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immunohistochemical studies localized MCT2, MCT7, and MCT8 proteins in the cattle rumen, abomasum, jejunum, and caecum.
The marked phenotypic abnormalities observed in the D3-deficient mouse, including perinatal mortality, growth retardation, and central hypothyroidism in adult animals, require expression of MCT8, confirming the interdependent relationship between the TH transport into cells and the deiodination processes.
Data indicate silymarin, an extract of the milk thistle, to be a potent inhibitor of T3 thyroid hormone (show PTH Proteins) uptake by solute carrier (show SERTAD2 Proteins) 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 Proteins) 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 Proteins), MCT2, and MCT4 (show SLC16A3 Proteins) are expressed in the PNS. While DRG neurons express MCT1 (show MCTS1 Proteins), myelinating Schwann cells.
Cerebral cortex hyperthyroidism of newborn mct8-deficient mice transiently suppressed by lat2 (show SLC7A8 Proteins) inactivation.
Mct8 deficiency has important metabolic consequences in the brain
Transporters MCT8 and OATP1C1 (show SLCO1C1 Proteins) maintain murine brain thyroid hormone (show PTH Proteins) homeostasis.
in Parkinson's disease, the levels of MCT1 (show MCTS1 Proteins), MCT2 and GLUT1 (show SLC2A1 Proteins) is not changed following dopaminergic neurodegeneration
Mct10 participates in tissue-specific TH transport and also contributes to the generation of the unusual serum TH profile characteristic for Mct8 deficiency
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 Proteins) 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 Proteins)-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 Proteins) 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)