TSHR recombinant protein
- Known as:
- TSHR Rec. protein
- Catalog number:
- BRP1093
- Product Quantity:
- 100 μg
- Category:
- -
- Supplier:
- Biospect
- Gene target:
- TSHR recombinant protein
Related genes to: TSHR recombinant protein
- Gene:
- TSHR NIH gene
- Name:
- thyroid stimulating hormone receptor
- Previous symbol:
- -
- Synonyms:
- LGR3
- Chromosome:
- 14q24-q31
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-05
- Date modifiied:
- 2019-04-23
Related products to: TSHR recombinant protein
Related articles to: TSHR recombinant protein
- Subclinical hypothyroidism (SH) in childhood is frequently idiopathic and usually follows a benign course. Heterozygous loss-of-function variants in the thyrotropin receptor (TSHR) gene have emerged as a genetic cause of isolated hyperthyrotropinemia; however, data regarding long-term outcomes and management are limited. - Source: PubMed
Publication date: 2026/06/05
Yaşar AyşeYarar Murat HakkıKırmızıbekmez HevesDursun Fatma - Anaplastic thyroid cancer (ATC) patient develops resistance to radioactive iodine (RAI) due to diminished sodium-iodide symporter (NIS) expression and mislocalization to the cell membrane. MAPK pathway inhibitors have demonstrated efficacy in enhancing RAI avidity in radioiodine-refractory papillary thyroid carcinoma and ATC. Elucidating this mechanism may lead to novel therapeutic approaches for ATC treatment. The cytotoxic effects of three MAPK pathway inhibitors (selumetinib, vemurafenib, dabrafenib) were assessed in ATC cell lines and xenograft models via viability assays and F-FDG PET/CT. We investigated their impact on radioiodine metabolism by analyzing the expression of key genes (NIS, TSHR, and TPO) and trafficking regulators (ARF4, PIGU, and β-catenin) via Western blotting, and assessing NIS localization and function through immunofluorescence and uptake assays. The protein interaction between NIS and ARF4 was examined via co-immunoprecipitation (co-IP) and immunofluorescence. MAPK pathway inhibitors reduced the viability of ATC cell lines. ATC cells exhibited restored iodine metabolism-related gene expression after treatment, and pronounced increases in membrane-localized NIS were detected via the promotion of ARF4 expression. Furthermore, MAPK pathway inhibitors increased radioiodine uptake in ATC cells. The MAPK pathway inhibitors enhance NIS function through two mechanisms: upregulation of NIS expression and increased ARF4-mediated NIS membrane transport. - Source: PubMed
Publication date: 2026/06/04
Wang JunfangZeng ZhenzhenXu ShashaWang XiaoxianWu KeliuChang YongguangWang GuanzhengLiu BaopingWang RuihuaHan Xingmin - Diethylene glycol dibenzoate (DEGDB), an emerging eco-friendly plasticizer, remains critically understudied with mechanistic and molecular-level evidence linking it to clear cell renal cell carcinoma (ccRCC) progression, representing a major knowledge gap. To fill this gap, we conducted a cross-scale investigation using network toxicology, WGCNA, machine learning, SHAP explainable modeling, and molecular docking as methodological tools to elucidate DEGDB‑induced ccRCC progression. By jointly mining the ChEMBL, PubChem, SwissADME, STRING, and GEO repositories, we rigorously distilled a high-confidence set of 42 target genes, among which TSHR, ADORA2B, ANPEP, CA9, CYP3A4, JUN, NR1I3, and PHGDH were highlighted. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that DEGDB may propel ccRCC progression by disrupting neuro-endocrine-immune network regulation, activating chemical carcinogenesis-related receptors, and perturbing metabolic-degradation pathways such as nitrogen metabolism and lysosomal signaling. Subsequently, 113 machine-learning algorithms were leveraged to construct predictive models, and SHAP-based interpretation pinpointed five core genes-CA9, NR1I3, PHGDH, GABRA2, and ANPEP. Validation against The Cancer Genome Atlas (TCGA) datasets demonstrated that CA9 exhibits marked expression divergence in ccRCC (box-plot analysis) and is strongly associated with unfavorable prognosis (Kaplan-Meier survival curves). Molecular-docking simulations further confirmed robust binding affinities between DEGDB and all five core target proteins (binding energies < -5 kcal/mol). In vitro assays additionally revealed that DEGDB significantly promotes 786-O and A498 proliferation and up-regulates CA9 protein expression. Collectively, our findings indicate that DEGDB accelerates ccRCC progression via the orchestrated modulation of cellular proliferation, disruption of neuro-endocrine-immune homeostasis, and activation of oncogenic receptors. This study provides a theoretical framework for assessing the environmentally relevant health risks posed by emerging plasticizers and for devising preventive strategies against DEGDB‑induced ccRCC under real‑world exposure scenarios. - Source: PubMed
Publication date: 2026/05/22
Yanping MaGuolin TianTao YangAngyang DuJiaxin LiBo TaoYajie LiYaodong JiaYuelong FengHao YangLihong NieRuining Zhao - Activation of thyroid-stimulating hormone receptor (TSHR) by autoantibodies is the primary cause of the autoimmune diseases Graves' hyperthyroidism and Graves' ophthalmopathy. Thus, recent pharmaceutical research has focused on blocking pathogenic TSHR activation. While this has potential to offer first-in-class disease-modifying medications to treat Graves' disease, the success of targeting drugs requires understanding of how TSHR-stimulating autoantibodies activate the receptor and mediate signalling. This study comprehensively characterized in vitro pharmacological profiles of two human TSHR-stimulating autoantibodies, M22 and K1-18, relative to bovine TSH (bTSH) in a HEK293A cell background expressing recombinant human TSHR. M22 and K1-18 exhibited subtle, G protein-specific, differences in activating Gα proteins, with both antibodies generally less potent and/or efficacious than bTSH. While both antibodies were equivalent in activation of most G proteins, K1-18 was less potent than M22 in activation of Gαs-short and Gαz. Interestingly, bTSH, M22 and K1-18 more potently activated Gα15 compared to other Gα proteins. In addition, M22 and K1-18 activated Gαs-dependent cAMP production and Gαq-coupled signalling (IP accumulation and iCa mobilisation), recruited β-arrestin 1 and 2, and stimulated receptor internalization to early endosomes. K1-18 was less potent than bTSH in all these assays, while M22 was less potent than bTSH in iCa mobilisation and β-arrestin recruitment. While M22 and K1-18 largely mirror the pharmacology of bTSH, quantification of revealed relative to bTSH they exhibit bias towards Gα12 activation, and away from β-arrestin 2 recruitment and iCa mobilization relative to Gs and cAMP. Thus, these findings offer insight into the action of TSHR-stimulating antibodies. - Source: PubMed
Publication date: 2026/05/30
Nguyen Huong T MGerrard ElliotStrachan RyanKlein UweSexton Patrick MWootten Denise - Organ-specific autoimmune diseases, particularly Graves' disease (GD) and its extrathyroidal manifestation, Graves' orbitopathy (GO), are characterized by systemic autoimmunity that may extend its impact to the central nervous system (CNS). While thyroid-stimulating hormone receptor (TSHR) is the primary driver of pathological remodeling in the thyroid and orbital tissues, emerging evidence suggests it is also expressed in the brain and may participate in neuroimmune signaling. However, the molecular mechanisms linking peripheral TSHR-driven autoimmunity to these extended systemic features remain unclear. Thus, GD and GO provide a unique window to investigate how peripheral autoantibodies influence CNS involvement as part of its broader pathological spectrum. - Source: PubMed
Publication date: 2026/05/27
Zhang HaiyangJiang ShufanZhu TianyiLiu YutingLi JipengFang SijieLi YinweiSun JingHe XinhengTong ChuanjunGao ZhengrunFan XianqunZhou Huifang