Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion. - Wikidata - awgldk - TriplyDB

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

http://www.wikidata.org/entity/Q34090117

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Inherited defects in thyroid hormone cell-membrane transport and metabolism Thyroid iodide efflux: a team effort?The syndromes of reduced sensitivity to thyroid hormone Controversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cells Diiodothyropropionic acid (DITPA) in the treatment of MCT8 deficiency Juvenile cataract-associated mutation of solute carrier SLC16A12 impairs trafficking of the protein to the plasma membrane.Thyroid hormone regulation of metabolism Inherited defects of thyroid hormone-cell-membrane transport: review of recent findings.Iodide transport: implications for health and disease.Mechanisms of thyroid hormone action Distinct roles of deiodinases on the phenotype of Mct8 defect: a comparison of eight different mouse genotypes.Increased oxidative metabolism and neurotransmitter cycling in the brain of mice lacking the thyroid hormone transporter SLC16A2 (MCT8)A mouse model suggests two mechanisms for thyroid alterations in infantile cystinosis: decreased thyroglobulin synthesis due to endoplasmic reticulum stress/unfolded protein response and impaired lysosomal processing.The nuclear receptor corepressor (NCoR) controls thyroid hormone sensitivity and the set point of the hypothalamic-pituitary-thyroid axis The Thyroid Hormone Analog DITPA Ameliorates Metabolic Parameters of Male Mice With Mct8 Deficiency Liver X receptor β controls thyroid hormone feedback in the brain and regulates browning of subcutaneous white adipose tissue Conditional deletion of insulin receptor in thyrocytes does not affect thyroid structure and function.Disruption of the melanin-concentrating hormone receptor 1 (MCH1R) affects thyroid function.The Type 3 Deiodinase Is a Critical Determinant of Appropriate Thyroid Hormone Action in the Developing Testis.Recent insights into the cell biology of thyroid angiofollicular units.Changes in thyroid status during perinatal development of MCT8-deficient male mice.Transporters MCT8 and OATP1C1 maintain murine brain thyroid hormone homeostasis Primary and secondary thyroid hormone transporters.Different causes of reduced sensitivity to thyroid hormone: diagnosis and clinical management.Thyroid hormone transporters--functions and clinical implications.Loss of sorting nexin 5 stabilizes internalized growth factor receptors to promote thyroid cancer progression.Chemistry and Biology in the Biosynthesis and Action of Thyroid Hormones.Hypomyelinating leukodystrophies - a molecular insight into the white matter pathology.Thyroid Hormone Signaling in Oligodendrocytes: from Extracellular Transport to Intracellular Signal.Manipulation of PBF/PTTG1IP phosphorylation status; a potential new therapeutic strategy for improving radioiodine uptake in thyroid and other tumors Overexpression of Interleukin-4 in the Thyroid of Transgenic Mice Upregulates the Expression of Duox1 and the Anion Transporter Pendrin.High T3, Low T4 Serum Levels in Mct8 Deficiency Are Not Caused by Increased Hepatic Conversion through Type I Deiodinase.Adeno Associated Virus 9-Based Gene Therapy Delivers a Functional Monocarboxylate Transporter 8, Improving Thyroid Hormone Availability to the Brain of Mct8-Deficient Mice.Iodine excess exposure during pregnancy and lactation impairs maternal thyroid function in rats Understanding the hypothalamus-pituitary-thyroid axis in mct8 deficiency.MCT8 Deficiency in Male Mice Mitigates the Phenotypic Abnormalities Associated With the Absence of a Functional Type 3 Deiodinase Time for T...(T3, T4, rT3)? Focus on "Acute inhibition of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel by thyroid hormones involves multiple mechanisms".Differential Regulation of Thyroid Hormone Metabolism Target Genes during Non-thyoidal Illness Syndrome Triggered by Fasting or Sepsis in Adult Mice.Identification, functional analysis, prevalence and treatment of monocarboxylate transporter 8 (MCT8) mutations in a cohort of adult patients with mental retardation.Evidence of G-protein-coupled receptor and substrate transporter heteromerization at a single molecule level.

P2860

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P2860

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

http://www.wikidata.org/entity/Q34090117

description

2010 nî lūn-bûn

@nan

2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@ast

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@en

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@nl

type

label

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@ast

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@en

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@nl

prefLabel

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@ast

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@en

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@nl

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P2860

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P1433

Journal of Clinical Investigation

P1476

Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion.

@en

P2093

Alexandra M Dumitrescu

http://www.w3.org/2001/XMLSchema#string

Caterina Di Cosmo

http://www.w3.org/2001/XMLSchema#string

Nancy J Philp

http://www.w3.org/2001/XMLSchema#string

Roy E Weiss

http://www.w3.org/2001/XMLSchema#string

Samuel Refetoff

http://www.w3.org/2001/XMLSchema#string

Xiao-Hui Liao

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P2860

Cloning of two human thyroid cDNAs encoding new members of the NADPH oxidase family

Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS)

A novel syndrome combining thyroid and neurological abnormalities is associated with mutations in a monocarboxylate transporter gene

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Iodotyrosine dehalogenase 1 (DEHAL1) is a transmembrane protein involved in the recycling of iodide close to the thyroglobulin iodination site

Identification of monocarboxylate transporter 8 as a specific thyroid hormone transporter

The Thyrotropin Receptor and the Regulation of Thyrocyte Function and Growth*

Plasma membrane transport of thyroid hormones and its role in thyroid hormone metabolism and bioavailability.

Association between mutations in a thyroid hormone transporter and severe X-linked psychomotor retardation.

The monocarboxylate transporter 8 linked to human psychomotor retardation is highly expressed in thyroid hormone-sensitive neuron populations.

P304

3377-3388

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scholarly article

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10.1172/JCI42113

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P433

9

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P478

120

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2010-08-02T00:00:00Z

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45461869

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20679730

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P932

2929715

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