Ask about this productRelated genes to: SLC16A12 antibody
- Gene:
- SLC16A12 NIH gene
- Name:
- solute carrier family 16 member 12
- Previous symbol:
- -
- Synonyms:
- MCT12
- Chromosome:
- 10q23.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-24
- Date modifiied:
- 2016-10-05
Related products to: SLC16A12 antibody
Related articles to: SLC16A12 antibody
- Creatine, α-N-methyl-guanidino-acetic acid, plays a fundamental role in the storage and regeneration of high-energy phosphate in the brain. Defects in the creatine transporter gene (CRT/SLC6A8) result in a significant reduction in brain creatine levels and severe neurological symptoms such as intellectual disability. Clarifying creatine dynamics in the brain is essential to increase our understanding of CRT deficiency syndrome (CRTD) pathology and the development of CRTD therapeutics. This review comprehensively summarizes the pathophysiological roles of transporters in dynamics of creatine and related guanidine compounds in the brain barriers and brain parenchyma. Brain creatine dynamics are regulated by the cooperative actions of various influx and efflux transporters of creatine, guanidinoacetate, creatinine, and creatine biosynthetic enzymes. These transporters include CRT/SLC6A8 as a creatine/guanidinoacetate/creatinine influx transporter, MCT12/SLC16A12, and SLC22A15 for creatine efflux transport, TauT/SLC6A6, GAT2/SLC6A13, and GAT3/SLC6A11 for guanidinoacetate influx transport, and OCT3/SLC22A3 for creatinine influx transport. Transporters and creatine biosynthetic enzymes, such as arginine-glycine amidinotransferase and guanidinoacetate N-methyltransferase, exhibit cell-type specific spatio-temporal expression at the brain barrier and in neurons, astrocytes, and oligodendrocytes. To date, no effective therapeutics have been developed for the treatment of CRTD. The link between low brain creatine level and the mechanism of neurological dysfunction remains unclear. Creatine prodrugs, molecular chaperones, and adeno-associated virus-based gene therapies are potential therapeutic options for CRTD. Advanced technologies, such as omics and genetic engineering, will open new avenues for CRTD therapeutics. - Source: PubMed
Tachikawa Masanori - Despite advancements in targeted therapies, the prognosis for clear cell renal cell carcinoma (ccRCC) remains poor, particularly for metastatic cases. PANoptosis, a newly discovered programmed cell death pathway involving crosstalk among pyroptosis, apoptosis, and necroptosis, has an undefined role in ccRCC pathogenesis and prognosis, representing a critical knowledge gap. - Source: PubMed
Publication date: 2025/11/18
Zhao QiyueXie HuadongLi ChaofuXiong YanxiangFan YongyiHuang YuanbiZhan YiZeng Siping - To date, few studies have specifically explored the placental transcriptome of an animal model of fetal growth restriction (FGR) with nitric oxide (NO) deficiency. The aim of this study was to use NG-nitro-L-arginine methyl ester (L-NAME) to establish a mouse model of FGR with NO deficiency and explore the histological changes and the transcriptomic complexity of the placenta. We established a FGR mouse model via L-NAME administration (n = 6 per group). We assessed the biometric phenotypes of the fetuses and the placentas and analyzed placental and cellular morphology to confirm the pathological changes that occur in FGR placentas. Finally, we applied RNA-seq to analyze the placental transcriptome from the L-NAME-induced mouse model of FGR. We established a mouse model of FGR using L-NAME with biometric and pathological changes. Transcriptomic analysis identified eight differentially expressed genes (DEGs) between the FGR-affected and normal placentas, including six upregulated genes (solute carrier family 6 (neurotransmitter transporter), member 14 (Slc6a14), matrix metallopeptidase 9 (Mmp9), RAS guanyl releasing protein 1 (Rasgrp1), ATP-binding cassette, subfamily B member 1B (Abcb1b), solute carrier family 16 (monocarboxylic acid transporters), member 12 (Slc16a12), and transmembrane protein 255A (Tmem255a)) and two downregulated genes (protein tyrosine phosphatase receptor type N polypeptide 2 (Ptprn2) and meiosis 1 associated protein (M1ap)). These DEGs are highly involved in angiogenesis, the immune system, and inflammatory signaling pathways, underscoring the multifaceted nature of FGR pathology. This study contributes to the understanding of FGR pathophysiology, emphasizing the importance of the immune-related molecular markers and offering potential targets for therapeutic intervention. - Source: PubMed
Huang ShiyunHe XinBian XiaotaoTong JiameiLi ZhengpengChen Yi - Clear cell renal cell carcinoma is the most predominant type of renal malignancies, characterized by high aggressiveness and probability of distant metastasis. Renin angiotensin system (RAS) plays a crucial role in maintaining fluid balance within the human body, and its involvement in tumorigenesis is increasingly being uncovered, while its role in ccRCC remains unclear. - Source: PubMed
Publication date: 2025/03/03
Chang QinzhengZhao ShuoSun JiajiaGuo WeiYang LinQiu LaiyuanZhang NianzhaoFan YidongLiu Jikai - Creatine is essential for ATP regeneration in energy-demanding cells. Creatine deficiency results in severe neurodevelopmental impairments. In the brain, creatine is synthesized locally by oligodendrocytes to supply neighboring neurons. Neuronal uptake is mediated by SLC6A8. However, it is still unknown how creatine is released from the producing cells. Here, we investigated the function of the transporter SLC22A15, which exhibits strikingly high amino acid sequence conservation. The release of substrates from 293 cells via heterologously expressed human and rat SLC22A15 was analyzed by mass spectrometry. A number of zwitterions were identified as substrates, with similar efflux transport efficiencies. However, in absolute numbers, the efflux of creatine far outweighed all other substrates. In contrast to the permanent creatine efflux mediated by SLC16A12 and SLC16A9, SLC22A15 was, by default, completely inactive, thereby preventing continuous creatine loss from producing cells. External substrates such as guanidinoacetic acid, GABA, or MPP trigger creatine release through a one-to-one exchange. Human and mouse mRNA profiles indicate that SLC22A15 expression is highest in oligodendrocytes and bone marrow. Single-cell RNA sequencing data substantiate the hypothesis that SLC22A15 depends on high intracellular creatine concentrations: high SLC22A15 counts, as in oligodendrocytes and macrophages, correlate with high counts of the creatine synthesis enzymes AGAT and GAMT in both humans and mice, whereas in proximal tubular cells and hepatocytes, AGAT counts are high, but SLC22A15 is absent. Our findings establish SLC22A15 as the pivotal transporter for controlled creatine release from oligodendrocytes, filling a critical gap in understanding creatine metabolism in the brain. - Source: PubMed
Publication date: 2025/01/10
Flögel SvenjaStrater MiriamFischer DietmarGründemann Dirk