作者: Keltoum Anflous-Pharayra , Nha Lee , Dawna L. Armstrong , William J. Craigen
DOI: 10.1016/J.BBABIO.2010.09.007
关键词: Mitochondrial membrane transport protein 、 Respiratory enzyme 、 Cell biology 、 Oxidative phosphorylation 、 Mitochondrion 、 Biology 、 Inner mitochondrial membrane 、 VDAC1 、 VDAC3 、 Biochemistry 、 Voltage-dependent anion channel
摘要: Voltage-dependent anion channel (VDAC) is an abundant mitochondrial outer membrane protein. In mammals, three VDAC isoforms have been characterized. We previously reported alterations in the function of mitochondria when assessed situ different muscle types VDAC1 deficient mice (Anflous et al., 2001). present report we extend study to VDAC3 muscles and measure respiratory enzyme activity both muscles. While heart absence causes a decrease apparent affinity for ADP, gastrocnemius, mixed glycolytic/oxidative muscle, ADP remains unchanged. The multiple defects complex activities muscle. However, defect restricted only IV. These functional correlate with structural aberrations mitochondria. results demonstrate that, unlike VDAC1, there muscle-type specificity therefore vivo these two may fulfill physiologic functions.