Key features and details
- Mouse monoclonal [4C1] to TSH Receptor/TSH-R
- Suitable for: IP, Flow Cyt, IHC-Fr, WB, IHC-P
- Reacts with: Human
- Isotype: IgG2a
Product nameAnti-TSH Receptor/TSH-R antibody [4C1]
See all TSH Receptor/TSH-R primary antibodies
DescriptionMouse monoclonal [4C1] to TSH Receptor/TSH-R
SpecificityAb27974 recognises TSH receptor/TSH-R.
Tested applicationsSuitable for: IP, Flow Cyt, IHC-Fr, WB, IHC-Pmore details
Unsuitable for: ELISA
Species reactivityReacts with: Human
Synthetic peptide corresponding to Human TSH Receptor/TSH-R. Specific to the external domain.
EpitopeAb27974 reacts with an epitope located in the extracellular region of TSH receptor.
- Human Thyroid gland.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term.
Storage bufferpH: 7.40
Preservative: 0.09% Sodium azide
Concentration information loading...
PurityProtein G purified
Purification notesAb27974 was purified by affinity chromatography, from tissue culture supernatant.
Our Abpromise guarantee covers the use of ab27974 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IP||Use at an assay dependent concentration.|
|Flow Cyt||1/100 - 1/1000.
Use 10µl of the suggested working dilution for 106 cells.
ab170191 - Mouse monoclonal IgG2a, is suitable for use as an isotype control with this antibody.
|IHC-Fr||Use at an assay dependent concentration.|
|WB||1/1000. Predicted molecular weight: 87 kDa.|
|IHC-P||Use at an assay dependent concentration. Antigen retrieval is not required.|
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
ab27974 has been referenced in 5 publications.
- Mather Q et al. A novel protein expression signature differentiates benign lipomas from well-differentiated liposarcomas. Mol Clin Oncol 7:315-321 (2017). PubMed: 28781809
- Liu T et al. Downregulated expression of TSHR is associated with distant metastasis in thyroid cancer. Oncol Lett 14:7506-7512 (2017). PubMed: 29344196
- Pu J et al. Isolated double adrenocorticotropic hormone-secreting pituitary adenomas: A case report and review of the literature. Oncol Lett 12:585-590 (2016). IHC-P ; Human . PubMed: 27347184
- Guest PC et al. Proteomic analysis of the maternal protein restriction rat model for schizophrenia: identification of translational changes in hormonal signaling pathways and glutamate neurotransmission. Proteomics 12:3580-9 (2012). PubMed: 23071080
- Romagnani P et al. Expression of IP-10/CXCL10 and MIG/CXCL9 in the thyroid and increased levels of IP-10/CXCL10 in the serum of patients with recent-onset Graves' disease. Am J Pathol 161:195-206 (2002). PubMed: 12107104