SLC25A25

Last update 08 May 2025

Basic Info

Synonyms

APC3, Calcium-binding mitochondrial carrier protein SCaMC-2, KIAA1896

+ [10]

Introduction

Electroneutral antiporter that most probably mediates the transport of adenyl nucleotides through the inner mitochondrial membrane. Originally identified as an ATP-magnesium/inorganic phosphate antiporter, it could have a broader specificity for adenyl nucleotides. By regulating the mitochondrial matrix adenyl nucleotide pool could adapt to changing cellular energetic demands and indirectly regulate adenyl nucleotide-dependent metabolic pathways.

100 Clinical Results associated with SLC25A25

100 Translational Medicine associated with SLC25A25

0 Patents (Medical) associated with SLC25A25

Literatures (Medical) associated with SLC25A25

01 Mar 2025·Journal of the European Academy of Dermatology and Venereology

Hair regrowth in alopecia areata and re‐pigmentation in vitiligo in response to treatment: Commonalities and differences

Review

Author: Yamaguchi, Yuji ; Yamaguchi, Hiroki L. ; Peeva, Elena

AbstractBoth alopecia areata (AA) and vitiligo share common pathogenesis involving, interferon‐γ (IFN‐γ) and interleukin‐15 (IL‐15) signalling pathways that activate cytotoxic CD8+ T lymphocytes. These shared mechanisms may explain why both diseases respond to currently available treatments (e.g. topical/systemic corticosteroid) and emerging treatment modalities. As compared with the speed of re‐pigmentation in vitiligo lesions, the regeneration of pigmented terminal hair follicles in AA lesions appears fast in response to treatments targeting the inhibition of the Janus kinases (JAKs) and other kinases. We summarize the commonalities and differences between AA and vitiligo focusing on the treatment modalities, followed by recent findings associated with hair follicle stem cells (HFSC) in hair bulge (HBg) and melanocyte stem cells (McSC) in HBg and hair germ (HGm). We then discuss how HFSC and HGm‐McSC are involved in the initiation of anagen phase, followed by pigmented terminal hair regrowth in the recovering AA lesions in association with immunology. We also discuss how HBg‐McSC contribute to the migration of fully dendritic mature melanocytes into interfollicular epidermis and the equal distribution of melanin in recovering vitiligo lesions. Finally, we present four hypotheses to elucidate the delayed distribution of melanin by mature melanocytes in depigmented vitiligo lesions from the aspects of stem cell biology, as compared with quick hair recovery in AA: (1) McSC are less abundant than HFSC. (2) McSC require a long travel, whereas HFSC reside close to hair regeneration trigger point. (3) Keratinocyte scaffold to accept melanin is not well preserved, whereas scaffold for hair regrowth is well preserved. (4) Inhibitors targeting JAKs and other kinases have less direct effects on melanocyte proliferation and differentiation in vitiligo than hair regrowth in AA. Our review provides an overview of treatment modalities and bridges the gap between scientific advancement and clinical practice in AA and vitiligo management.

01 Nov 2023·Heliyon

Integrated bioinformatics and validation to construct lncRNA-miRNA-mRNA ceRNA network in status epilepticus

Article

Author: Yang, Bin ; Liang, Risheng ; Wen, Hanyu ; Lin, Yaojing ; Wang, Chunhua

BackgroundStatus epilepticus (SE) is a neurologic emergency with characteristic of prolonged seizure activity. However, the investigation of lncRNA based competing endogenous RNAs (ceRNAs) network in SE still requires further elucidation. This study aims to construct the ceRNA network and uncover the related mechanism in SE.MethodsThe C57BL/6 mice pilocarpine-induced (SE) model was established (i.p. injection, 300 mg/kg) (n = 3). RNA-Sequencing was carried out and identified the differential expressed genes (DEGs). GO annotations, KEGG, and GSEA analysis were performed to study the underlying mechanism and pathways of the DEGs. Further, the protein-protein interaction (PPI) network and ceRNA network were visualized by Cytoscape software. The expression level of differential expressed genes involved in the ceRNA network was detected by qRT-PCR.ResultsA total of 345 DE-mRNAs, 84 DE-lncRNAs, and 5 DE-miRNAs were screened out. Subsequently, the functional analysis suggested that angiogenesis, inflammation, and neuron related biological processes were enriched in SE. The constructed ceRNA network-1 contained 7 up-regulated DE-mRNAs (Arid5a, Adm, Insig1, Midn, Btaf1, Per1, Slc25a25), 1 down-regulated DE-miRNA (mmu-miR-6413), and 1 up-regulated DE-lncRNA (Zmiz1os1). The ceRNA network-2 contained 2 down-regulated DE-mRNAs (Rab27a and Lrp2), 1 up-regulated DE-miRNAs (mmu-miR-139-5p), and 1 down-regulated DE-lncRNA (Gm15883).ConclusionFor the first time this study present the expression profile and potential function of lncRNAs in C57BL/6 mice with SE. These results provided novel insights into the discovery of genetic biomarkers for SE.

01 Nov 2023·IUBMB Life

Adenine nucleotide carrier protein dysfunction in human disease

Review

Author: Mishra, Gargi ; Coyne, Liam P. ; Chen, Xin Jie

AbstractAdenine nucleotide translocase (ANT) is the prototypical member of the mitochondrial carrier protein family, primarily involved in ADP/ATP exchange across the inner mitochondrial membrane. Several carrier proteins evolutionarily related to ANT, including SLC25A24 and SLC25A25, are believed to promote the exchange of cytosolic ATP‐Mg2+ with phosphate in the mitochondrial matrix. They allow a net accumulation of adenine nucleotides inside mitochondria, which is essential for mitochondrial biogenesis and cell growth. In the last two decades, mutations in the heart/muscle isoform 1 of ANT (ANT1) and the ATP‐Mg2+ transporters have been found to cause a wide spectrum of human diseases by a recessive or dominant mechanism. Although loss‐of‐function recessive mutations cause a defect in oxidative phosphorylation and an increase in oxidative stress which drives the pathology, it is unclear how the dominant missense mutations in these proteins cause human diseases. In this review, we focus on how yeast was productively used as a model system for the understanding of these dominant diseases. We also describe the relationship between the structure and function of ANT and how this may relate to various pathologies. Particularly, mutations in Aac2, the yeast homolog of ANT, were recently found to clog the mitochondrial protein import pathway. This leads to mitochondrial precursor overaccumulation stress (mPOS), characterized by the toxic accumulation of unimported mitochondrial proteins in the cytosol. We anticipate that in coming years, yeast will continue to serve as a useful model system for the mechanistic understanding of mitochondrial protein import clogging and related pathologies in humans.

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SLC25A25

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