Disease relevance of SLC25A14

• The present results indicate that BMCP1 may be involved in pathogenesis of mitochondrial dysfunction in neurons induced by aging or neurodegenerative disorders, and perhaps in energy balance in the brain [1].
• Exacerbation of cytotoxicity, oxidative stress and modification of MMP with reduced UCP5 expression in the face of MPP(+) toxicity suggest that UCP5 might be physiologically important in the pathology of oxidative stress-induced neurodegeneration [2].
• The objective of this study is to demonstrate the effectiveness and feasibility in treating empyema after pulmonary resection with a modified Clagett procedure performed at the bedside (BMCP) [3].

High impact information on SLC25A14

• In the nervous system, BMCP1 was present in cortex, basal ganglia, substantia nigra, cerebellum, and spinal cord [4].
• To study the effect of BMCP1 expression on mitochondrial function, neuronal (GT1-1) cell lines with stable overexpression of BMCP1 were generated [4].
• We explored the effects of reduced UCP5 expression on mitochondrial membrane potential (MMP), oxidative stress, ATP levels, and cell viability, under normal and MPP(+)-induced cytotoxic conditions, in human catecholaminergic SH-SY5Y cells [2].
• The increase in ROS production may be attenuated by UCP4 and UCP5 up-regulation [5].
• Particular attention has been paid to the roles of UCP2 to UCP5 as agents mediating thermogenesis, and to the concept of limited or "mild" uncoupling as a means of reducing oxidative stress [6].

Biological context of SLC25A14

• Molecular cloning of rat brain mitochondrial carrier protein-1 cDNA and its up-regulation during postnatal development [1].
• We investigated the relationship between skeletal muscle UCP5 expression and in vivo energy metabolism in 36 non-diabetic Pima Indians [7].
• However, UCP5 knockdown increased MPP(+)-induced cytotoxicity by 15% and oxidative stress levels by 40%, and partially restored MPP(+)-induced mitochondrial depolarization by 57% [2].
• UCP4 and UCP5 are interesting in light of their abundant expression in the brain, which may signal an important metabolic function in thermogenesis or regulation of reactive oxygen species in that tissue [8].
• Transgenic mice expressing murine UCP5(L), the long isoform of UCP5, using an inducible metallothionine promoter (to drive expression of the transgene in liver, testis, heart, lung, spleen, intestine, kidney and brain) did not display any overt metabolic phenotype, despite liver UCP5(L) mRNA expression equivalent to that of normal mouse brain [8].

Anatomical context of SLC25A14

• In 48-h fasted or insulin-induced hypoglycemic rats, BMCP1 mRNA expression in the hypothalamus slightly, but significantly, decreased compared with that in their appropriate controls [1].
• The effects of classical uncouplers, fatty acids, uncoupling proteins (UCP1-UCP5) and thyroid hormones on the efficiency of OxPhos are described [9].

Other interactions of SLC25A14

• The UCP signature excluding BMCP1 was also found in the second matrix segment: [positively charged residue]-(Pro/ del-Leu/del)-[positively charged residue]-phi-X-Gly/Ser-Thr/n-X-NH/[negatively charged residue]-Ala-phi [10].
• Phylogenetic analysis indicates that there are at least three clades of UCPs in invertebrates, which are closely related to vertebrate UCP1-3, UCP4, and UCP5, respectively, and shows early evolutionary divergence of UCPs, which pre-dates the divergence of protostomes and deuterostomes [11].

Analytical, diagnostic and therapeutic context of SLC25A14

• Three patients underwent BMCP as an outpatient, whereas the other two had BMCP during their hospitalizations [3].

References