Ask about this productRelated genes to: SLC25A6 antibody
- 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 antibody
Related articles to: SLC25A6 antibody
- Topical and transdermal drug and cosmetic development is advancing across industry; however, the efforts may in part be hindered by paucity of data on the fate of chemicals in human skin, which depend on protein-mediated transport and biotransformation of such chemicals. A label-free mass spectrometry-based proteomics approach was used to comprehensively quantify drug metabolizing enzymes and transporters in the fractionated epidermis and dermis of 17 healthy Caucasian human skin samples. Over 1000 proteins were identified for cytosolic and membrane components, and abundance were obtained using a modified HiN (high 3/2 ion intensity) approach (without using standards). Key findings included high interindividual variability in the expression of phase I and II enzymes (eg, aldehyde dehydrogenase 2, carboxylesterase 1, glutathione S-transferase P1, and glutathione peroxidase 3) and solute carrier transporters (eg, SLC25A5, SLC25A6). Notably, several metabolic enzymes, previously uncharacterized in human skin, were quantified in the membrane fractions, including glutathione S-transferases (GSTs) such as GSTM3 (12.2 pmol/mg protein) and GSTP1 (5.55 pmol/mg protein). Subcellular localization analysis revealed that many quantified proteins were associated with mitochondrial or membrane compartments, reinforcing the functional diversity and compartmentalized nature of dermal metabolism. Furthermore, strong correlations in enzyme and transporter expression were observed between the dermis and epidermis (Spearman's ρ > 0.85). This dataset provides the most detailed quantification to date of drug metabolizing enzymes and transporters in human skin and offers critical input parameters for dermal physiologically based pharmacokinetic modeling applications. These quantitative insights improve the accuracy and clinical relevancy of in vitro in vivo extrapolations related to dermal drug metabolism and disposition for chemicals applied to the skin or those that come into contact with the skin inadvertently. Integration of this proteomic dataset into physiologically based pharmacokinetic frameworks will enhance the scientific reliability, applicability across product applications and regulatory acceptance of skin-based models for drug development and safety evaluation. SIGNIFICANCE STATEMENT: Understanding drug metabolism and transport in human skin is essential for predicting dermal absorption and safety. This study provides the most comprehensive proteomic dataset of metabolizing enzymes and transporters in epidermis and dermis, revealing high interindividual variability, previously unquantified enzymes, and strong layer correlations, supporting improved dermal physiologically based pharmacokinetic model development. - Source: PubMed
Publication date: 2026/04/29
Seriki SeunRostami-Hodjegan AminWarwood StaceyTan Ming-LiangTsakalozou EleftheriaBarber JillAl-Majdoub Zubida M - Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, largely due to late diagnosis, rapid progression, and the development of chemoresistance. Mitochondrial metabolic reprogramming has emerged as a critical driver of tumor progression and drug resistance. Sirtuin-3 (SIRT3), a mitochondrial NAD -dependent deacetylase, plays a context-dependent role in cancer biology; however, its function and underlying mechanism in GC progression and cisplatin (DDP) resistance remain unclear. This study aimed to explore the biological role and molecular mechanism of SIRT3 in GC. - Source: PubMed
Publication date: 2026/06/08
Meng WenjunLang ChunlanGan JiadiMu XiaoliTang LianshaWang JialingLiu YihaoZhu YuetingDu YangZhang HaolingHe QinqinLiu Jiyan - India possesses a rich diversity of indigenous cattle that are well adapted to varied agro-climatic regions. These populations exhibit remarkable variation in stature (height at withers), ranging from short-statured types such as Vechur, Punganur, Malnad Gidda, and Khariar to tall and heavy breeds like Kankrej, Ongole and other milch breeds (Sahiwal, Gir, etc.). The short-statured breeds offer potential advantages in feed efficiency, disease resilience, and cultural value besides being economical to maintain. However, their genetic basis for stature remains underexplored. This study leverages whole-genome resequencing (WGS) data on short-statured (n = 19) and tall (Kankrej as representative; n = 19) Indian cattle to delineate the copy number variation (CNV) landscape and selection signatures underpinning stature divergence. Post-quality control, CNVs were detected from duplicate-marked bam files using CNVnator with read-depth methodology, filtered (q0 < 0.5, p < 0.01, size 1 kb-5 Mb), and concatenated into CNV regions (CNVRs). Selection signatures were identified using cross population extended haplotype homozygosity (XP-EHH) methodology for inter-population comparison of short-statured cattle with tall cohort. Genes harboured under CNVRs and sweep windows were annotated using GALLO, with functional mining from literature databases. In short-statured cattle, 41,913 CNVs were concatenated into 10,075 CNVRs, with 8.01% genomic coverage. A total of 25 genes were found to be common across two analyses i.e., unique (non-overlapping) CN regions in 70% short-statured individuals and scan of selection signature. Key genes across the analyses included IGF1R (cell proliferation), FGFR3 (skeletal growth), SOX6 (body size), EXT2/LGR4 (bone density), PRKCD (developmental regulation), ADAMTSL2 (extracellular matrix integrity), SLC25A6 (glucose metabolism), and SDHA (energy supply). Unique non-overlapping copy number regions (e.g., 78 regions found in 100% of dwarf individuals) harbored several genes, including ARL13B (osteogenesis), AXIN2 (bone remodeling), CCND2 (myogenesis), and TNNT1 (muscle contraction). This comprehensive CNV map and scan for signatures of selection unveil stature-associated genomic variants, informing conservation strategies for threatened short-statured breeds by enhancing their socio-economic value through targeted breeding. The findings underscore CNVs as pivotal drivers of phenotypic diversity in cattle populations, with implications for livestock genomics and sustainable agriculture. - Source: PubMed
Publication date: 2026/06/08
Ahmad Sheikh FirdousAarif OvaisHassan Mir MehrozChand RoshniGangwar MunishT Sarath KumarKumar Amit - Turner syndrome is a rare disorder resulting from abnormalities in the number or structure of a single X chromosome. It stands as the sole survivable monosomy observed in humans. Individuals affected by Turner syndrome commonly face significant complications, including impaired gonadal development, short stature, and intellectual disabilities. Despite extensive research, the complete understanding of the pathogenesis behind Turner syndrome remains elusive. - Source: PubMed
Publication date: 2026/04/01
Liang HuishengLi ZhongyangZhang Fei - 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