Ask about this productRelated genes to: SLC16A1 antibody
- Gene:
- SLC16A1 NIH gene
- Name:
- solute carrier family 16 member 1
- Previous symbol:
- -
- Synonyms:
- MCT, MCT1
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-16
- Date modifiied:
- 2016-10-05
Related products to: SLC16A1 antibody
Related articles to: SLC16A1 antibody
- The transition from mitosis to meiosis represents a fundamental cell-fate decision that requires coordinated remodeling of transcriptional and metabolic programs. While key transcriptional regulators of meiotic entry have been defined, how metabolic flux directly governs this process remains unclear. Here, we identify a monocarboxylate transporter1 (MCT1)-dependent metabolic checkpoint that controls meiotic progression in mammalian spermatogenesis. Through integrative single-cell transcriptomics, metabolic profiling, and computational perturbation modeling, we show that Stra8-driven meiotic initiation is coupled to a metabolic switch favoring monocarboxylic acid metabolism, prominently involving MCT1 (encoded by Slc16a1). Germ cell-specific deletion of Slc16a1 results in a complete arrest at the pachytene stage, characterized by defective homologous recombination, persistent DNA damage, and failure to activate the meiotic transcriptional program. Multi-omic analyses reveal that loss of MCT1 induces a metabolic stress-like state, suppresses expression of key meiotic regulators, and disrupts progression through the pachytene checkpoint. Mechanistically, we demonstrate that MCT1-mediated lactate influx drives histone H4 lysine 12 lactylation (H4K12la) at promoters of meiotic genes, thereby epigenetically licensing their expression. In the absence of MCT1, H4K12la deposition is lost at meiotic loci and redistributed toward stress-response pathways. Together, our findings suggest MCT1-mediated metabolism as an instructive signal that integrates metabolic state with epigenetic regulation to govern meiotic cell-fate progression, defining a previously unrecognized metabolic checkpoint at pachytene. - Source: PubMed
Publication date: 2026/04/30
Wang NingZhang XiaoyuLiu Yan - The transition from mitosis to meiosis represents a fundamental cell-fate decision that requires coordinated remodeling of transcriptional and metabolic programs. While key transcriptional regulators of meiotic entry have been defined, how metabolic flux directly governs this process remains unclear. Here, we identify a monocarboxylate transporter1 (MCT1)-dependent metabolic checkpoint that controls meiotic progression in mammalian spermatogenesis. Through integrative single-cell transcriptomics, metabolic profiling, and computational perturbation modeling, we show that -driven meiotic initiation is coupled to a metabolic switch favoring monocarboxylic acid metabolism, prominently involving MCT1 (encoded by ). Germ cell-specific deletion of results in a complete arrest at the pachytene stage, characterized by defective homologous recombination, persistent DNA damage, and failure to activate the meiotic transcriptional program. Multi-omic analyses reveal that loss of MCT1 induces a metabolic stress-like state, suppresses expression of key meiotic regulators, and disrupts progression through the pachytene checkpoint. Mechanistically, we demonstrate that MCT1-mediated lactate influx drives histone H4 lysine 12 lactylation (H4K12la) at promoters of meiotic genes, thereby epigenetically licensing their expression. In the absence of MCT1, H4K12la deposition is lost at meiotic loci and redistributed toward stress-response pathways. Together, our findings suggest MCT1-mediated metabolism as an instructive signal that integrates metabolic state with epigenetic regulation to govern meiotic cell-fate progression, defining a previously unrecognized metabolic checkpoint at pachytene. - Source: PubMed
Publication date: 2026/04/22
Zhang XiaoyuLiu YanWang Ning - In head and neck squamous cell carcinoma (HNSCC), solute carrier family 16 member 1 (SLC16A1) is associated with tumor advancement and reduced sensitivity to ferroptosis, yet the molecular basis of these effects remains unclear. This study seeks to uncover how SLC16A1 contributes to HNSCC tumorigenesis. - Source: PubMed
Publication date: 2026/04/22
Tian ChunhuiXie WeipinLi WenGu HuaiyuLiu XuebaoTong BushengLiu YehaiZong Huaiyuan - Propionate, a gut microbiota-derived short-chain fatty acid, influences fetal development and postnatal metabolic programming. Although the fetus lacks microbiota and endogenous propionate production, human pregnancies show a fetal-to-maternal propionate concentration ratio greater than unity, suggesting concentrative transport across the placenta. However, its underlying mechanism remains undefined. The present study aimed to identify the transporter responsible for transplacental transport of propionate across the syncytiotrophoblast (SynT) layer. Transporter knockdown in human choriocarcinoma JEG-3 cells revealed that MCT1 (SLC16A1) silencing reduced [H]propionate uptake, whereas knockdown of other anion transporters had no effect. Functional assays using Xenopus oocytes demonstrated that the expression of human MCT1, but not MCT4 (SLC16A3), increased [H]propionate transport. In human trophoblast stem cell (hTSC)-derived SynT, [H]propionate uptake was pH-dependent and significantly inhibited by MCT1-selective inhibitors. Subsequently, to evaluate transcellular transport, we performed quantitative permeability assays using a hTSC-derived placental barrier model. [H]Propionate permeability was significantly higher than that of [C]d-mannitol, a paracellular marker. MCT1 inhibition reduced [H]propionate permeability in both apical-to-basal and opposite directions, whereas MCT4 inhibition had minimal effects. Notably, the hTSC-derived model exhibited a directional bias in [H]propionate transfer, reflecting the fetal-directed enrichment observed in vivo. Mathematical model analysis further indicated that MCT1 functions at both the apical and basal membranes to facilitate bidirectional transport of propionate. Together, these findings identify MCT1 as the predominant mediator of propionate transfer across the human SynT layer, providing mechanistic insights into how the placenta governs fetal exposure to maternal microbiota-derived metabolites. KEY POINTS: The fetus relies on maternal-derived propionate for development, but the molecular mechanism responsible for its concentrative transport across the human placenta remains undefined. Using multiple human trophoblast models and functional expression assays, we identified MCT1, but not MCT4, as the primary mediator of propionate transport. A human trophoblast stem cell-derived placental barrier model successfully exhibited a directional bias in propionate transfer, reflecting the fetal-directed enrichment observed in vivo. Mathematical modelling of the permeability data from the human trophoblast stem cell-derived barrier model indicates that MCT1 functions at both the apical and basal membranes of the syncytiotrophoblast to facilitate bidirectional transport. These findings establish MCT1 as a key gateway for transplacental propionate transfer, providing mechanistic insights into how the placenta regulates fetal exposure to maternal microbiota-derived metabolites. - Source: PubMed
Publication date: 2026/04/24
Tsuchitani ToshiakiMidorikawa RinKasuya AkariNoguchi SakiYamamoto KoheiNishimura TomohiroKaji HirokazuHori TakeshiTomi Masatoshi - Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disorder characterized by persistent fatigue and post-exertional symptom exacerbation, frequently associated with immune and metabolic disturbances. To evaluate the therapeutic potential of a probiotic formula, HH-205M, we employed a composite mouse model combining forced swimming stress (FSS) and repeated lipopolysaccharide (LPS) administration. FSS-LPS exposure induced pronounced fatigue-like phenotypes, including reduced physical endurance capacity in treadmill and weight-loaded swimming tests, delayed recovery in post-swim grooming behavior, and increased thermal pain sensitivity. These behavioral impairments were accompanied by elevated serum creatine kinase (CK), lactate dehydrogenase (LDH), and lactate levels, indicating systemic metabolic stress. At the tissue level, FSS-LPS increased lipid peroxidation and upregulated pro-inflammatory cytokine expression while suppressing antioxidant gene expression in the gastrocnemius muscle. Furthermore, expression of lactate-related genes, (GPR81) and (MCT1), was reduced, suggesting disruption of lactate transport and sensing pathways under chronic stress and inflammatory conditions. HH-205M supplementation attenuated the elevations in circulating fatigue-related biomarkers, moderated oxidative and inflammatory responses, and restored and expression. These molecular changes were paralleled by improvements in endurance performance and nociceptive sensitivity. HH-205M administration was also associated with distinct shifts in gut microbial composition, including enrichment of and and reduced relative abundance of . Collectively, these findings indicate that the FSS-LPS composite model recapitulates inflammation-associated metabolic disturbances relevant to fatigue-like conditions and that HH-205M administration is associated with concurrent improvements in behavioral and molecular parameters in this model. - Source: PubMed
Publication date: 2026/04/10
Song Jae GwangBae Hyun JinLee Dong HwanSeo JoeunLee BomiShin Kum-JooChung Eui-ChunLee JeongwookKim Hyung WookOh Nam Su