Key features and details
- Rabbit polyclonal to TSH Receptor/TSH-R
- Suitable for: IHC-P, Flow Cyt
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
Product nameAnti-TSH Receptor/TSH-R antibody
See all TSH Receptor/TSH-R primary antibodies
DescriptionRabbit polyclonal to TSH Receptor/TSH-R
Tested applicationsSuitable for: IHC-P, Flow Cytmore details
Species reactivityReacts with: Mouse, Rat, Human
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.09% Sodium azide
Constituents: 0.01% BSA, 50% Glycerol
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab202960 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/100 - 1/500. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.
Use at 1/50 - 1/200 with fluorescent detection methods.
ab171870 - Rabbit polyclonal IgG, is suitable for use as an isotype control with this antibody.
FunctionReceptor 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).
Tissue specificityExpressed in the thyroid.
Involvement in diseaseDefects 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.
Hypothyroidism, congenital, non-goitrous, 1
Familial gestational hyperthyroidism
Sequence similaritiesBelongs to the G-protein coupled receptor 1 family. FSH/LSH/TSH subfamily.
Contains 7 LRR (leucine-rich) repeats.
Cellular localizationCell membrane.
- Information by UniProt
- CHNG1 antibody
- hTSHR I antibody
- hTSHRI antibody
Immunohistochemical analysis of formalin-fixed and paraffin embedded Mouse spleen tissue labeling TSH Receptor/TSH-R using ab202960 at 1/200 dilution, followed by conjugation to the secondary antibody and DAB staining.
Immunohistochemical analysis of formalin-fixed and paraffin-embedded Rat brain tissue labeling TSH Receptor/TSH-R using ab202960 at 1/200 dilution, followed by Goat Anti-Rabbit IgG, Cy3 conjugated secondary antibody at 1/200 dilution.
Flow Cytometry analysis of Mouse thymocytes labeling TSH Receptor/TSH-R using ab202960 at 1/100 dilution (green) followed by a FITC conjugated secondary compared to control cells (blue).
ab202960 has been referenced in 1 publication.
- Wang M et al. Periostin silencing suppresses the aggressive phenotype of thyroid carcinoma cells by suppressing the Akt/thyroid stimulating hormone receptor axis. Cytotechnology 70:275-284 (2018). PubMed: 28965266