protein

TSHR Immunizing Peptide

MBS427575

0.1 mg

190 USD

Blocking Peptide

TSHR Immunizing Peptide

[TSHR]

[TSHR; thyroid stimulating hormone receptor; CHNG1; LGR3; MGC75129; hTSHR-I; TSH-R; seven transmembrane helix receptor; thyroid-stimulating hormone receptor; thyrotropin receptor; thyrotropin receptor-I, hTSHR-I; TSHR (aa101-115)]

[thyrotropin receptor isoform 1; Thyrotropin receptor; thyrotropin receptor; thyroid stimulating hormone receptor; Thyroid-stimulating hormone receptor; TSH-R]

[TSHR]

[TSHR]

[TSHR; TSHR; LGR3; CHNG1; hTSHR-I; LGR3; TSH-R]

TSHR_HUMAN

Human, Cow

764

C-SKVTHIEIRNTRNLT

Shipped at ambient temperature, store at -20°C

The peptide was used in the production of Goat Anti-TSHR (aa101-115) Antibody. It is currently untested in blocking applications.

. Supplied As: 100 ug of Lyophilized peptide, formulation 5pmol/uL in 5% (v/v) acetonitrile/H2O.Reconstitute pellet in distilled water where required water where required. For blocking studies, reconstitute pellet in 200 uL distilled water to obtain a 0.5 mg/ml peptide solution.

64085121

NP_000360.2

NM_000369.2

Arf6 Signaling Events Pathway (138034); Arf6 Trafficking Events Pathway (137954); Autoimmune Thyroid Disease Pathway (83121); Autoimmune Thyroid Disease Pathway (533); Class A/1 (Rhodopsin-like Receptors) Pathway (1269545); G Alpha (s) Signalling Events Pathway (1269575); GPCR Downstream Signaling Pathway (1269574); GPCR Ligand Binding Pathway (1269544); Hormone Ligand-binding Receptors Pathway (1269559); Neuroactive Ligand-receptor Interaction Pathway (83053)

The protein encoded by this gene is a membrane protein and a major controller of thyroid cell metabolism. The encoded protein is a receptor for thyrothropin and thyrostimulin, and its activity is mediated by adenylate cyclase. Defects in this gene are a cause of several types of hyperthyroidism. Three transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Dec 2008]

TSHR: 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). Defects in TSHR are found in patients affected by hyperthyroidism with different etiologies. Somatic, constitutively activating TSHR mutations and/or constitutively activating G(s)alpha mutations have been identified in toxic thyroid nodules (TTNs) that are the predominant cause of hyperthyroidism in iodine deficient areas. These mutations lead to TSH independent activation of the cAMP cascade resulting in thyroid growth and hormone production. TSHR mutations are found in autonomously functioning thyroid 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). Autoantibodies against TSHR are directly responsible for the pathogenesis and hyperthyroidism of Graves disease. Antibody interaction with TSHR results in an uncontrolled receptor stimulation. Defects in TSHR are the cause of congenital hypothyroidism non-goitrous type 1 (CHNG1); also known as congenital hypothyroidism due to TSH resistance. CHNG1 is 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. CHNG1 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. Defects in TSHR are the cause of familial gestational hyperthyroidism (HTFG). HTFG is a condition characterized by abnormally high levels of serum thyroid hormones occurring during early pregnancy. Defects in TSHR are the cause of hyperthyroidism non- autoimmune (HTNA). It is 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. Belongs to the G-protein coupled receptor 1 family. FSH/LSH/TSH subfamily. 2 isoforms of the human protein are produced by alternative splicing. Protein type: Receptor, GPCR; GPCR, family 1; Membrane protein, integral; Membrane protein, multi-pass. Chromosomal Location of Human Ortholog: 14q31. Cellular Component: integral to plasma membrane; plasma membrane; receptor complex. Molecular Function: peptide receptor activity, G-protein coupled; protein binding; thyroid-stimulating hormone receptor activity. Biological Process: adenylate cyclase activation; cell-cell signaling; G-protein coupled receptor protein signaling pathway; G-protein signaling, adenylate cyclase activating pathway; G-protein signaling, coupled to cyclic nucleotide second messenger; hormone-mediated signaling; nervous system development; positive regulation of cell proliferation. Disease: Hyperthyroidism, Familial Gestational; Hyperthyroidism, Nonautoimmune; Hypothyroidism, Congenital, Nongoitrous, 1

0.1 mg

190 USD