-
MCT1 haploinsufficiency promotes resistance to hepatic steatosis by altering lipid metabolism though a modulation of AMPK activity.
-
Silencing or genetic deletion of MCT1 in vivo inhibited migration, invasion, and spontaneous metastasis.
-
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.
-
Exercise-induced changes in tumour LDH-B and MCT1 expression are modulated by oestrogen-related receptor alpha in breast cancer-bearing BALB/c mice
-
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.
-
This study showed that mouse MCT1, MCT2, and MCT4 are expressed in the PNS. While DRG neurons express MCT1, myelinating Schwann cells.
-
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
-
in Parkinson's disease, the levels of MCT1, MCT2 and GLUT1 is not changed following dopaminergic neurodegeneration
-
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.
-
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
-
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
-
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.
-
MCT1 and MCT4 protein expression increased by 92 and 61%, respectively, after 12 days of functional overload (p < 0.05).
-
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.
-
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.
-
Basigin gene products bind MCT1 with moderate affinity, but L1cam does not bind MCT1.
-
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.
-
hydrophobic residues at the N- and C-termini of the putative transmembrane domain of Basigin interact with MCT1, but the glutamate plays no role
-
Results demonstrate beyond doubt that MCT1 is by far the predominant monocarboxylate transporter present in cultured cortical astrocytes from newborn mice.
-
changes in MCT1 are complex, depending not only the accumulated exercise but also on the stage of training.
