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Validated All-in-One™ qPCR Primer for TGFBR1(NM_004612.3) Search again
Product ID:
HQP110590
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AAT5, ACVRLK4, ALK-5, ALK5, ESS1, LDS1, LDS1A, LDS2A, MSSE, SKR4, TBR-i, TBRI, TGFR-1, tbetaR-I
Gene Description:
transforming growth factor beta receptor 1
Target Gene Accession:
NM_004612.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene forms a heteromeric complex with type II TGF-beta receptors when bound to TGF-beta, transducing the TGF-beta signal from the cell surface to the cytoplasm. The encoded protein is a serine/threonine protein kinase. Mutations in this gene have been associated with Loeys-Dietz aortic aneurysm syndrome (LDAS). Multiple transcript variants encoding different isoforms have been found for this gene.
Gene References into function
- TGF beta type I receptor mRNA concentration on the surface of human osteoblasts is increased by 1 alpha,25-dihydroxyvitamin D3 due to changes in receptor mRNA stability not associaed with an increase in the rate of gene transcription.
- present in diabetic foot ulcer
- Hypertrophic maturation of chondrocytes in induced by the TGF-beta type I receptors.
- CD44 interaction with the TGF-betaRI kinase promotes activation of multiple signaling pathways required for ankyrin-membrane interaction, tumor cell migration, and oncogenic events during HA and TGF-beta-mediated metastatic breast tumor progression
- elucidation of smad requirement in transforming growth factor-beta type I receptor-induced responses
- TGF-beta1 receptor expression in peritoneal fibroblasts was increased by hypoxia or hypoxia plus TGF-beta1, but decreased by TGF-beta1 alone.
- a C-to-T single-nucleotide polymorphism (C-509T) in the TGF-beta1 gene promoter may be associated with altered gene expression and asthma phenotype
- expression values for TGF 1 and its receptors I, II, and III were twice as high in the group of patients with a diagnosis of high-grade lymphomas as in the group of patients diagnosed with low-grade lymphomas
- Blocking Smad7 expression by RNA interference inhibits association of GADD34-PP1c complex with TbetaRI.
- combined production of the immunosuppressants IL-10 and TGF-beta, as well as coexpression of TGF-beta RI and RII (required for cellular response to TGF-beta), may act to down-modulate host anti-Mycobacterium tuberculosis immunity
- that an increased TGFbetaRI:TGFbetaRII ratio may underlie aberrant TGFbeta signaling in SSc and contribute to elevated basal collagen production
- transforming growth factor-beta signaling has a role in receptor RI induction by histone deacetylase activity inhibition in breast cancer cells
- endogenous IGFBP-3 directly inhibits proliferation of human intestinal smooth muscle cells by activation of TGF-betaRI and Smad2, an effect that is independent of its effect on IGF-I-stimulated growth.
- sphingosine 1-phosphate receptors and the transforming growth factor beta-type I receptor serine/threonine kinase are essential for activation of Smad3 by lysophospholipids
- Mutation in the TGFBR1 gene is associated with carcinomas of the kidney and bladder
- Dpr2 binds to the TGFbeta receptors ALK5 and ALK4, and accelerates lysosomal degradation of these receptors
- NEDD4-2 functions like Smurfs 1 and 2 in that it associates with TGF-beta type I receptor via Smad7, and induces its ubiquitin-dependent degradation
- Bikunin neither decreased expression of TGF-beta receptors (TbetaRI and TbetaRII) in cancer cells nor altered the specific binding of 125I TGF-beta1 to the cells.
- TGF-beta induces biglycan expression through ALK5 and GADD45beta
- Genetic alterations reflecting mismatch repair of TGFBR1 gene do not occur in small bowel carcinoid tumors.
- IL-6 increases trafficking of TGF-beta1 receptors to non-lipid raft-associated pools resulting in augmented TGF-beta1 Smad signaling
- possible role of heterozygous mutation in a newly described human phenotype that includes widespread perturbations in cardiovascular, craniofacial, neurocognitive and skeletal development
- the Int7G24A variant of the TGFBR1 gene predisposes to small cell lung cancer risk (meta-analysis)
- Pituitary cells, which demonstrate reduced expression of dopamine beta2 receptor, also show reduction of TGFbeta1 type I receptor.
- TGFbeta1/ALK5 may alleviate scarring in chronic fibrotic disease.
- HCV NS5A modulates TGF-beta signaling through interaction with TbetaR-I
- Int7G24A variant of transforming growth factor-beta receptor type I is associated with invasive breast cancer
- ALK5 plays unique, non-redundant cell-autonomous roles during facial development in K14-Cre transgenic mice.
- A comprehensive genetic analysis of TGFBR1 was performed in patients with Marfan syndrome or Marfan-related phenotypes.
- TGF-beta type I receptor kinase has a role in progression of growth and metastasis of mouse mammary carcinoma
- Mutations in either TGFBR1 or TGFBR2 predispose patients to aggressive and widespread vascular disease (Loeys-Dietz syndrome)
- The majority of systemic sclerosis (SSc) fibroblasts exhibit elevated levels of transforming growth factor beta type I receptor (TGFbetaRI).
- Synthesis of TGFbeta-1 and type I TGFbeta-receptor increases over time in recipients developing chronic allograft nephropathy.
- The mRNA expressions of TGFbeta receptor type I (TGFbetaRI) in hMSCs increased with the length of cell culture.
- Enhances tumor invasion and angiogenesis by stimulating expression of matrix metalloproteinase MMP-9.
- Epac1 inhibits TGFbeta-dependent regulation of cell migration and adhesion through TbetaRI
- a distinct BMP and TGFbeta-receptor repertoire may explain the reduced chondrogenic capacity of adipose tissue stromal cells in vitro
- common variants in TGFBR1 gene do not strongly influence genetic susceptibility to diabetic nephropathy in an Irish Caucasian population.
- mRNA codifying for TbetaRI was found in platelets.
- Our analysis definitely excludes the possibility of the TGFBR1*6A allele increasing the risk of colorectal neoplasia in our sample population.
- data provide limited support for the hypothesis that sequence variation in TGFBR1 defined by the TGFBR1*6A allele confers an elevated risk of colorectal cancer
- no evidence to support the hypothesis that TGFBR1*6A is associated with lung cancer.
- mutations in the TGFBR1,2 gene may be associated with greater phenotypic heterogeneity than previously reported
- ALK5-dependent Smad3 signaling is the responsible pathway inducing CTGF expression.
- 4 new variants of T beta RI in malignant effusion tumor cells identified; characterization of 2 elements controlling its stability & transcriptional activation; expression of one variant bestowed cancer cells with growth advantage in presence of TGFbeta
- The identification of the splice variants T beta RIB and the novel isoform T beta RIIC in man clearly contributes to the growing complexity of the TGF-beta family.
- the TGFBR1(*)6A variant may be associated with an increased risk of low-risk familial breast cancer and might be a marker for poorly differentiated breast cancer.
- Somatic acquisition of TGFBR1*6A by epithelial and stromal cells during head and neck and colon cancer development.
- Pronounced changes in the expression and localization of the TGF-beta receptors Tgfbr1 were noted as mouse lungs progressed through the canalicular, saccular, and alveolar stages of development.
- The aim of this study was to analyse the profile of TGF-beta1 and the expression of its receptor (TbetaR I, TbetaR II and TbetaR III-betaglycan) genes in IPAH and in secondary forms of pulmonary arterial hypertension [Eisenmenger's syndrome patients].
- TGF-beta-mediated activation of the ALK5-Smad 3 pathway plays a role in SHH promoted motility and invasiveness of gastric cancer cells
- TGF-beta1, TbetaRI, and TbetaRII loss of expression correlates with differentiation in human oral squamous cell carcinomas
- TGF-beta mediates its effects on proteoglycan synthesis in VSMCs via the ALK5/Smad2/3 phosphorylation pathway as well as via the p38 MAP kinase signaling cascade.
- TGF-beta complexes assemble cooperatively through recruitment of the low-affinity (type I) receptor by the ligand-bound high-affinity (type II) pair.
- A direct effect of TGF-beta signaling via ALK5 on the regulation of TNF-alpha synthesis in macrophages
- TGFBR1*6A may contribute to cancer progression through RhoA activation in a TGF-beta signaling-independent manner
- both ALK1 and ALK5 are needed for TGF-beta-induced phosphorylation of intracellular mediators Smad1/5, whereas only ALK5 is essential for TGF-beta1-induced phosphorylation of Smad3
- reduced TGF beta R1 expression could contribute to the development of malignant phenotype of non-small cell lung cancer
- Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5.
- T beta RI sumoylation controls responsiveness to TGF-beta, with implications for tumour progression
- TGF-beta receptor I kinase has a role in the pathobiology of ineffective hematopoiesis
- MT1-MMP-dependent TGFbeta signaling through Alk5 is also required for PGE(2)-induced endothelial cord formation in vitro, and Alk5 kinase activity is required for PGE(2)-induced neovascularization in vivo.
- The high expression of genes coding TGFbetaRI, TGF-betaRII and TGF-betaRIII receptors in all the polyps and healthy tissues, show readiness to transduction of TGFbeta
- study showed that germline allele-specific expression(ASE)of the TGFBR1 gene is a quantitative trait occuring in 10 to 20% of colorectal cancer (CRC) patients & 1 to 3% of controls; estimates suggest ASE confers a substantially increased risk of CRC
- Mutations in TGFBR1 and TGFBR2 rarely cause sporadic BAV.
- TGF-beta specifically activates TAK1 through interaction of TbetaRI with TRAF6, whereas activation of Smad2 is not dependent on TRAF6.
- 177 colorectal cancer patients were genotyped for either the major form of the TGFBR1 receptor gene, homozygous for an internal segment of 9 alanines (9A/9A), or the lesser form, heterozygous for the polymorphism containing 6 alanines (9A/6A).
- Mutations and polymorphisms in TGFBR1 and TGFBR2 in patients with Marfan syndrome, Loeys-Dietz syndrome and related disorders are described.
- Behcets disease cases had lower incidence of TGFBR1(transforming growth factor beta receptor 1) *6A polymorphism compared with controls
- 7 different common variants in TGFB1 and TGFBR1 were not associated with an increased risk of bladder cancer
- analysis of genetic polymorphisms of transforming growth factor-beta1 and its receptors and colorectal cancer susceptibility
- these data are consistent with a role for the activin receptor-like kinase 5 in the progression of idiopathic pulmonary arterial hypertension