FITC标记的促甲状腺素受体抗体（C端）
产品名称： FITC标记的促甲状腺素受体抗体（C端）
英文名称： Anti-TSHR (CT)/FITC
产品编号： HZ-0206R-FITC
产品价格： null
产品产地： 中国/上海
品牌商标： HZbscience
更新时间： 2023-08-17T10:24:20
使用范围： IF=1:50-200
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Rabbit Anti-TSHR (CT)/FITC Conjugated antibody
FITC标记的促甲状腺素受体抗体（C端）
| 英文名称 | Anti-TSHR (CT)/FITC |
| 中文名称 | FITC标记的促甲状腺素受体抗体（C端） |
| 别 名 | hTSHR I; hTSHRI; LGR 3; LGR3; MGC75129; Thyroid adenoma hyperfunctioning; Thyroid carcinoma with thyrotoxicosis; Thyroid Stimulating Hormone Receptor; Thyrotropin Receptor; Thyrotropin receptor I; TSH R; TSHR; Thyroid stimulating hormone receptor; TSHR_HUMAN. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 研究领域 | 细胞生物 生长因子和 细胞膜受体 内分泌病 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Rat, Chicken, Pig, Cow, Horse, Rabbit, Guinea Pig, |
| 产品应用 | IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 86kDa |
| 细胞定位 | 细胞膜 |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human TSHR |
| 亚 型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 储 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存条件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| 产品介绍 | background: The glycoprotein hormone receptor family consists of the luteinizing hormone receptor, the follicle-stimulating hormone receptor, and the thyroid stimulating hormone(TSH) receptor. TSH, which is released from the pituitary gland, binds to the TSH receptor on thyroid cells to control size and function of the thyroid gland (De Felice et al. 2004). The TSH receptor signals through Gs to elevate intracellular cAMP in the thyroid gland, which regulates iodide uptake, and transcription of thyroglobulin (Tg), thyroid peroxidase (TPO), and sodium-iodide symporter. The TSH receptor also signals Gq and phospholipase C to regulat iodide efflux, H2O2 production, and thyroglobulin iodination. Autoimmunity to the TSH receptor causes hyperthyroidism (Graves disease) or hypothyroidism (Hashimoto thyroiditis) when the autoantibodies function as agonists or antagonists, respectively, at the TSH receptor (Rapoport and McLachlan, 2001; Davies et al., 2002). Millipore’s cloned human TSH receptor-expressing cell line is made in the Chem-10 host, which supports high levels of recombinant TSH receptor expression on the cell surface and contains high levels of the promiscuous G protein to couple the receptor to the calcium signaling pathway. Thus, the cell line is an ideal tool for screening for antagonists of interactions between TSH and its ligands. Function: Receptor for thyrothropin. Plays a central role in controlling thyroid cell metabolism. The activity of this receptor is mediated by G proteins which activate adenylate cyclase. Also acts as a receptor for thyrostimulin (GPA2+GPB5). Subunit: Interacts (via the PDZ-binding motif) with SCRIB; regulates TSHR trafficking and function. Subcellular Location: Cell membrane; Multi-pass membrane protein. Tissue Specificity: Expressed in the thyroid. DISEASE: Note=Defects in TSHR are found in patients affected byhyperthyroidism with different etiologies. Somatic, constitutivelyactivating TSHR mutations and/or constitutively activatingG(s)alpha mutations have been identified in toxic thyroid nodules (TTNs) that are the predominant cause of hyperthyroidism in iodinedeficient areas. These mutations lead to TSH independent activationof the cAMP cascade resulting in thyroid growth and hormoneproduction. TSHR mutations are found in autonomously functioning nodules (AFTN), toxic multinodular goiter (TMNG) and hyperfunctioning thyroid adenomas (HTA). TMNG encompasses a spectrum of different clinical entities, ranging from a single hyperfunctioning nodule within an enlarged thyroid, to multiple hyperfunctioning areas scattered throughout the gland. HTA are discrete encapsulated neoplasms characterized by TSH-independent autonomous growth, hypersecretion of thyroid hormones, and TSH suppression. Defects in TSHR are also a cause of thyroid neoplasms (papillary and follicular cancers). Note=Autoantibodies against TSHR are directly responsible for the pathogenesis and hyperthyroidism of Graves disease. Antibody interaction with TSHR results in an uncontrolled receptor stimulation. Hypothyroidism, congenital, non-goitrous, 1 (CHNG1) [MIM:275200]: A non-autoimmune condition characterized by resistance to thyroid-stimulating hormone (TSH) leading to increased levels of plasma TSH and low levels of thyroid hormone. It presents variable severity depending on the completeness of the defect. Most patients are euthyroid and asymptomatic, with a normal sized thyroid gland. Only a subset of patients develop hypothyroidism and present a hypoplastic thyroid gland. Note=The disease is caused by mutations affecting the gene represented in this entry. Familial gestational hyperthyroidism (HTFG) [MIM:603373]: A condition characterized by abnormally high levels of serum thyroid hormones occurring during early pregnancy. Note=The disease is caused by mutations affecting the gene represented in this entry. Hyperthyroidism, non-autoimmune (HTNA) [MIM:609152]: A condition characterized by abnormally high levels of serum thyroid hormones, thyroid hyperplasia, goiter and lack of anti-thyroid antibodies. Typical features of Graves disease such as exophthalmia, myxedema, antibodies anti-TSH receptor and lymphocytic infiltration of the thyroid gland are absent. Note=The disease is caused by mutations affecting the gene represented in this entry. Similarity: Belongs to the G-protein coupled receptor 1 family. FSH/LSH/TSH subfamily. Contains 7 LRR (leucine-rich) repeats. Database links: Entrez Gene: 7253 Human Omim: 603372 Human SwissProt: P16473 Human Unigene: 123078 Human Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. TSHR(Thyroid stimulating hormone receptor)是垂体前叶嗜碱细胞分泌的一种糖蛋白，直接作用于甲状腺，并能影响其结构功能。该抗体主要用于垂体肿瘤功能性分类的研究 |
糖蛋白受体家族由促黄体受体、促卵泡受体和促甲状腺（TSH）受体组成。从垂体中释放的TSH与甲状腺细胞上的TSH受体结合，以控制甲状腺的大小和功能（De Felice等）。2004）。TSH受体通过Gs信号上调甲状腺细胞内cAMP，调节碘摄取、甲状腺球蛋白（TG）、甲状腺过氧化物酶（TPO）和碘化钠转运体的转录。TSH受体还提示GQ和磷脂酶C调节碘排出物、H2O2生成和甲状腺球蛋白碘化。TSH受体自身免疫导致甲状腺功能亢进（Graves病）或甲状腺功能减退（Hashimoto thyroiditis），当自身抗体在TSH受体上分别起激动剂或拮抗剂作用时（拉波波特和克劳克兰，2001；戴维斯等人，2002）。Millipore克隆的人TSH受体表达细胞系是在Chem-10宿主中建立的，该细胞系在细胞表面支持高水平的重组TSH受体表达，并含有高水平的混杂G蛋白以将受体与钙信号途径结合。因此，细胞系是筛选TSH及其配体相互作用拮抗剂的理想工具。