Examination of bioenergetic function in the inner mitochondrial membrane peptidase 2-like (Immp2l) mutant mice

被引:19
作者
Bharadwaj, Manish S. [1 ]
Zhou, Yu [2 ]
Molina, Anthony J. [1 ]
Criswell, Tracy [2 ]
Lu, Baisong [2 ]
机构
[1] Wake Forest Univ Hlth Sci, Dept Internal Med, Sect Gerontol & Geriatr Med, Winston Salem, NC 27157 USA
[2] Wake Forest Univ Hlth Sci, Wake Forest Inst Regenerat Med, Winston Salem, NC 27157 USA
基金
美国国家卫生研究院;
关键词
Immp2l; Cytochrome c1; GPD2; Complex III; Mitochondrial respiration; SKELETAL-MUSCLE MITOCHONDRIA; COMPLEX-III; HEART-MITOCHONDRIA; HYDROGEN-PEROXIDE; GENE IMMP2L; DEHYDROGENASE; EXPRESSION; SUBUNIT; PROTEIN; YEAST;
D O I
10.1016/j.redox.2014.08.006
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inner mitochondrial membrane peptidase 2-like (IMMP2L) protein is a mitochondrial inner membrane peptidase that cleaves the signal peptide sequences of cytochrome cl (CYC1) and mitochondrial glycerol phosphate dehydrogenase (GPD2). Immp2l mutant mice show infertility and early signs of aging. It is unclear whether mitochondrial respiratory deficiency underlies this phenotype. Here we show that the intermediate forms of GPD2 and CYC1 have normal expression levels and enzymatic function in Immp2l mutants. Mitochondrial respiration is not diminished in isolated mitochondria and cells from mutant mice. Our data suggest that respiratory deficiency is not the cause of the observed Immp2l mutant phenotypes. (C) 2014 The Authors. Published by Elsevier B.V.
引用
收藏
页码:1008 / 1015
页数:8
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