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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Oct 2014.

Thyroid stimulating hormone, beta

TSH beta
The four human glycoprotein hormones chorionic gonadotropin (CG), luteinizing hormone (LH), follicle stimulating hormone (FSH), and thyroid stimulating hormone (TSH) are dimers consisting of alpha and beta subunits that are associated noncovalently. The alpha subunits of these hormones are identical, however, their beta chains are unique and confer biological specificity. Thyroid stimulating hormone functions in the control of thyroid structure and metabolism. The protein encoded by this gene is the beta subunit of thyroid stimulating hormone. Mutations in this gene result in congenital hypothyroidism.[provided by RefSeq, Nov 2009] (from NCBI)
Top mentioned proteins: Prolactin, HAD, Thyrotropin-Releasing Hormone, CD45, ACID
Papers on TSH beta
Falsely undetectable TSH in a cohort of South Asian euthyroid patients.
New
Dlott et al., San Diego, United States. In J Clin Endocrinol Metab, Apr 2014
Discordant samples were evaluated on up to 8 FDA-approved TSH immunoassays and the TSHβ gene was sequenced.
Serum TSH and risk of papillary thyroid cancer in nodular thyroid disease.
GeneRIF
Vitti et al., Pisa, Italy. In J Clin Endocrinol Metab, 2012
Data suggest that likelihood of papillary thyroid carcinoma is reduced when serum TSH is lower, as in thyroid autonomy, and increased when serum TSH is higher, as in thyroid autoimmunity. [Meta-Analysis; REVIEW]
The natural history of the normal/mild elevated TSH serum levels in children and adolescents with Hashimoto's thyroiditis and isolated hyperthyrotropinaemia: a 3-year follow-up.
GeneRIF
Loche et al., Bolzano - Bozen, Italy. In Clin Endocrinol (oxf), 2012
Data suggest that a progressive increase in TSH are predictive factors for thyroid failure in Hashimoto's thyroiditis (HT) patients.
Changes of thyroid hormone levels and related gene expression in zebrafish on early life stage exposure to triadimefon.
Zhu et al., Hangzhou, China. In Environ Toxicol Pharmacol, 2011
Thyroid hormones levels and the expression of related genes in the hypothalamic-pituitary-thyroid (HPT) axis, including thyroid-stimulating hormone (TSH-beta), deiodinases (dio1 and dio2) and the thyroid hormone receptor (thraa and thrb) were evaluated.
T3 rapidly modulates TSHβ mRNA stability and translational rate in the pituitary of hypothyroid rats.
GeneRIF
Nunes et al., São Paulo, Brazil. In Mol Cell Endocrinol, 2011
These data add new insight to an important role of T3 in rapidly regulating TSH beta gene expression at posttranscriptional level.
Immunological regulation of metabolism--a novel quintessential role for the immune system in health and disease.
GeneRIF
Klein et al., Houston, United States. In Faseb J, 2011
Studies indicate that immune system-derived TSH, in particular, a splice variant of TSHbeta that is preferentially made by cells of the immune system, is produced by a subset of hematopoietic cells that traffic to the thyroid.
Two novel mutations of the TSH-beta subunit gene underlying congenital central hypothyroidism undetectable in neonatal TSH screening.
GeneRIF
Belgorosky et al., Buenos Aires, Argentina. In J Clin Endocrinol Metab, 2010
Novel mutations of the TSH-beta subunit gene underlying congenital central hypothyroidism undetectable in neonatal TSH screening.
Resistance to thyroid hormone due to a novel thyroid hormone receptor mutant in a patient with hypothyroidism secondary to lingual thyroid and functional characterization of the mutant receptor.
Mori et al., Maebashi, Japan. In Thyroid, 2010
It also had a clear dominant negative effect on genes negatively, but not positively, regulated by thyroid hormone, including the TSH-releasing hormone and TSHbeta genes.
Contribution of TNF-alpha and nuclear factor-kappaB signaling to type 2 iodothyronine deiodinase activation in the mediobasal hypothalamus after lipopolysaccharide administration.
Lechan et al., Boston, United States. In Endocrinology, 2010
The LPS-induced increase in Ikappa-Balpha in the pars tuberalis was associated with increased TSHbeta gene expression in this tissue, but cAMP response element-binding protein (CREB) phosphorylation was observed only in a subset of alpha tanycytes.
W194XProp1 and S156insTProp1, both of which have intact DNA-binding domain, show a different DNA-binding activity to the Prop1-binding element in human Pit-1 gene.
Okimura et al., Kōbe, Japan. In Mol Cell Endocrinol, 2010
Prop1 activates POU1F1 (Pit-1) gene expression, which in turn stimulates GH, PRL, TSHbeta and GHRH receptor gene expressions.
Transient hypothyroxinemia in juvenile glycoprotein hormone subunit B5 knock-out mice.
Fliers et al., Amsterdam, Netherlands. In Mol Cell Endocrinol, 2010
During hypothyroidism, despite similar serum T(4), pituitary TSHbeta mRNA was 2-fold lower in GPB5(-/-) mice compared to WT. Adult mice displayed increased pituitary deiodinase type 2 during euthyroidism and decreased serum T(4) during hypothyroidism in GPB5(-/-).
Hes1 regulates formations of the hypophyseal pars tuberalis and the hypothalamus.
Kameda et al., Sagamihara, Japan. In Cell Tissue Res, 2010
Both the rostral tip of Rathke's pouch (pars tuberalis primordium) and the pars tuberalis expressed alphaGSU mRNA, and were immunoreactive for LH, chromogranin A, and TSHbeta in mice.
New cases of isolated congenital central hypothyroidism due to homozygous thyrotropin beta gene mutations: a pitfall to neonatal screening.
GeneRIF
Polak et al., Paris, France. In Thyroid, 2010
we describe two new sibships with isolated congenital central hypothyroidism due to two different homozygous TSHbeta gene mutations (c.Q49X and c.C105fs114X).
Expression patterns of hormones, signaling molecules, and transcription factors during adenohypophysis development in the chick embryo.
Ryan et al., Montréal, Canada. In Dev Dyn, 2010
RT-PCR detected low levels of Fshbeta (gonadotropes) and Pomc (corticotropes, melanotropes) mRNA at E4 and Gh (somatotropes), Prl (lactotropes), and Tshbeta (thyrotropes) mRNA at E8.
Dissecting the Relation between a nuclear receptor and GATA: binding affinity studies of thyroid hormone receptor and GATA2 on TSHβ promoter.
GeneRIF
Santos et al., São Carlos, Brazil. In Plos One, 2009
T3 weakens TRb1 binding to a negative regulatory element in the TSHbeta promoter.
Thyrotropin in teleost fish.
Review
Miller et al., College Station, United States. In Gen Comp Endocrinol, 2009
Descriptive studies have found increased TSHbeta expression associated with life history events thought to be promoted by thyroid hormones.
Basic science and clinical research advances in the pituitary transcription factors: Pit-1 and Prop-1.
Review
Ridgway et al., Aurora, United States. In Curr Opin Endocrinol Diabetes Obes, 2008
Among these findings include: the effects of the Pit-1 coactivators, GATA-2 and TRAP-220, on the transcriptional regulation of the TSHbeta gene and thyrotropin expression, characterization of a novel pituitary regulator of Pit-1 expression, Atbf1, elucidation of the roles of Wnt and Notch signaling on Prop-1-mediated specification of the Pit-1 cell lineage and gonadotropes, and the identification of regulatory regions of the Prop-1 gene.
Initially elevated TSH and congenital central hypothyroidism due to a homozygous mutation of the TSH beta subunit gene: case report and review of the literature.
Review
Pohlenz et al., Esslingen, Germany. In Exp Clin Endocrinol Diabetes, 2006
Congenital central hypothyroidism (CCH) is a rare disease which can be caused by mutations in the gene for the thyrotropin (TSH) beta subunit ( TSHB).
[Progress on pituitary-specific transcription factor (POU1F1) in poultry].
Review
Yang et al., Beijing, China. In Yi Chuan, 2004
Prolactin (PRL),Growth Hormone (GH), and Thyroid-stimulating Hormone-beta(TSHbeta), secreting by chicken anterior pituitary, are essential hormones affecting chicken laying ability, growth rate, and immunity via regulating chicken broodiness, development, and immune response.
Hypothyroidism in siblings due to a homozygous mutation of the TSH-beta subunit gene.
Review
White et al., New Orleans, United States. In J Pediatr Endocrinol Metab, 2004
Sequencing of the TSH-beta subunit gene revealed a homozygous single nucleotide deletion in codon 105, producing a frame shift and resulting in inactive TSH.
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