TSHR sirna

TSHR siRNA (Rat)

Cat. Num. AAA8236230

• Gene Names: Tshr; TSHRA
• Reactivity: Rat
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: TSHR; TSHR siRNA (Rat); Thyrotropin receptor; Thyroid-stimulating hormone receptor; TSH-R; TSHR sirna

• Host: Synthetic
• Reactivity: Rat
• Specificity: TSHR siRNA (Rat) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 764

• Applicable Applications for TSHR sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of rat TSHR gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for TSHR sirna

siRNA to inhibit TSHR expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 6981680
• NCBI GeneID: 25360
• NCBI Accession #: NP_037020.1
• NCBI GenBank Nucleotide #: NM_012888.1
• UniProt Accession #: P21463
• Molecular Weight: 86,475 Da
• NCBI Official Full Name: thyrotropin receptor
• NCBI Official Synonym Full Names: thyroid stimulating hormone receptor
• NCBI Official Symbol: Tshr
• NCBI Official Synonym Symbols: TSHRA
• NCBI Protein Information: thyrotropin receptor
• UniProt Protein Name: Thyrotropin receptor
• Protein Family: Thyrotropin receptor
• UniProt Gene Name: Tshr
• UniProt Synonym Gene Names: TSH-R
• UniProt Entry Name: TSHR_RAT

NCBI Description

acts as a G-protein coupled receptor for thyroid-stimulating hormone; induces increased cAMP levels [RGD, Feb 2006]

Uniprot Description

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: Membrane protein, multi-pass; Membrane protein, integral; Receptor, GPCR; GPCR, family 1

Cellular Component: plasma membrane; integral to membrane; receptor complex; lipid raft

Molecular Function: thyroid-stimulating hormone receptor activity

Biological Process: regulation of locomotion; inner ear receptor stereocilium organization and biogenesis; adult locomotory behavior; inner ear receptor cell development; B cell differentiation; positive regulation of cell proliferation; positive regulation of multicellular organism growth; G-protein signaling, adenylate cyclase activating pathway