Ask about this productRelated genes to: SLC25A6 Blocking Peptide
- Gene:
- SLC25A6 NIH gene
- Name:
- solute carrier family 25 member 6
- Previous symbol:
- ANT3
- Synonyms:
- ANT3Y, MGC17525
- Chromosome:
- Xp22.32 and Yp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-08-03
- Date modifiied:
- 2016-02-18
Related products to: SLC25A6 Blocking Peptide
Related articles to: SLC25A6 Blocking Peptide
- Glutamine addiction is a key metabolic vulnerability in cancer. However, the mechanisms governing the limited efficacy of glutamine metabolism inhibitor (GMI) monotherapy require further investigation. Via single-cell monitoring using a caspase-3 activity indicator, we identified SLC25A6 as a key mediator of GMI-induced apoptosis in colorectal cancer cells. SLC25A6 overexpression enhanced apoptosis both in vitro and in vivo. SLC25A6 promoted mitochondrial fragmentation and dysfunction and upregulated the expression of mitochondrial fission markers. Notably, mitofission inhibitors largely abolished SLC25A6-related mitochondrial dysfunction and intrinsic apoptosis. Mechanistically, SLC25A6 directly interacted with MIC60, competitively inhibiting MIC19 binding; both MIC60 and MIC19 are key components of the mitochondrial contact site and cristae organizing system (MICOS). The SLC25A6 T126A mutant failed to bind MIC60 and lost its ability to destabilize the MICOS complex and facilitate mitofission. Upregulation of SLC25A6 expression induced by the glutaminase inhibitor CB-839 sensitized cancer cells to the Bcl-2 inhibitor ABT-199. Combined CB-839 and ABT-199 treatment showed strong synergistic antitumor effects in colorectal cancer xenograft models. Our findings reveal a novel function of SLC25A6 that links metabolic stress to mitochondrial apoptosis via disruption of the MICOS complex. Combination treatments with mitochondrial apoptotic inducers represent a promising avenue for maximizing the efficacy of GMIs in cancer treatment. - Source: PubMed
Publication date: 2026/04/23
Wang YinongWang BingzhiLiu YuZhou ChengYuan JunhuZhang FanyuMa LingMa YimingWang Hongying - Microproteins represent a class of short polypeptides with very diverse cellular functions. Microproteins frequently escape proteomics-based identification, making the extent and potential functions of small proteins largely elusive. Some microproteins originate from transcripts that are annotated as long noncoding RNAs (lncRNAs). Here, we functionally characterize SMIM26, a microprotein localized to mitochondria. In biochemical and single-molecule tracking studies, we found that SMIM26 interacts with VDAC1/2 in the outer mitochondrial membrane and with SLC25A6 in the inner mitochondrial membrane. It spans the intermembrane space and is phosphorylated at distinct residues. Knockout cells are viable, but respiratory chain activity is strongly reduced. Interestingly, knockout mice are not viable and die at early developmental stages. Zebrafish homozygous mutants are viable but show reduced fitness and survival compared with their wild-type or heterozygous siblings. Consistent with the mitochondrial phenotype in cell lines, respiration is also reduced in homozygous zebrafish embryos. Our work suggests that SMIM26 coordinates metabolite transport through the inner and outer mitochondrial membranes and is essential for respiratory chain function in vivo. - Source: PubMed
Publication date: 2026/04/16
Heizler KevinChugunova AnastasiaHofmann MaraProchazkova MichaelaProcházka JanHo-Xuan HungFallmann JoergStejskal KarelKrssakova GabrielaBader StefanieKocak ErmanYasar DogukanLuckner PatriciaLehmann GerhardKöngeter JulianRiester MarisaRoitinger ElisabethWetzel ChristianDiederichs SvenSedlacek RadislavBruckmann AstridGebhardt J Christof MPauli AndreaMeister Gunter - X-prolyl aminopeptidase 2 (XPNPEP2), which is abundantly expressed in vascular endothelial cells (ECs), has been reported to be associated with cardiovascular disease and angiogenesis. However, its function in ECs and its involvement in the pathogenesis of angiogenesis remain unclear. In this study, we revealed that XPNPEP2 is essential for EC function and angiogenesis via modulation of mitochondrial function. , XPNPEP2 deletion led to pathological changes in the pulmonary artery wall and renal tissue, decreased venous blood vessel density in the proximal region of superficial retinal vessels, and significantly slowed wound healing and tumor growth in mice. , XPNPEP2 deficiency impaired EC proliferation, migration, and tubulogenesis, which was accompanied by diminished mitochondria-associated membranes and dysfunctional mitochondria, including insufficient ATP, excessive mitochondrial reactive oxygen species (mROS), and disrupted respiration chain function. XPNPEP2 was found to interact with SLC25A6. The overexpression of XPNPEP2 restored impaired EC angiogenesis and the reduction in SLC25A6 caused by XPNPEP2 ablation. Moreover, inhibition of XPNPEP2 downregulated SLC25A6 via Siah E3 ubiquitin protein ligase 1 (SIAH1)-mediated degradation. Additionally, attenuated EC angiogenesis was achieved solely by silencing SLC25A6. Our findings highlight that XPNPEP2 regulates angiogenesis via modulation of mitochondrial function, which may represent a new strategy for the treatment of angiogenesis-related diseases. - Source: PubMed
Publication date: 2026/01/07
Yang ChenxiLu YijunXia YuWang BingyingXu JieZhang YuchenYan JiaxuanLiu MinChen TingZhao XiaoxuCang XiaohuiMao JianhuaJiang Pingping - Endometrial receptivity is essential for successful pregnancy, and endometriosis is widely recognized as a disruptor of this process. Poor endometrial receptivity is also a key factor contributing to recurrent implantation failure. Although some molecular mechanisms related to endometrial receptivity have been identified, their specific roles in endometriosis and recurrent implantation failure remain unclear. This study aimed to elucidate the shared molecular mechanisms affecting endometrial receptivity in endometriosis and recurrent implantation failure using multi-omics data analysis. We sourced datasets from the NCBI GEO database and employed weighted gene co-expression network analysis to identify gene modules associated with these conditions, followed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Single-cell sequencing analysis and immunofluorescence were used for expression analysis. We identified 3690 and 4892 upregulated genes and 2675 and 5065 downregulated genes in endometriosis and recurrent implantation failure, respectively. Functional enrichment analysis and validation identified 15 hub genes including SRPRB, SLC35B1, and SLC25A6. Receiver operating characteristic curve analysis demonstrated that these genes are associated with high diagnostic accuracy. Single-cell sequencing analysis indicated that these genes are predominantly expressed in basal epithelial cells, with RBM3 being particularly prominent. This study provides new insights into the molecular mechanisms underlying endometrial receptivity and identifies potential targets for the diagnosis and treatment of endometriosis and recurrent implantation failure. - Source: PubMed
Publication date: 2025/12/29
Yu JieWang WeiLi QiongLan LanJiang Li-LiHe Xin-RongJiang Xiao-WeiYan Yu-LinYao Xiao-MingWang Meng-YueDuan Ping-MeiHuang Lin-ChunQi Hai-FengYu Ting-He - Alpha-enolase (ENO1), the enzyme catalyzing 2-phosphoglycerate conversion to phosphoenolpyruvate, is highly expressed in diffuse large B-cell lymphoma (DLBCL) and correlates with adverse clinical outcomes. Thus, understanding the relationship between ENO1-related gene (ERG) network and DLBCL is imperative. Here, we integrated multi-omics profiling (RIP-seq, RNA-seq, and protein interactome analysis) to identify ERGs and established a prognostic model by machine learning algorithms. - Source: PubMed
Publication date: 2025/10/23
Yan WenliLiu XiaoxiGao BeibeiZhang ShanshanRen JinhongLu YangAi LimeiYan JinsongWang Haina