Ask about this productRelated genes to: SLC16A1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: SLC16A1 Blocking Peptide
- Intestinal mucosal healing is a key indicator for evaluating therapeutic efficacy and predicting long-term prognosis in ulcerative colitis (UC). Short-chain fatty acids (SCFAs) play an important role in maintaining intestinal homeostasis and promoting mucosal repair; however, their quantitative association with UC mucosal healing has not been fully elucidated. This study aimed to investigate the association between SCFA levels and endoscopic mucosal healing in UC patients and evaluate their clinical value as predictive biomarkers. - Source: PubMed
Publication date: 2026/06/13
He Ben-QiuLai Xiang-QuanYang XueZhou Jin - Combined hepatocellular-cholangiocarcinoma (cHCC-CCA) is a rare, biologically heterogeneous primary liver cancer with conflicting reported outcomes. The prognostic impact of viral hepatitis in cHCC-CCA remains unclear. Given its established influence in hepatocellular carcinoma, we evaluated whether viral etiology is associated with distinct clinical and genomic features in cHCC-CCA. - Source: PubMed
Publication date: 2026/05/18
Puttagunta NehaFriedman MatthewKhandakar BinnyBrown Timothy JGrewal Udhayvir SinghHornstein Nicholas - This study aims to investigate the causal relationship between SLC16A1 lactylation modification and systolic blood pressure (SBP) and diastolic blood pressure (DBP), as well as the potential mediating role of lipidomics-triglyceride (50:3/50:1) in this association. - Source: PubMed
Publication date: 2026/05/11
Zhao WeikunLi XiaopingHuang RongjieLuo Zuchun - 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: 2026/04/30
Zhang XiaoyuLiu YanWang Ning - 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