Autor: |
Solberg A; Clinic for Diagnostics and Intervention and Institute of Medical Microbiology, Oslo University Hospital, Rikshospitalet, 0027 Oslo, Norway., Robertson AB, Aronsen JM, Rognmo Ø, Sjaastad I, Wisløff U, Klungland A |
Jazyk: |
angličtina |
Zdroj: |
Journal of molecular cell biology [J Mol Cell Biol] 2013 Jun; Vol. 5 (3), pp. 194-203. Date of Electronic Publication: 2013 Apr 08. |
DOI: |
10.1093/jmcb/mjt012 |
Abstrakt: |
Mammals have nine homologues of the Escherichia coli AlkB repair protein: Alkbh1-8, and the fat mass and obesity associated protein FTO. In this report, we describe the first functional characterization of mouse Alkbh7. We show that the Alkbh7 protein is located in the mitochondrial matrix and that an Alkbh7 deletion dramatically increases body weight and body fat. Our data indicate that Alkbh7, directly or indirectly, facilitates the utilization of short-chain fatty acids, which we propose is the likely cause for the obesity phenotype observed in the Alkbh7(-/-) mice. Collectively, our data provide the first direct demonstration that murine Alkbh7 is a mitochondrial resident protein involved in fatty acid metabolism and the development of obesity. |
Databáze: |
MEDLINE |
Externí odkaz: |
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