Ask about this productRelated genes to: SLC25A3 antibody
- Gene:
- SLC25A3 NIH gene
- Name:
- solute carrier family 25 member 3
- Previous symbol:
- PHC
- Synonyms:
- -
- Chromosome:
- 12q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-14
- Date modifiied:
- 2016-02-18
Related products to: SLC25A3 antibody
Related articles to: SLC25A3 antibody
- The Solute carrier family 25 member 3 (SLC25A3), a mitochondrial solute carrier protein, has been implicated in tumor progression. Nonetheless, the connection between SLC25A3 and hepatocellular carcinoma (HCC) remains ambiguous. - Source: PubMed
Publication date: 2026/01/24
Bie BeibeiLiu LibingWang FurongMeng XianingWu MengdiSun Jin - Mitochondrial protein import and transporter systems play essential roles in maintaining metabolic competence and proteostasis in stem cells. However, the transcriptional architecture of mitochondrial translocase (TOM/TIM) complexes and transporter genes in human spermatogonial stem cells (SSCs) remains poorly defined. We performed an integrative analysis combining bulk microarray profiling of human SSC-enriched populations (n=3 biological replicates per group) with complementary single-cell RNA-sequencing (scRNA-seq) datasets. Differential expression (limma; |log₂FC| ≥ 2, adj. P < 0.05), co-expression network construction (WGCNA), protein-protein interaction mapping (STRING/cytoHubba), and miRNA-mRNA regulatory inference were used to identify key mitochondrial transporter nodes. Validation of hub-gene expression patterns was performed using an independent scRNA-seq dataset. Cell-type identity of SSC-enriched cultures was confirmed by immunocytochemistry for established SSC markers. Integrated multi-omics analyses revealed a coordinated enrichment of mitochondrial transporter genes in SSCs, including upregulation of TOMM and TIMM family members and selected ATPase and SLC transporters relative to fibroblasts. Hub genes (TOMM22, TIMM17A, ATP6V1A, SLC25A3) showed high network centrality and were consistently enriched in undifferentiated SSC clusters across multiple scRNA-seq datasets. miRNA-mRNA interaction modeling identified several SSC-expressed miRNAs (e.g., hsa-miR-4732-3p, hsa-miR-6503-3p) as potential post-transcriptional regulators of mitochondrial transporter networks. Human SSCs exhibit a distinctive mitochondrial transporter gene program characterized by enhanced expression of protein-import machinery and metabolic transport components. These findings provide a comprehensive molecular framework for understanding mitochondrial regulation in SSCs and establish new candidate targets for probing germline metabolism and stem-cell maintenance. - Source: PubMed
Publication date: 2026/03/02
Mahforoozmahalleh Zahra HasaniAzizi HosseinSkutella Thomas - Copper (Cu) is an essential trace element required for mitochondrial respiration via its incorporation into cytochrome c oxidase (CuCOX), the terminal enzyme of the electron transport chain. Here, we employed size-exclusion chromatography coupled with inductively coupled plasma mass spectrometry (SEC-ICP-MS), UV-Vis spectroscopy, and immunoblotting to identify and validate a high molecular weight Cu-containing peak in the SEC-ICP-MS chromatogram as representative of CuCOX activity. We demonstrate that this CuCOX peak is enhanced under metabolic conditions inducing oxidative phosphorylation, such as high Cu supplementation or galactose-containing media, and correlates with increased mitochondrial respiration. Using exogenous Cu tracing, we characterized the time- and dose-dependent incorporation of newly acquired Cu into CuCOX under elevated Cu conditions in renal cancer cells, modeling advanced clear cell renal cell carcinoma (ccRCC). RNA interference experiments targeting key Cu transporters revealed that CuCOX formation is independent of the high-affinity Cu importer CTR1, but instead relies on alternative transporters, including DMT1, LAT1, and the mitochondrial carrier SLC25A3, with transporter contributions dynamically reshaped during chronic adaptation to high Cu availability. In contrast, under standard low-Cu conditions, CTR1 remains required for cellular Cu uptake and CuCOX metallation. Together, these findings define context-dependent Cu trafficking pathways in renal cancer and establish SEC-ICP-MS as a sensitive platform for assessing CuCOX metallation and mitochondrial metabolism, with potential applications in biomarker discovery and therapeutic targeting in RCC. - Source: PubMed
Publication date: 2026/02/12
Secic DinaBischoff Megan ESchmidt LucasPanmanee WarunyaYang JuechenMeller JarekVest Katherine ECunningham John TLandero Julio ACzyzyk-Krzeska Maria F - Hepatocellular carcinoma (HCC) represents one of the most life-threatening malignancies globally. Despite significant advancements in the treatment of HCC in recent years, therapeutic outcomes remain unsatisfactory, particularly for patients with advanced, inoperable HCC. Thus, there is an urgent need to identify novel therapeutic targets and develop combination therapies to enhance treatment efficacy. The aim of this study is to elucidate the role and mechanism of solute carrier family 25 member A3 (SLC25A3) in HCC. - Source: PubMed
Publication date: 2025/12/29
Deng ShuangyaFu Jie - Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease in preterm infants, characterized by dysregulated macrophage polarization and oxidative stress. While mesenchymal stem cell-derived exosomes (MSC-Exos) have shown protective effects against BPD, the role of exosomes derived from hypoxia-preconditioned MSCs (Hypo-Exos) remains unclear. This study aimed to investigate whether Hypo-Exos alleviate BPD by modulating alveolar macrophage (AM) polarization and oxidative stress via the mitochondrial transporter SLC25A3. We utilized in vitro models of LPS-induced M1 polarization and HO-induced oxidative stress in AMs, as well as an in vivo rat model of BPD induced by intermittent hypoxia. Our data demonstrate that hypoxic preconditioning enhanced exosome secretion from MSCs. Furthermore, hypoxic preconditioning promoted the packaging of SLC25A3 into these exosomes. Hypo-Exos significantly suppressed M1 polarization, reduced oxidative stress, and ameliorated lung injury and dysfunction in BPD rats. Silencing SLC25A3 in MSCs abolished these protective effects. Mechanistically, SLC25A3 interacted with PTEN, leading to inhibition of PTEN expression and activation of the PI3K/AKT signaling pathway. Overexpression of PTEN reversed the beneficial effects of SLC25A3 on macrophage polarization and oxidative stress. These findings reveal that Hypo-Exos deliver SLC25A3 to AMs, thereby downregulating PTEN, activating PI3K/AKT signaling, promoting M2 polarization, attenuating oxidative damage, and ultimately mitigating BPD progression. This study provides important mechanistic insights and suggests potential therapeutic avenues for exosome-based treatment of BPD. - Source: PubMed
Zhang YanfangZhang AiminYang JialeHuang FurongZhao MenghuaHuang LiWang Juanmei