SLC25A14 Membrane Protein Introduction

Introduction of SLC25A14

UCP5 (SLC25A14) was first described and named as brain mitochondrial carrier protein-1 (BMCP1), which is a member of the mitochondrial solute carrier 25 (SLC25) family. The oxidative phosphorylation of UCPs separated from ATP synthesis, the energy is dissipated as heat, the process of which is also known as mitochondrial proton leakage. UCPs promote the transfer of anions from the inner to outer mitochondrial membranes, as well as the reflow of protons from the outer to the inner mitochondrial membrane. They also reduce the mitochondrial membrane potential of mammalian cells. The exact method by which tissue specificity occurs in different UCPs and UCPs to transfer H+/OH is unknown. UCPs contain three homologous protein domains of MACPs.

Basic Information of SLC25A14
Protein Name Brain mitochondrial carrier protein 1
Gene Name SLC25A14
Aliases Mitochondrial uncoupling protein 5 (UCP 5), Solute carrier family 25 member 14
Organism Homo sapiens (Human)
UniProt ID O95258
Transmembrane Times 6
Length (aa) 325

Function of SLC25A14 Membrane Protein

SLC25A14 is widely expressed in many tissues. And it has a high expression in the brain and testis. The gene product has an n-terminal hydrophobic domain that is absent from other UCPs. This gene has found two mosaic variants. The expression of SLC25A14 is enhanced in human cerebral ischemic injury in vitro, and its expression has a long-term effect on neuroprotection because it reduces the potential of the mitochondrial membrane and thus reduces the production of reactive oxygen species. The reduction in oxygen can be determined by the increased activity of superoxide degrading enzymes and SLC25A14.

Oxidative phosphorylation in mitochondrial electron transport chain (ETC), and proton leak via uncoupling proteins (UCPs). Fig.1 Oxidative phosphorylation in mitochondrial electron transport chain (ETC), and proton leak via uncoupling proteins (UCPs). (Ramsden, 2012)

Application of SLC25A14 Membrane Protein in Literature

  1. Mortensen O.H., et al. Developmental Programming by High Fructose Decreases Phosphorylation Efficiency in Aging Offspring Brain Mitochondria, Correlating with Enhanced UCP5 Expression. Journal of Cerebral Blood Flow & Metabolism. 2014, 34 (7): 1205-1211. PubMed ID: 24756078

    The results show that the high fructose diet during pregnancy and lactation has a long-term effect on brain mitochondrial function in older rats (fetal planning), which appears to be associated with increased levels of SLC25A14 protein.

  2. Choi K. H., et al. Expression Profiles of Mitochondrial Genes in the Frontal Cortex and the Caudate Nucleus of Developing Humans and Mice Selectively Bred for High and Low Fear. PLoS ONE. 2012, 7 (11): e49183. PubMed ID: 23152871

    These results suggest that MAOB, SLC25A14 and TUBB3 are involved in mitochondrial function in the PFC, thus playing a key role in brain development and fear-related behavior.

  3. Anitha A., et al. Brain Region-Specific Altered Expression and Association of Mitochondria-Related Genes in Autism. Molecular Autism. 2012, (3): 12. PubMed ID: 23116158

    This study found that the expression of SLC25A14 had been reduced in at least two of the brain regions of autism patients.

  4. Gutiérrez-Aguilar M., Baines C.P. Physiological and pathological roles of mitochondrial SLC25 carriers. The Biochemical journal. 2013, 454(3):371-386. PubMed ID: 23988125

    This review covers the current knowledge on the role of SLC25 transporters in health and disease.

  5. Dahlin, Amber., et al. Expression Profiling of the Solute Carrier (SLC) Gene Family in the Mouse Brain. The Journal of pharmacology and experimental therapeutics2009,329 (2): 558-570. PubMed ID: 19179540

    This review is mainly about the studies on the role of SLC genes in neurophysiological and pathological processes.

SLC25A14 Preparation Options

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  1. Ramsden D. B., et al. (2012). Human neuronal uncoupling proteins 4 and 5 (UCP4 and UCP5): structural properties, regulation, and physiological role in protection against oxidative stress and mitochondrial dysfunction. Brain and behavior 2.4 : 468-478.

All listed customized services & products are for research use only, not intended for pharmaceutical, diagnostic, therapeutic or any in vivo human use.

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