Ask about this productRelated genes to: TSHR antibody
- 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 antibody
Related articles to: TSHR antibody
- Transient congenital hypothyroidism (TCH) is characterized by congenital hypothyroidism (CH) which spontaneously resolves in the first years of life. While most cases are sporadic, several studies from worldwide showed variants in , genes in the etiology of TCH. The aim of our study is to evaluate the genetic etiology of TCH. - Source: PubMed
Publication date: 2026/05/12
Köprülü ÖzgeAcar SezerUzman Ceren YılmazErbaş İbrahim MertNalbantoğlu ÖzlemHazan FilizGürsoy SemraKorkmaz Hüseyin AnılÖzkan Behzat - Thyroid cancer (TC) is the most common endocrine malignancy, and challenges persist in preoperative diagnosis of indeterminate nodules and postoperative monitoring when thyroglobulin (Tg) assays are compromised by interfering anti-Tg antibodies (Tg-Ab). Extracellular vesicles (EVs) carry molecular cargo reflective of cells of origin and are increasingly explored as biomarker sources. In this study, we investigated whether thyroid-derived EVs retain the expression of thyroid-specific thyrotropin-receptor (TSHR), a suitable target in immunoaffinity-based EV isolation, and explored the presence of Tg in EV cargo as potential surrogate for serum Tg. EVs from thyroid cell lines (Nthy-Ori 3-1, TPC-1, OCUT2) and plasma of patients with benign, malignant tumors and recurrent TC were isolated by differential ultracentrifugation and characterized via nanoparticle tracking and Dot and Western blot analyses. EVs derived from Nthy-Ori 3-1 and TPC-1 cell lines were positive for surface TSHR and vesicular Tg, but not OCUT2. All plasma-derived EVs were positive for TSHR and Tg, while their electrophoretic profiles from vesicles differed compared to tissue lysate. Tg was detectable in EVs isolated from recurrent TC samples, even in Tg-Ab positive cases. Together, these results support the use of TSHR for targeted EV isolation and point to vesicular Tg as a potential recurrence marker. - Source: PubMed
Publication date: 2026/04/14
Bobar NevenaMitić NinoslavKosanović MajaŠelemetjev SonjaIšić Denčić TijanaTaušanović KatarinaJanković Miljuš Jelena - Thyroid-stimulating hormone beta subunit () gene, a member of the glycoprotein hormone beta subunit family, has been detected in ovarian tissues and granulosa cells (GCs) of several species, suggesting a potential involvement in ovarian function. However, its molecular regulatory mechanisms and functional roles in Duolang sheep remain unclear. - Source: PubMed
Publication date: 2026/05/01
Sun HuiPingZhu LeXiaoShahbaz GulMuhammadGu RuoHuaiHe ChengLongChen ShuXinWang ChaoFanXing FengYan XiangLin - Iodine is crucial for growth and development. Given that persistent iodine imbalance impairs thyroid function and can trigger various pathologies, this study preliminarily investigated the effects and underlying mechanisms of long-term iodine deficiency or excess on thyroid proliferation in rats. We established rat models of iodine deficiency and excess through long-term intervention with a low-iodine diet and deionized water containing different concentrations of potassium iodide. Our results revealed distinct molecular profiles under these conditions: iodine deficiency significantly upregulated the expression of TSHR and PKA-cat, whereas long-term iodine excess markedly suppressed them. Despite these divergent signaling initiations, both conditions resulted in a significant increase in the protein expression of PCNA and Pax8, unequivocally indicating enhanced thyroid follicular cell proliferation. Furthermore, key nodes of the Ras/MAPK pathway, RAS and BRAF, demonstrated a clear upward trend in the late intervention phase in both groups. These findings collectively demonstrate that both iodine deficiency and excess can promote thyroid proliferation; however, the mechanisms involved in driving this proliferative response are likely distinct. Deficiency acts by activating the TSH-TSHR-PKA pathway and synergistically enhancing RAS/BRAF signaling. In contrast, long-term iodine excess promotes thyroid proliferation by enhancing RAS/BRAF activation through inhibition of the TSHR-PKA axis. - Source: PubMed
Publication date: 2026/05/01
Cheng JunshuaiGao ZifanZhao YuanSong QiuyiWang YuXu TingtingLv KaiLi YanleiZhang WanqiLiu JuanTan Long - To determine the genetic polymorphisms of and genes with susceptibility to Graves` ophthalmopathy among patients with Graves' disease. - Source: PubMed
Publication date: 2026/04/29
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