THRB antibody - middle region (ARP37995_P050)
- Known as:
- THRB (anti-) - middle region (ARP37995_P050)
- Catalog number:
- arp37995_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- THRB antibody - middle region (ARP37995_P050)
Related genes to: THRB antibody - middle region (ARP37995_P050)
- Gene:
- THRB NIH gene
- Name:
- thyroid hormone receptor beta
- Previous symbol:
- ERBA2, PRTH
- Synonyms:
- THRB1, THRB2, NR1A2, THR1, ERBA-BETA, GRTH
- Chromosome:
- 3p24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-31
- Date modifiied:
- 2016-02-23
Related products to: THRB antibody - middle region (ARP37995_P050)
Related articles to: THRB antibody - middle region (ARP37995_P050)
- G protein-coupled receptors (GPCRs) are the most widely targeted class of signaling proteins, comprising ∼30% of FDA-approved drugs. Their therapeutic potential arises from their ability to translate diverse extracellular cues into intracellular signals G proteins, arrestins, and other effectors. This signaling versatility creates opportunities for functional selectivity, where ligands preferentially engage particular pathways. However, few endogenous receptor systems display well-defined ligand-dependent divergence across multiple signaling levels. Protease-activated receptor 1 (PAR1) is a candidate model. Thrombin canonically cleaves PAR1 at Arg41, whereas activated protein C (aPC) has been reported to cleave PAR1 at Arg46 in endothelial and co-receptor-supported settings, creating distinct tethered peptide ligands. Thrombin cleavage drives canonical Gαq- and Gα12/13-dependent prothrombotic and barrier-disruptive signaling, whereas aPC cleavage has been associated with anticoagulant, cytoprotective, and anti-inflammatory signaling. However, PAR1's transducer-wide coupling profile, transcriptional consequences, and physiological outputs remain incompletely characterized. - Source: PubMed
Publication date: 2026/05/25
Fallon Braden SCampbell Robert AEnglish Justin G - Resistance to thyroid hormone beta (RTHβ) is a rare genetic disorder characterized by reduced tissue responsiveness to thyroid hormones despite elevated circulating levels. The coexistence of RTHβ and ectopic thyroid tissue is exceptionally rare and presents significant diagnostic and management challenges. We report an eight-year-old girl diagnosed with congenital hypothyroidism through neonatal screening, with thyroid scintigraphy demonstrating a lingual ectopic thyroid. Levothyroxine maintained free thyroxine within the upper reference range and clinical euthyroidism; however, biochemical control as judged by TSH was persistently suboptimal. Genetic sequencing identified a heterozygous THRB c.1312 C > T (p.Arg438Cys) mutation, confirming RTHβ. At seven years of age, the patient developed progressive sublingual swelling with markedly elevated thyroglobulin levels. Positron emission tomography demonstrated metabolic activity consistent with functioning thyroid tissue. Surgical excision was undertaken after multidisciplinary discussion in view of progressive enlargement and chronic TSH stimulation. Histopathology revealed benign hyperplastic thyroid tissue, and BRAF mutation testing was negative. The patient remains clinically stable on levothyroxine replacement. This case highlights the diagnostic delay that may occur when RTHβ coexists with congenital hypothyroidism due to ectopic thyroid, and underscores that persistent unexplained TSH elevation despite clinical euthyroidism on levothyroxine should prompt reassessment for RTHβ even when an alternative diagnosis is established. - Source: PubMed
Publication date: 2026/06/02
Awad Mohammad HosnyThalange NanduAbiary Mohamed El - Mitochondrial metabolism (MM) abnormalities have been implicated in multiple diseases, but its contribution to sepsis-associated encephalopathy (SAE) remains insufficiently understood. The purpose of this research was to explore the candidate biomarkers associated with MM in SAE and the underlying mechanisms. - Source: PubMed
Publication date: 2026/05/22
Zhou RanFang HaoLi HeruiZhang YunhuiSu Xiaosan - Antifouling biocides are marine pollutants intentionally used on vessels and are frequently detected in aquatic environments. The effects of Diuron and Irgarol 1051 (Irgarol), persistent antifouling biocides in the marine environment, on various aquatic organisms remain incompletely understood. In this study, we investigated whether Diuron and Irgarol disrupt thyroid hormone function in fish, using zebrafish larvae as a model. Both compounds induced reductions in survival and hatching rates. Notably, Diuron caused edema and posterior swim bladder noninflation even at a concentration as low as 0.6 mg/L. According to the adverse outcome pathway (AOP) published by the Organisation for Economic Co-operation and Development for thyroid hormone disruption, posterior swim bladder noninflation is one of the adverse outcomes. Based on this, we examined changes in the expression of thyroid-related genes. Diuron exposure significantly decreased dio1 and tshb expression, while significantly increasing thrb expression. Dio1 is an enzyme responsible for converting T4 to T3, and its inhibition is identified as a key event in the published AOP. In contrast, Irgarol exposure significantly increased thrb expression but did not cause significant changes in other thyroid-related genes. These findings suggest that both Diuron and Irgarol affect embryonic development and hatching in zebrafish and that Diuron has the potential to disrupt thyroid hormone function. - Source: PubMed
Publication date: 2026/05/08
Horie YoshifumiChihaya YutoJiang Jheng-Jie - - Source: PubMed
Publication date: 2026/05/05
Chen JunJiang Xinquan