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MCT8 encodes an integral membrane protein that functions as a transporter of thyroid hormone. Additionally we are shipping Monocarboxylate Transporter 8 Antibodies (29) and Monocarboxylate Transporter 8 Proteins (4) and many more products for this protein.
immunohistochemical studies localized MCT2 (show SLC16A7 ELISA Kits), MCT7, and MCT8 proteins in the cattle rumen, abomasum, jejunum, and caecum.
Data indicate silymarin, an extract of the milk thistle, to be a potent inhibitor of T3 thyroid hormone (show PTH ELISA Kits) uptake by solute carrier family 16 (monocarboxylic acid transporters), member 2 protein (MCT8).
Data show that diiodothyropropionic acid (DITPA) mainly ameliorated the hypermetabolism of monocarboxylate transporter 8 (MCT8) knockout mice.
The data demonstrate that OATP1c1 (show SLCO1C1 ELISA Kits) and MCT8 expression are regulated in a parallel manner during inflammation at the blood-brain barrier of rodents.
This study showed that mouse MCT1 (show MCTS1 ELISA Kits), MCT2 (show SLC16A7 ELISA Kits), and MCT4 (show SLC16A3 ELISA Kits) are expressed in the PNS. While DRG neurons express MCT1 (show MCTS1 ELISA Kits), myelinating Schwann cells.
Cerebral cortex hyperthyroidism of newborn mct8-deficient mice transiently suppressed by lat2 (show SLC7A8 ELISA Kits) inactivation.
Mct8 deficiency has important metabolic consequences in the brain
Transporters MCT8 and OATP1C1 (show SLCO1C1 ELISA Kits) maintain murine brain thyroid hormone (show PTH ELISA Kits) homeostasis.
in Parkinson's disease, the levels of MCT1 (show MCTS1 ELISA Kits), MCT2 (show SLC16A7 ELISA Kits) and GLUT1 (show SLC2A1 ELISA Kits) is not changed following dopaminergic neurodegeneration
Mct10 (show SLC16A10 ELISA Kits) participates in tissue-specific TH transport and also contributes to the generation of the unusual serum TH profile characteristic for Mct8 deficiency
These studies indicate that the high serum T3 in MCT8 deficiency increases the total energy expenditure and fails to maintain weight despite adequate calorie intake.
MCT8 Mutation is associated with Allan-Herndon-Dudley Syndrome.
brain damage in MCT8 deficiency is diffuse, without evidence of focal lesions, and present from fetal stages despite apparent normality at birth
Specific mutations of MCT8 located in transmembrane helix 2 (del230F, V235M, and ins236V) increase the capacity of MCT8 variants to dimerize.
we report 4 Allan-Herndon-Dudley syndrome patients in unrelated Turkish families harboring novel MCT8 mutations
two SNPs in MCT8 were related to circulating thyroid hormone (show PTH ELISA Kits) levels in men but not in women: the rs5937843 polymorphism (G/T) was inversely associated with FT4 levels and the rs6647476 (T/C) polymorphism related negatively to circulating FT3
A reduction in MCT8 expression in the intrauterine growth retardation fetal brain could further compromise Thyroid hormone (show PTH ELISA Kits)-dependent brain development.
We describe three new SLC16A2 mutations associated with different levels of clinical severity in patients with psychomotor retardation disorders.
Monocarboxylate transporter 8 modulates the viability and invasive capacity of human placental cells and fetoplacental growth in mice.
A boy with Allan-Herndon-Dudley syndrome and his heterozygous mother had a point mutation in exon 3 of the MCT8 gene 1201G>A:G401R which changes the properties of the protein.
MCT8 mutations in Allan-Herndon-Dudley Syndrome patients may have tissue-specific effects on thyroid hormone (show PTH ELISA Kits) transport.
This gene encodes an integral membrane protein that functions as a transporter of thyroid hormone. The encoded protein facilitates the cellular importation of thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (rT3) and diidothyronine (T2). This gene is expressed in many tissues and likely plays an important role in the development of the central nervous system. Loss of function mutations in this gene are associated with psychomotor retardation in males while females exhibit no neurological defects and more moderate thyroid-deficient phenotypes. This gene is subject to X-chromosome inactivation. Mutations in this gene are the cause of Allan-Herndon-Dudley syndrome.
monocarboxylate transporter 8
, MCT 8
, Monocarboxylate transporter 8 (MCT 8) (X-linked PEST-containing transporter)
, X-linked PEST-containing transporter
, solute carrier family 16 member 2
, monocarboxylate transporter 7
, solute carrier family 16 (monocarboxylic acid transporters), member 2
, solute carrier family 16, member 2 (monocarboxylic acid transporter 8)