Solute Carrier Family 16, Member 1 (Monocarboxylic Acid Transporter 1) (SLC16A1) ELISA Kits

Human Solute Carrier Family 16, Member 1 (Monocarboxylic Acid Transporter 1) (SLC16A1) interaction partners

1. MCT1 mRNA expression in esophageal squamous cell carcinoma (ESCC) was analyzed in The Cancer Genome Atlas database and in ESCC cells. MCT1 expression was found to correlate with neoplasm stage. Survival analysis showed that patients in a highMCT1 group had a lower overall and progressionfree survival. Downregulation of MCT1 suppressed proliferation and survival of ESCC cells in vitro.

2. Activation of autophagy can promote metastasis and glycolysis in HCC cells, and autophagy induces MCT1 expression by activating Wnt/beta-catenin signaling.

3. Study shows that proton-driven lactate flux is enhanced by the intracellular carbonic anhydrase CAII, which is colocalized with the monocarboxylate transporter MCT1 in MCF-7 breast cancer cells; the results suggest that CAII features a moiety that exclusively mediates proton exchange with the MCT to facilitate transport activity.

4. 7ACC2 is an inhibitor of mitochondrial pyruvate transport; the blockade of pyruvate import into mitochondria prevents extracellular lactate uptake as efficiently as a MCT1 inhibitor

5. the MCT1 A allele is associated with forward soccer player status

6. High MCT-1 expression is associated with clear cell renal cell carcinoma.

7. Metabolism-dependent clonal growth of HCT15 colorectal cancer cells was induced by Nrf2-dependent activation of MCT1-driven lactate exchange.

8. These results demonstrate that Monocarboxylate transporters tend to play a role in the aggressive breast cancer subtypes through the dynamic interaction between breast cancer cells and adipocytes.

9. Sub-Saharan African groups show extremely high values of the T allele of 1470T > A polymorphism. The TT genotype preeminence in African groups could explain the better predisposition to sprint/power performances of African athletes. Caucasian and Asian populations show variable proportions of TT and AA genotypes allowing inter-individual differences in lactate transport.

10. Using in vitro models, we demonstrate that tumor-excreted branched-chain amino acid (BCKA)s can be taken up and re-aminated to BCAAs by tumor-associated macrophages. Our data further suggest that the anti-proliferative effects of MCT1 knockdown observed by others might be related to the blocked excretion of BCKAs.

11. Study demonstrated that the high mRNA level of both MCT1 and GLUT1 correlated with poor prognosis, high- Fuhrman grade clear-cell renal cell carcinoma and metabolic reprogramming.

12. Hypoxia-induced MCT1 supports glioblastoma glycolytic phenotype, being responsible for lactate efflux and an important mediator of cell survival and aggressiveness

13. our finding that the expression of MCT1 and MCT4 is reduced in mutant IDH1 gliomas highlights the unusual metabolic reprogramming that occurs in mutant IDH1 tumors and has important implications for our understanding of these tumors and their treatment

14. MCT1 expression, independent of transporter activity, is required for growth factor-induced tumor cell motility.

15. TOMM20, MCT1, and MCT4 expression was significantly different in Hodgkin and Reed Sternberg (HRS) cells. HRS have high expression of MCT1, while tumor associated macrophages have absent MCT1 expression. Tumor-infiltrating lymphocytes have absent MCT1 expression. Reactive lymph nodes in contrast to cHL tumors had low TOMM20, MCT1, and MCT4 expression in lymphocytes and macrophages.

16. TOMM20 and MCT1 were highly expressed in diffuse large B-cell lymphoma lymphocytes, indicating an OXPHOS phenotype, whereas non-neoplastic lymphocytes in the control samples did not express these markers.

17. Data suggest that targeting monocarboxylate transporter 1 (MCT1) in both tumor cells and brain endothelial cells (EC) may be a promising therapeutic strategy for the treatment of Glioblastoma (GBM).

18. The structures and functions of hMCT1 and hMCT4 transporters.

19. MCT1 inhibitor AZD3965 increased MCT4-dependent accumulation of intracellular lactate, inhibiting monocarboxylate influx and efflux.

20. Silencing or genetic deletion of MCT1 in vivo inhibited migration, invasion, and spontaneous metastasis.

Zebrafish Solute Carrier Family 16, Member 1 (Monocarboxylic Acid Transporter 1) (SLC16A1) interaction partners

1. Data indicate that monocarboxylate transporters (MCTs1-4) were all found to be expressed in brains of embryos, and were localized in both neurons and astrocyte.

Horse (Equine) Solute Carrier Family 16, Member 1 (Monocarboxylic Acid Transporter 1) (SLC16A1) interaction partners

1. The expression of monocarboxylic acid transporter 1 (MCT1), MCT2, and CD147 in 3 horse breeds with different atheletic demands is reported.[MCT1; MCT2]

2. Results indicated that a single IET resulted in transient increases in MCT1 and MCT4 mRNA expression and protein content in untrained and trained horses.

3. The coding sequence of MCT1, MCT4, and CD147 in healthy horses, and the incidence of polymorphisms of these proteins in horses with excercise-induced myopathy are reported.

4. MCT1 protein content in GMM samples obtained when the horses were 24 months old was significantly higher than at 2 months of age. However, MCT4 protein content remained unchanged throughout the study period.

Mouse (Murine) Solute Carrier Family 16, Member 1 (Monocarboxylic Acid Transporter 1) (SLC16A1) interaction partners

1. In MCT1 (+/-) heterozygotes, which express half of the normal complement of MCT1, the retina developed normally and retained normal function, indicating that MCT1 is expressed at sufficient levels to support outer retinal metabolism.

2. MCT1 haploinsufficiency promotes resistance to hepatic steatosis by altering lipid metabolism though a modulation of AMPK activity.

3. Silencing or genetic deletion of MCT1 in vivo inhibited migration, invasion, and spontaneous metastasis.

4. It was concluded that both MCT1 and CAII are involved in the homeostatic control of pH in skeletal muscle, both at rest and at the onset of exercise. The improved muscle function and resistance to fatigue in MCT1(+/-) mice remain unexplained.

5. Exercise-induced changes in tumour LDH-B and MCT1 expression are modulated by oestrogen-related receptor alpha in breast cancer-bearing BALB/c mice

6. Chronic lactate administration after exercise increases MCT1 protein expression, which can be involved in the regulation of the observed increase in muscle glycogen storage after exercise training.

7. This study showed that mouse MCT1, MCT2, and MCT4 are expressed in the PNS. While DRG neurons express MCT1, myelinating Schwann cells.

8. These data for the first time demonstrate that MCT1 is critical for regeneration of both sensory and motor axons in mice following sciatic nerve crush

9. in Parkinson's disease, the levels of MCT1, MCT2 and GLUT1 is not changed following dopaminergic neurodegeneration

10. results suggest that a reduction in mitochondria is a result, rather than the cause, of the metabolic deficiency observed in Basigin-null mice, and likely occurs because of reduced metabolic activity in the absence of MCT1 expression.

11. miR-29a, miR-29b selectively target MCT1 3'UTR ; the miR-29 isoforms are highly expressed in islets and contribute to silencing Mct1 in beta cells; miR-29 isoforms contribute to beta-cell-specific silencing of the MCT1 transporter and may affect insulin release

12. monocarboxylate transporter 1 (MCT1), is highly enriched within oligodendroglia and disruption of this transporter produces axon damage and neuron loss in animal and cell culture models; in addition, this same transporter is reduced in patients with, and in mouse models of, amyotrophic lateral sclerosis, suggesting a role for oligodendroglial MCT1 in pathogenesis

13. It was shown that forced overexpression of MSlc16a1 in beta-cells replicates the key features of exercise-induced hyperinsulinism and highlights the importance of this transporter's absence from these cells for the normal control of insulin secretion.

14. MCT1 and MCT4 protein expression increased by 92 and 61%, respectively, after 12 days of functional overload (p < 0.05).

15. Data suggest that basigin interacts with MCT1 and MCT2 to locate them properly in the membrane of spermatogenic cells and that this may enable sperm to utilize lactate as an energy substrate contributing to cell survival.

16. MCT-1 contributes to NOX-2 expression via late phase activation of NF-kappaB in a ROS-dependent manner in ATDC5 cells exposed to IL-1beta.

17. Basigin gene products bind MCT1 with moderate affinity, but L1cam does not bind MCT1.

18. In situ hybridization survey of MCT subtypes in placenta detected intense mRNA expression of MCT1, MCT4, & MCT9 (gestational day 11.5 through day 18.5); subcellular localization of MCT1 & MCT4 in cell membrane is opposite polarity found in human.

19. hydrophobic residues at the N- and C-termini of the putative transmembrane domain of Basigin interact with MCT1, but the glutamate plays no role

20. Results demonstrate beyond doubt that MCT1 is by far the predominant monocarboxylate transporter present in cultured cortical astrocytes from newborn mice.

Cow (Bovine) Solute Carrier Family 16, Member 1 (Monocarboxylic Acid Transporter 1) (SLC16A1) interaction partners

1. This study confirmed age-dependent changes of MCT1 expression in the rumen epithelium of newborn calves and showed that its expression might be affected by liquid feed type.

2. These findings show that MCT 1 increases with the development of rumen function and also in adult animals MCT 1 may change with the feeding.

3. The expression and distribution of monocarboxylate transporter 1 along the gastrointestinal tract of calves suggest it may play a role in transport of short chain fatty acids and their metabolites.

4. This study investigated the distribution and expression of monocarboxylate transporter 1 (MCT1) in the livers of pre-ruminant calves and adult bovines (bulls and cows), using different molecular biological techniques.

5. The results show that monocarboxylate transporter 1 (MCT1) is a major route for short chain fatty acids (SCFA) efflux across the basolateral membrane of bovine large intestine and that it could play a role in the regulation of intracellular pH.