ReviewCurrent opinion in endocrinology, diabetes, and obesity2013
Inherited defects of thyroid hormone-cell-membrane transport: review of recent findings.
Review in Current opinion in endocrinology, diabetes, and obesity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 35 citations in OpenAlex.
- Tsh Induces Agrp1 Neuron Proliferation in Oatp1c1-Deficient Zebrafish.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Prenatal Treatment of Thyroid Hormone Cell Membrane Transport Defect Caused byThyroid : official journal of the American Thyroid Association · 2021Article
- Monocarboxylate Transporter 8 Deficiency: From Pathophysiological Understanding to Therapy Development.Frontiers in endocrinology · 2021Review
- Thyroid Hormone Availability and Action during Brain Development in Rodents.Frontiers in cellular neuroscience · 2017Article
- MCT8 Deficiency in Male Mice Mitigates the Phenotypic Abnormalities Associated With the Absence of a Functional Type 3 Deiodinase.Endocrinology · 2016Article
- Nongenomic actions of thyroid hormone.Nature reviews. Endocrinology · 2016Review
- Placenta passage of the thyroid hormone analog DITPA to male wild-type and Mct8-deficient mice.Endocrinology · 2014Article
- Structure and function of thyroid hormone plasma membrane transporters.European thyroid journal · 2014Review
- Altered behavioral performance and live imaging of circuit-specific neural deficiencies in a zebrafish model for psychomotor retardation.PLoS genetics · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of reviewThis review summarizes the most significant findings over the last year regarding human and animal models deficient in thyroid hormone cell-membrane transporters (THCMTs). Although several THCMTs have been modelled in genetically engineered mice, the only THCMT defect known in humans is that caused by mutations in the monocarboxylate transporter 8 (MCT8) gene. RECENT
findingsThe importance of several amino acid residues has been assessed in vitro to further our understanding on the structure-function of the MCT8. The administration of the thyromimetic compound, diiodothyropropionic acid, has been tested in patients with MCT8 gene mutations, following studies of its use in mice. Another thyroid hormone analogue, 3,3',5,5'-tetraiodothyroacetic acid, was tested in Mct8-deficient mice. The phenotypes of L-type aminoacid transporter 2 and organic anion transporting polypeptide 1C1 deficiencies have been studied in mouse models. Mct8/organic anion transporting polypeptide 1C1 double knockout mice have been shown to manifest neurodevelopmental deficits. Zebrafish is emerging as another vertebrate model that may be useful to study the role of Mct8 in brain development. SUMMARY: Studies on the pathogenesis and therapy of MCT8 deficiency are in progress, and new vertebrate models that are suitable to study the neurological consequences of the syndrome are being explored.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.