Ask about this productRelated genes to: SLC25A35 Blocking Peptide
- Gene:
- SLC25A35 NIH gene
- Name:
- solute carrier family 25 member 35
- Previous symbol:
- -
- Synonyms:
- FLJ40217
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-03
- Date modifiied:
- 2015-12-08
Related products to: SLC25A35 Blocking Peptide
Related articles to: SLC25A35 Blocking Peptide
- Shenzhu granules (SG) are composed of five traditional Chinese herbal medicines, all of which are frequently used in different kinds of functional foods. This study systematically evaluates the anti-fatigue effects of SG and explores the underlying mechanisms to support its potential as a functional food. The anti-fatigue effects of SG were assessed through a functional anti-fatigue test and measurement of serum oxidative stress markers. Additionally, multi-omics approaches, including metabolomics, transcriptomics, and proteomics were used to investigate the mechanisms underlying the anti-fatigue effects of SG. - Source: PubMed
Publication date: 2026/03/23
Zhang HongmingLi XingxingLi MengGuo WenjunZhang ManqiGao XiaohanLiu JiaxinLin YanlingXie ShengxuZhang DianwenLiu YueXu Yajuan - Mitochondria provide a variety of metabolites, in addition to ATP, to meet cell-specific needs. One such metabolite is phosphoenolpyruvate (PEP), which contains a higher-energy phosphate bond than ATP and has diverse biological functions. However, how mitochondria-generated PEP is delivered to the cytosol and fulfills cell-specific requirements remains elusive. Here, we show that SLC25A35 regulates mitochondrial PEP efflux and glyceroneogenesis in lipogenic cells that utilize the pyruvate-to-PEP bypass. Reconstitution and structural studies demonstrated PEP transport by SLC25A35 in a pH gradient-dependent manner. Loss of SLC25A35 in adipocytes impaired the conversion of mitochondrial PEP into glycerol-3-phosphate, thereby reducing glycerolipid synthesis. Significantly, hepatic inhibition of SLC25A35 in obese mice alleviated steatosis and improved systemic glucose homeostasis. Together, these results suggest that mitochondria facilitate glycerolipid synthesis by providing PEP via SLC25A35, offering lipogenic mitochondria as a target to limit glycerolipid synthesis, a pivotal step in the pathogenesis of hepatic steatosis and type 2 diabetes. - Source: PubMed
Publication date: 2026/03/17
Yamamuro TadashiKatoh DaisukeSilva Guilherme MartinsNishida HiroshiOikawa SatoshiHiguchi YusukeWang DandanFujimoto MasanoriYoshida NaofumiLi MarkShin JihoonZhao ZezhouYook Jin-SeonSun LijunKajimura Shingo - Evidence on short-term black carbon (BC) exposure on mental health and underlying mechanisms involving mitochondrial function remains limited. In the Guangxi Eco-Environmental Health and Aging Study with 2271 middle-aged and older adults, we addressed this knowledge gap and explored potential DNA methylation signatures involving mitochondrial regulatory genes. Short-term BC exposure was significantly associated with a 0.494-point and 0.348-point increase in PHQ-9 and GAD-7 scores, respectively, and higher odds of depression (odds ratio [OR] = 1.554, 95 %CI: 1.276-1.901) and anxiety (OR = 1.628, 95 %CI:1.330-1.999) symptoms. These adverse effects could be mitigated by good sleep quality, defined as the PSQI score < 7. In 573 participants with available DNA methylation data, we identified 113 CpG sites in mitochondrial regulatory genes significantly associated with 28-day BC exposure. Particularly, three and five sites were associated with PHQ-9 scores and depression symptoms, while 16 were associated with GAD-7 scores and five with anxiety symptoms, respectively. Mediation analysis revealed that three CpG sites mapped on SLC25A38, SLC25A37, and SLC25A35 mediated the impact of BC on depression, with mediation proportions ranging from approximately12.19 % to 24.84 %. Our findings suggest that short-term BC exposure may affect mental health outcomes through the epigenetic regulation of mitochondrial function, highlighting a potentially modifiable biological pathway linking environmental pollution to brain health. - Source: PubMed
Publication date: 2026/01/07
Liu ShuzhenLuo YaxinCai JianshengWang YutingRong JiahuiMo XiaotingLiang YujianYe ZeyanTang XuNiu SiyuanZhang TiantianLuo LeiZhao LinhaiGuo PeifengJiang MeijieLi YouPang WeiyiQin JianZhang ZhiyongGao Xu - Mitochondria provide a variety of metabolites, in addition to ATP, to meet cell-specific needs. One such metabolite is phosphoenolpyruvate (PEP), which contains a higher-energy phosphate bond than ATP and has diverse biological functions. However, how mitochondria-generated PEP is delivered to the cytosol and fulfills cell-specific requirements remains elusive. Here, we show that SLC25A35 regulates mitochondrial PEP efflux and glyceroneogenesis in lipogenic cells that utilize the pyruvate-to-PEP bypass. Reconstitution and structural studies demonstrated PEP transport by SLC25A35 in a pH gradient-dependent manner. Loss of SLC25A35 in adipocytes impaired the conversion of mitochondrial PEP into glycerol-3-phosphate, thereby reducing glycerolipid synthesis. Significantly, hepatic inhibition of SLC25A35 in obese mice alleviated steatosis and improved systemic glucose homeostasis. Together, these results suggest that mitochondria facilitate glycerolipid synthesis by providing PEP via SLC25A35, offering lipogenic mitochondria as a target to limit glycerolipid synthesis, a pivotal step in the pathogenesis of hepatic steatosis and Type 2 diabetes. - Source: PubMed
Publication date: 2026/03/10
Yamamuro TadashiKatoh DaisukeSilva Guilherme MartinsNishida HiroshiOikawa SatoshiHiguchi YusukeWang DandanFujimoto MasanoriYoshida NaofumiLi MarkShin JihoonZhao ZezhouYook Jin-SeonSun LijunKajimura Shingo - Mitochondria dysfunction has been closely linked to a wide spectrum of human cancers, whereas the molecular basis has yet to be fully understood. SLC25A35 belongs to the SLC25 family of mitochondrial carrier proteins. However, the role of SLC25A35 in mitochondrial metabolism reprogramming, development and progression in human cancers remains unclear. Here, we found that SLC25A35 markedly reprogramed mitochondrial metabolism, characterized by increased oxygen consumption rate and ATP production and decreased ROS level, via enhancing fatty acid oxidation (FAO). Meanwhile, SLC25A35 also enhanced mitochondrial biogenesis characterized by increased mitochondrial mass and DNA content. Mechanistic studies revealed that SLC25A35 facilitated FAO and mitochondrial biogenesis through upregulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) via increasing acetyl-CoA-mediated acetylation of PGC-1α. Clinically, SLC25A35 was highly expressed in HCC and correlated with adverse patients' survival. Functionally, SLC25A35 promoted the proliferation and metastasis of HCC cells both in vitro and in vivo, as well as the carcinogenesis in a DEN-induced HCC mice model. Moreover, we found that SLC25A35 upregulation is caused, at least in part, by decreased miR-663a in HCC cells. Together, our results suggest a crucial oncogenic role of SLC25A35 in HCC by reprogramming mitochondrial metabolism and suggest SLC25A35 as a potential therapeutic target for the treatment of HCC. - Source: PubMed
Publication date: 2025/03/10
Yu Heng-ChaoBai LuJin LiangZhang Yu-JiaXi Zi-HanWang De-Sheng