SLC25A5 is encoded by SLC25A5 gene which is located on Xq24-q26. And the molecular mass of SLC25A5 is about 32 kDa. It mainly expressed in proliferative and undifferentiated cells. SLC25A5 belongs to the mitochondrial carrier (TC 2.A.29) family of which members are thought to have six transmembrane α-helical spanners and take part in transporting nucleotides, amino acids, inorganic ions and co-factors, keto acids, across the mitochondrial inner membrane.
|Basic Information of SLC25A5|
|Protein Name||ADP/ATP translocase 2|
|Aliases||ADP,ATP carrier protein 2, ADP,ATP carrier protein, fibroblast isoform, Adenine nucleotide translocator 2, ANT 2, Solute carrier family 25 member 5|
|Organism||Homo sapiens (Human)|
|Transmembrane Times||Multi-pass membrane|
SLC25A5 mainly acts as an antiporter for ADP/ATP, facilitating the exchange of cytoplasmic ADP with mitochondrial ATP across the mitochondrial inner membrane. Expression of SLC25A5 is activated during cell proliferation and is repressed when cells become growth arrested. Accordingly, SLC25A5 also participates in the formation of the mitotic spindle-associated MMXD complex, so it may function in chromosome segregation. Besides, SLC25A5 is related to adenine transmembrane transporter activity, RNA binding and ubiquitin protein ligase binding. What’ s more, the expression of SLC25A5 is an important index of carcinogenesis because it is related to the rate of glycolytic metabolism. Compared with F1F0-ATPase, SLC25A5 has the opposite effect in the mitochondrial matrix, but their functions together maintain the mitochondrial membrane potential and ensure cell survival and proliferation. Beyond that, SLC25A5 can regulate the selective elimination of senescent cells targeted by mitochondrial. It has been shown that SLC25A5 directly bound to sesaminol, which pleiotropically upregulate cyclin D1 expression with protein stabilization and mTORC1 activation.
Fig.1 Role of ANT isoforms (including SLC25A5) in oxidative phosphorylation and glycolysis (Chevrollier, 2011).
This article focuses on cellular senescence, a kind of cycle arrest. Authors find that ANT2, also named SLC25A5, is related to the selective elimination of senescent cells targeted by mitochondrial, downregulation of SLC25A5 in nonsenescent cells promoted their MitoTam-triggered elimination, while restoration has the opposite effect.
MicroRNA is abnormal in many cancers, authors of this article study the function of SLC25A5 shRNA-regulated miRNAs in the pathogenesis of HCC. SLC25A5 can regulate the expression of miR-19a and miR-96, which leads to the suppression of tumor growth.
This article reveals that SLC25A5 binds to sesaminol, which may pleiotropically upregulate cyclin D1 expression at the mRNA level and protein level with mammalian target of rapamycin complex 1 (mTORC1) activation and protein stabilization.
Authors of this article want to study the therapeutic potential of ANT2, also named SLC25A5, inhibition to EGFR tyrosine kinase inhibitor (EGFR-TKI) resistance in non-small cell lung cancer. In the end, they find that the overexpression of SLC25A5 is related to the EGFR-TKI resistance, and SLC25A5 targeting may a novel strategy for solving this problem.
This article reveals differences between cytokine effects in mouse and human cells and mechanistically implicates the TGFβ/SMAD pathway, via induction of NADPH oxidases and suppression of ANT2, as key mediators of IFNγ/TNFα-evoked genotoxicity and cellular senescence.
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