Ask about this productRelated genes to: SLC25A11 Blocking Peptide
- Gene:
- SLC25A11 NIH gene
- Name:
- solute carrier family 25 member 11
- Previous symbol:
- SLC20A4
- Synonyms:
- OGC
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-18
- Date modifiied:
- 2016-10-05
Related products to: SLC25A11 Blocking Peptide
Related articles to: SLC25A11 Blocking Peptide
- The central nervous system is highly sensitive to energy supply, and the hippocampus operates under sustained metabolic load due to continuous synaptic activity and information processing. Lysosomes couple nutrient status to cellular energetics through the mechanistic target of rapamycin complex 1 (mTORC1) and the autophagy-lysosome pathway, yet their -subcellular contribution to neuronal metabolic profiles remains unclear. To address this, we established an AAV-LysoTag/Lyso-IP workflow combined with metabolomics to quantify metabolites within mouse hippocampal lysosomes. An Lyso-IP platform and immunofluorescence provided cell-based validation. Under every-other-day fasting, hippocampal lysosomes exhibited reprogramming: small-molecule substrates derived from amino acids and fatty acids accumulated; bis(monoacylglycero)phosphate was upregulated, indicating enhanced intraluminal vesicle formation and lipid degradation/sorting; -sphingolipids and cardiolipin increased, consistent with selective mitophagy. Notably, high basal lysosomal levels of malic acid and α-ketoglutarate (α-KG) suggested additional sources beyond the mitochondria. Immunofluorescence further showed lysosomal localization of isocitrate dehydrogenase and fumarate hydratase, suggesting partial residency of these enzymes. The oxoglutarate carrier (SLC25A11) signals were observed in LAMP1 compartments, suggesting potential transmembrane exchange of α-KG and malic acid. Together, our data indicate that lysosomal tricarboxylic acid -related metabolites are maintained by three parallel routes: mitochondrial delivery to lysosomes, local production by resident enzymes, and transporter-mediated exchange. These metabolites supplement and reshape neuronal carbon flux and metabolic resilience at the subcellular level. Our findings elevate lysosomes from degradative endpoints to mobilizable metabolic hubs in the brain and provide both methodological and conceptual frameworks for neurometabolic adaptation under energy scarcity. - Source: PubMed
Publication date: 2026/02/19
Kong LiangliangTan HongyingZhu XiaotingWen YiqingLi Yang - YTH N-methyladenosine RNA binding protein F1 (YTHDF1) enables N-methyladenosine-containing RNA binding activity, involved in mRNA destabilization and positive regulation of translational initiation. Here we aimed to investigate the main molecular events associated with YTHDF1 during the course of metabolic dysfunction-associated steatotic liver disease (MASLD). YTHDF1 expression was detected by western blotting and real-time PCR. Ythdf1 hepatocyte-specific knockout mice were generated in this study. RNA sequencing and proteomic analyses were performed to investigate potentially involved molecular pathways. The protein levels of YTHDF1 were increased during MASLD progression. Under high-fat diet intervention, hepatocyte-specific Ythdf1-knockout mice exhibited a pronounced increase in both liver weight and liver-to-body weight ratio, accompanied by significant hepatic steatosis. YTHDF1 depletion promotes the progression of MASLD through enhanced peroxisome activation and mitochondria dysfunction, which are independent of its RNA N-methyladenosine reader activity. In particular, decreased YTHDF1 enhances the expression of acyl-CoA oxidase 1 (ACOX1), and peroxisome activation in a manner relies on YTHDF1 facilitating the formation of stress granules in MASLD. In addition, YTHDF1 was localized in the mitochondria and interacted with SLC25A11, affecting mitochondrial glutathione transport and its homeostasis. Finally, the identified lysine 191 methylation modification can reduce the stability of YTHDF1 protein, thereby achieving its protein expression regulation during MASLD progression. YTHDF1 inhibits MASLD progression by modulating stress granule sequestration of ACOX1 mRNA and maintaining mitochondrial homeostasis. - Source: PubMed
Publication date: 2026/04/10
Mu ChenyangTan JianWang YuefanYin HaozanDai ZhihuiWang ZenghanDing DongyangZhang ZhichaoWang SijieLiu HuiYang Fu - Metabolic reprogramming is one of the eight hallmarks of cancer, and in lung cancer, it is notably linked to ferroptosis-related lipid metabolism. Cancer stem cells, regarded as the initiating cells of cancer, can extensively influence the tumor microenvironment (TME). Nevertheless, their role in metabolic reprogramming within lung adenocarcinoma (LUAD) remains incompletely explored. In this study, through molecular biology experiments including RNA-seq, proteomics, RNA pulldown, and PCR, we discovered a novel and intricate mechanism by which the lncRNA ROLLCSC, derived from extracellular vesicles (EVs) of LUAD stem cells, regulates the tumor TME. Mechanistically, lncRNA ROLLCSC can interact with CDC42, a GTPase protein, mediating a positive feedback loop that promotes the entry of more EVs into recipient lung cancer cells (LLC). FTO-mediated m6A demethylation enhances the stability of ROLLCSC, which is recognized by the reader protein IGF2BP2 in recipient LLC cells. Most importantly, lncRNA ROLLCSC can reshape the lipid metabolism of LLC cells by targeting ACSL4 and , thereby enhancing their resistance to ferroptosis. Clinically, ROLLCSC and its targets are associated with distinct tumor expression patterns and have prognostic significance. Overall, our study elucidates how the lncRNA ROLLCSC derived from cancer stem cell (CSC)-derived EVs is efficiently transported to LUAD cells, subsequently reshaping the lipid metabolism of recipient cells and enhancing their resistance to ferroptosis. - Source: PubMed
Publication date: 2025/08/05
Zhang Yu-HanXie Jia-ChengYe TingGuo Shi-MengHan XueYang SiShi LeiLi Yi-ShiXing H RosieLi Jing-YuWang Jian-Yu - BACKGROUND: Biliary tract cancer is a group of highly heterogeneous and metastatic malignancies of the biliary tract. Current clinical treatment strategies and diagnostic methods need further improvement to effectively manage this disease. METHODS: We performed multiomics integrative and in silico analyses of selected SLC25 family members. Cell models with SLC25A11 overexpression or knockdown can be used for various biological function assays and cell imaging. Animal models and clinical specimens can be used to evaluate prognosis and treatment. RESULTS: SLC25A11 inhibition significantly reduced cell migration and proliferation both in vitro and in vivo. In addition, loss of SLC25A11 leads to accumulation of TCA-related metabolites, alters mitochondrial homeostasis, and reduces mitochondrial membrane potential. In addition, we confirmed that lipid peroxidation and lipid ROS aggregation in mitochondria by SLC25A11-knockdown model. Based on our RNA sequencing data, inhibition of SLC25A11 reduces NRF2 expression and translocation, resulting in loss of interaction affinity with the ferroptosis suppressor FSP1 and subsequent reactivation of the ferroptosis machinery. We also showed that low levels of SLC25A11 and knockdown models can activate lipid peroxidation and related molecules ACSL4, LPCAT3, and PEBP1, further inducing ferroptosis. Furthermore, recruitment of ferrostatin-1 (Fer-1) antagonizes the ferroptosis state by reducing lipid peroxidation and blocking the expression levels of these related molecules. CONCLUSIONS: Bringing all the evidence together, we added several important insights between ferroptosis and biliary tract cancer. We raised that SLC25A11 will serve as a novel prognostic factor and treatment strategy for biliary tract cancer. - Source: PubMed
Publication date: 2026/01/09
Lin Yu-YuKuo Han-HsiHe Zhao-JingChung Hsin-YiKim Cheorl-HoPan Yi-RuWu Meng-JuChan Ming-HsienYeh Chun-NanChiang Nai-JungChen Ming-HuangChang Yu-Chan - Chronic hypoxia is commonly associated with various cardiovascular diseases, with cardiomyocyte death being the most frequently observed alteration. Mitochondrial dysfunction is another consequence seen in the hypoxic heart. However, the mechanistic linkage between mitochondrial dysfunction and cardiomyocyte death in the hypoxic heart remains unclear. Solute carrier family 25 member 11 (SLC25A11) is essential for mitochondrial function via transporting glutathione to mitochondria and is possibly involved in ferroptosis. However, the role of SLC25A11 in chronic hypoxia-induced cardiomyocyte ferroptosis remains unknown. - Source: PubMed
Publication date: 2025/12/17
Li YansongXia JingwenWei YongHe MaorongHe GuibinZhu Yan