type (WT) animals. MOXI knockout mice also exhibit a profound reduction in exercise capacity, highlighting the role of MOXI in metabolic control. The functional characterization of MOXI provides insight into the regulation of mitochondrial metabolism and energy homeostasis and underscores the regulatory potential of additional micropeptides that have yet to be identified.
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