Acts as an import component of the TIM23 translocase complex. Stimulates the ATPase activity of HSPA9 (By similarity). Negative regulator of the mitochondrial respiratory chain. Prevents mitochondrial hyperpolarization state and restricts mitochondrial generation of ATP. Interacts with the TIM23 complex. Directly interacts with PAM16/MAGMAS; this interaction counteracts DNAJC15-dependent stimulation of HSPA9 ATPase activity (By similarity). Associates with complex I of the mitochondrial electron transfer chain; this interaction may interfere with the formation of supercomplexes that facilitate the transfer of electrons between complexes. Expressed at high levels in liver, heart, at moderate levels in kidney and, at very low levels, in lung (at protein level). High expression levels in testis. Highly expressed in CD8+ T-cells, but barely detectable in CD4+ T-cells (at protein level). Almost undetectable in B-cells. No visible phenotype. Mutant animals are viable. Both male and female are fertile and do not exhibit any obvious malformations or behavioral abnormalities. CD8+ T-cell mitochondria are hyperpolarized, compared to their wild-type counterparts. In fasted mutant animals, livers do not exhibit any signs of steatosis, but accumulate glycogen, possibly due to a sustained mitochondrial oxidation that leads to rapid metabolism of lipids, hence minimizing their accumulation in the liver and favoring glycogenesis. During fasting, loss of white fat is also more prominent than in wild type animals.