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Lactic acid and pyruvate transport across plasma membranes is catalyzed by members of the proton-linked monocarboxylate transporter (MCT) family, which has been designated solute carrier family-16. Additionally we are shipping Solute Carrier Family 16 (Monocarboxylic Acid Transporters), Member 3 Antibodies (61) and Solute Carrier Family 16 (Monocarboxylic Acid Transporters), Member 3 Kits (5) and many more products for this protein.
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MCT1 (show CMA1 Proteins) may be acting as an uptake transporter and MCT4 (show SLC16A4 Proteins) as an efflux system across the basolateral membrane for ferulic acid, and that this process is stimulated by butyric acid.
Ocular absorption of monocarboxylic acid drugs may be enhanced by MCT (show MCAT Proteins) transporter SLC16A3, and the absorption route provided by the transporter may be utilized to improve the bioavailability of topically applied ophthalmic drugs.
Gamma-hydroxybutyric acid (GHB) is a substrate for both MCT2 and MCT4 (show SLC16A4 Proteins).
MCT1 (show MCTS1 Proteins) inhibition impairs proliferation of glycolytic breast cancer cells co-expressing MCT1 (show MCTS1 Proteins) and MCT4 via disruption of pyruvate rather than lactate export.
This study demonstrated that MCT4 was up regulation in the brain afeter cerebral ischemia.
The soleus, liver and heart were the main tissues that showed improved the MCT1 (show MCTS1 Proteins) mRNA expression, indicating its important role in controlling MLSS concentration in mice.
MCT4-overexpressing mesenchymal stem cells preferentially induced cell death in cardiomyocytes.
MCT4 depletion induced cell death characterized by elevated reactive oxygen species and metabolic crisis. In xenograft models, MCT4 had a significant impact on tumor metabolism and was required for rapid tumor growth.
MCT4 is up-regulated in inflammation-activated macrophages and required for innate immune response.
Nitric oxide represents an intercellular signal to control MCT4 expression in astrocytes; in doing so, it facilitates lactate transfer to other surrounding cell types in the central nervous system.
MCT4 expression markedly increased the gradient between intracellular and extracellular pH from 0.14 to 0.43.
MCT1 (show MCTS1 Proteins) and MCT4 protein expression increased by 92 and 61%, respectively, after 12 days of functional overload (p < 0.05).
In situ hybridization survey of MCT (show MCAT Proteins) subtypes in placenta detected intense mRNA expression of MCT1 (show MCTS1 Proteins), MCT4, & MCT9 (gestational day 11.5 through day 18.5); subcellular localization of MCT1 (show MCTS1 Proteins) & MCT4 in cell membrane is opposite polarity found in human.
Results suggest that monocarboxylate transporter 4 (MCT4) can play an important role in the transport of short-chain fatty acid
Data indicate that monocarboxylate transporters (MCTs1 (show MCTS1 Proteins)-4) were all found to be expressed in brains of embryos, and were localized in both neurons and astrocyte.
Lactic acid and pyruvate transport across plasma membranes is catalyzed by members of the proton-linked monocarboxylate transporter (MCT) family, which has been designated solute carrier family-16. Each MCT appears to have slightly different substrate and inhibitor specificities and transport kinetics, which are related to the metabolic requirements of the tissues in which it is found. The MCTs, which include MCT1 (SLC16A1\; MIM 600682) and MCT2 (SLC16A7\; MIM 603654), are characterized by 12 predicted transmembrane domains (Price et al., 1998
monocarboxylate transporter 3
, monocarboxylate transporter 4
, solute carrier family 16 (monocarboxylic acid transporters), member 3
, solute carrier family 16, member 3 (monocarboxylic acid transporter 4)
, solute carrier family 16, member 3 (monocarboxylic acid transporter 4) b
, MCT 3
, MCT 4
, solute carrier family 16 member 3
, monocarboxylate transporter 4b