Ask about this productRelated genes to: SLC25A39 antibody
- Gene:
- SLC25A39 NIH gene
- Name:
- solute carrier family 25 member 39
- Previous symbol:
- -
- Synonyms:
- FLJ22407, CGI-69
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-21
- Date modifiied:
- 2016-10-05
Related products to: SLC25A39 antibody
Related articles to: SLC25A39 antibody
- Mitochondrial dysfunction drives persistent inflammation in severe asthma, yet its upstream metabolic regulation remains unclear. Induced sputum from patients with severe asthma was analyzed and integrated with transcriptomic datasets from independent cohorts. Two mouse models (C57BL/6J) were used for in vivo validation with multi-omics profiling, and mechanistic studies were performed in air-liquid interface-cultured primary human airway epithelial cells. Glutathione reduced form (GSHr) was markedly depleted in sputum and associated with poor disease control and mixed granulocytic inflammation in patients with severe asthma. Multi-omics analyses revealed coordinated disruption of glutathione (GSH) metabolism, including oxidized GSH accumulation, reduced synthesis and glutathione-S-transferase activity, and impaired mitochondrial GSH transport. GSH supplementation alleviated airway inflammation, oxidative stress, and mitochondrial dysfunction, whereas pharmacological inhibition of GST exacerbated these effects. Mitochondrial analyses identified suppressed SLC25A39 expression as a key mediator of defective GSH transport and redox imbalance. Transcriptomic profiling of airway biopsies showed upregulation of Neuropilin-1 (Nrp1), closely associated with altered glutathione pathways. Targeting the Nrp1 b1 domain restored mitochondrial GSH metabolism and attenuated airway inflammation. These findings identify an Nrp-centered metabolic pathway that disrupts mitochondrial homeostasis and drives inflammatory amplification, highlighting mitochondria-targeted therapeutic strategies for severe asthma. - Source: PubMed
Publication date: 2026/04/08
Huang JunwenZhao WenquChen YingChen YaoxinGong ZhaoqianMa YanyanLi YuemaoHu DapengHuang ShuyuFan KekeZhu BangPeng XiaoqianPeng XianruCai ShaoxiZhao Haijin - Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, with limited therapeutic options for advanced-stage patients. Here, we identify DLAT, a key enzyme in mitochondrial metabolism, as a critical driver of CRC progression. Multi-omics analyses revealed that DLAT was overexpressed in CRC tissues and correlated with poor patient prognosis. The results showed that DLAT promoted CRC growth by promoting the resistance to mitochondrial antioxidant stress and suppressing ferroptosis. Mechanistically, DLAT directly bond to the mitochondrial glutathione (mtGSH) transporter SLC25A39 and enhanced its protein stability independent of intracellular GSH levels, leading to the maintain of mitochondrial GSH (mtGSH) import and redox homeostasis. Knockdown of DLAT or SLC25A39 disrupted mtGSH transport, elevated lipid peroxidation, and sensitized CRC cells to ferroptosis. We further identified a small molecular drug GL-V9 as a DLAT degrader. GL-V9 bond to DLAT and induced DLAT degradation through ubiquitin-proteasome pathway. The disruption of DLAT-SLC25A39 axis by GL-V9 led to mtGSH depletion and oxidative stress, as well as the significant suppression of CRC growth. These findings establish DLAT as a metabolic vulnerability in CRC and highlight GL-V9 as a promising therapeutic agent. - Source: PubMed
Publication date: 2026/04/18
Zhang KunZhang XinHuang ChenqiYang JunyiDong LongxuanChen XijingXun ChenGuo Yongjian - Interleukin-17A inhibitors are therapeutic options in psoriatic arthritis (PsA), but response is not universal. Evidence from other inflammatory arthritides suggests differential gene expression may predict outcomes. This study aimed to identify transcriptomic predictive biomarkers of response in PsA patients commencing secukinumab. - Source: PubMed
Publication date: 2026/04/15
Jalil Nahdia Afiifah AbdulChinoy HectorJani MeghnaBarton AnneThompson CharlotteMartin PaulNair NishaBluett James - Solute carrier family 25 member 39 (SLC25A39) is a pivotal mitochondrial glutathione transporter and an emerging oncoprotein in hepatocellular carcinoma (HCC). While its cell-intrinsic roles are increasingly recognized, its comprehensive functions in modulating the tumor immune microenvironment (TIME) and epigenetic landscape within HCC remain undefined. To address this, we employed an integrated multi-omics and experimental approach, including TCGA, ssGSEA, CCK-8, Transwell, etc. Our study confirmed SLC25A39 upregulation and its pro-tumorigenic role. Notably, we provide several key novel insights: First, we establish the first link between promoter hypermethylation at specific CpG sites and poor patient prognosis, revealing an epigenetic regulatory layer in HCC. Second and most importantly, we pioneer the exploration of SLC25A39 in the HCC immune context, demonstrating its association with a distinct immunosuppressive TIME characterized by a Th2-skewed profile, reduced cytotoxic cell infiltration, and elevated immune checkpoint (CTLA-4, PD-1) expression. Furthermore, drug sensitivity analysis linked SLC25A39 to a broader spectrum of pharmacological agents beyond sorafenib. Collectively, our findings not only reinforce SLC25A39 as a therapeutic target but, for the first time, reposition it as a potential modulator at the intersection of tumor metabolism, epigenetics, and immunology in HCC, offering a rationale for its inhibition, particularly combined with immunotherapy. - Source: PubMed
Publication date: 2026/03/28
Mo YifeiDu ZhipengLiu Mei - Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, with poor prognosis driven by tumor heterogeneity and therapy resistance. Mitochondrial solute carriers (SLC25 family) are crucial for metabolic and redox regulation, yet their roles in HCC remain poorly understood. - Source: PubMed
Publication date: 2026/01/19
Liu WenxuanKuang TianruiDong KeshuaiLi ManDeng WenhongYu Jia