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Validated All-in-One™ qPCR Primer for TGFBR2(NM_003242.5) Search again
Product ID:
HQP018054
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AAT3, FAA3, LDS1B, LDS2, LDS2B, MFS2, RIIC, TAAD2, TBR-ii, TBRII, TGFR-2, TGFbeta-RII, tbetaR-II
Gene Description:
transforming growth factor beta receptor 2
Target Gene Accession:
NM_003242.5(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
This gene encodes a member of the Ser/Thr protein kinase family and the TGFB receptor subfamily. The encoded protein is a transmembrane protein that has a protein kinase domain, forms a heterodimeric complex with another receptor protein, and binds TGF-beta. This receptor/ligand complex phosphorylates proteins, which then enter the nucleus and regulate the transcription of a subset of genes related to cell proliferation. Mutations in this gene have been associated with Marfan Syndrome, Loeys-Deitz Aortic Aneurysm Syndrome, and the development of various types of tumors.
Gene References into function
- Altogether, these results identify a mechanism by which RhoB antagonizes TGF-beta action through transcriptional down-regulation of AP1 in T beta R-II promoter.
- treatment with the HDAC inhibitor induces TbetaRII promoter activity by the recruitment of the PCAF protein to the NF-Y complex, interacting with the inverted CCAAT box in the TbetaRII promoter
- Overexpression of a dominant negatively acting mutant of TGFBR2 in primitive hemopoietic progenitor cells renders them transiently unresponsive to both autocrine and paracrine TGF-beta signaling and leads to their enhanced survival and proliferation.
- TGF beta type II 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 associated with an increase in the rate of gene transcription.
- crystal structure of the human TbetaR2 ectodomain--TGF-beta3 complex
- present in diabetic foot ulcer
- TGFBII receptors were purified and refolded; they have an apparent molecular weight of 14 kDa as by size-exclusion chromatography
- data suggest the existence of a further definite subgroup of diffuse-type gastric carcinomas with altered TGFbeta-IIR expression, independent from a mutator phenotype with TGFbeta-IIR gene mutations
- Differential rates of frameshift alterations in four repeat sequences of hereditary nonpolyposis colorectal cancer tumors.These repeats consisted of (A)10 in the TGF beta RII, (G)8 in the BAX, (A)8 in the CASP1, and (CCA)7 in the APP genes.
- Coding region microsatellite mutations characteristic of defective mismatch repair Identification of TGFbetaRII coding region microsatellite mutations in vivo implicates this gene in the pathogenesis of human T-LBL/ALL.
- This protein was expressed locally in the media and adeventitia at injected arterial segments without any significant dissemination to remote areas.
- TGF-beta2 receptor expression in peritoneal fibroblasts was increased by hypoxia or hypoxia plus TGF-beta1, but decreased by TGF-beta1 alone.
- The loss of TbetaR-II expression in the primary tumor is associated with clinical stage (P <0.01) and predicts a significantly lower survival rate in renal cell carcinoma patients.
- Human breast tumors were screened for TGFBR2 mutation and/or altered expression of TGFBR2 protein. TGFBR2 was expressed in the epithelium and stroma of tumors, and was higher in patients having positive lymph nodes and/or negative ER and PR expression.
- role of a CCAAT box and three GC boxes in the regulation of the TbetaR-II promoters in embryonal carcinoma-differentiated cells
- Transforming growth factor beta1 receptor II is downregulated by E1A in adenovirus-infected cells.
- We observed subsequent loss of type II TGFbeta receptor (TBR2) expression in metastatic renal cell carcinomas [RCC}. We propose that loss of TBR3 is necessary for RCC carcinogenesis, and loss of TBR2 leads to acquisition of a metastatic phenotype.
- ERT mediates the expression of TGF-beta RII, and the transcriptional inhibition of ets-related transcription factor could be a one of the mechanisms of colonic carcinogenesis
- TbetaRII in transgenic mice plays a critical role in maintaining the nondifferentiated character of virgin mammary gland epithelium.
- 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
- TGFBR2 has a role in progression of estrogen receptor-negative breast cancer
- each of the five Ets proteins influences the TbetaR-II promoter in a unique manner because of important differences in their biochemical properties or their patterns of cellular expression
- NMR analysis of the extracellular domain of the human TGFbeta type II receptor in complex with monomeric TGFbeta3
- 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
- an increased TGFbetaRI:TGFbetaRII ratio may underlie aberrant TGFbeta signaling in systemic sclerosis and contribute to elevated basal collagen production
- Our studies show that RDH12 is associated with retinal dystrophy and encodes an enzyme with a unique, nonredundant role in the photoreceptor cells.
- The first characterized nonepithelial tumors in hereditary nonpolyposis colorectal cancer seem to carry a limited panel of dna replication errors, including a frameshift at the TGFBR2 gene.
- thrombin via PAR1 induced the internalization of endoglin and type-II TGF-beta receptor (TbetaRII) but not type-I receptors in human ECs
- transforming growth factor beta type II receptor promoter activity and acetylation of Sp1 by recruitment of PCAF/p300 to a Sp1.NF-Y complex are induced by Trichostatin A
- possible role of heterozygous mutation in a newly described human phenotype that includes widespread perturbations in cardiovascular, craniofacial, neurocognitive and skeletal development
- UV-induced down-regulation of TbetaRII and the concerted over-expression of Smad7 may trigger the inhibition of the TGF-beta-induced phosphorylation of Smad2.
- Identification of TGFBR2 mutations in Marfan syndrome type II provided the direct evidence of the relation in humans.
- blockade of TGF-beta after intramuscular transfer of the soluble type II TGF-beta receptor gene suppressed hepatic fibrosis
- Repression of type II TGF-beta receptor may act as significant determinant of lung adenocarcinoma invasiveness, an early step in tumor progression toward metastasis.
- TGFBR2 mutations is associated with deregulation of cdk4 and colon cancer
- Identification of a novel TGFBR2 gene mutation in a Korean patient with Loeys-Dietz aortic aneurysm syndrome; no mutation in TGFBR2 gene in 30 patients with classic Marfan's syndrome.
- prostate cancer cells mediate growth inhibition and differentiation of bone marrow endothelial cells through alteration of TGFbetaRII-mediated signal transduction.
- changes in TbetaRII levels by EGF are EGF receptor-kinase-dependent and are controlled by signals downstream of MEK1/2
- Down-regulation of TbetaRII in dermal cells or up-regulation of TbetaRII in epidermal cells reverses their migratory responses to serum and plasma, respectively.
- reduced transforming growth factor-beta type II receptor expression may play a critical role in determining the malignant phenotype of human adrenocortical carcinoma
- levels of TGFbeta-1 and TGFbeta R-2 were increased in the intimal matrices, smooth muscle cells, and macrophages, as well as in endothelial cells of atherosclerotic aorta
- Signaling through Tgfbr2 regulates the maintenance of boundaries in the sclerotome and developing axial skeleton in transgenic mice.
- A comprehensive genetic analysis of TGFBR2 was performed in patients with Marfan syndrome or Marfan-related phenotypes.
- Mice transgenic for directed expression of a dominant negative TGF beta receptor type II, under the CD4 promoter lacking the CD8 silencer, spontaneously develop features characteristic of primary biliary cirrhosis.
- Results from this family provides further evidence that mutations in TGFbetaR2 cause a distinct syndrome.
- Mutations in either TGFBR1 or TGFBR2 predispose patients to aggressive and widespread vascular disease (Loeys-Dietz syndrome)
- The human TbetaRII overexpressed in highly malignant K-ras-transformed thyroid cell clones is a functional receptor essential for a strong reduction of adhesive & migratory behaviour of these cells.
- epidermal growth factor (EGF)-mediated induction of TbetaRII expression may participate in a synergistic interplay between EGF and TGF-beta signaling pathway
- TGF-beta RII was not upregulated in cyclosporine-induced gingival growth in patients after kidney transplantation.
- Mutated TGFBR2 seems to play an important role in the abrogation of transforming growth factor beta signal transduction in giant cell carcinoma cells.
- mutations of the amino-acid residues, D55 and E142 of TbetaR-II, resulted in loss of TGF-beta binding and downstream signaling activity
- The variant alleles of the promoter polymorphisms, TGFB1 C-509T and TGFBR2 G-875A, were associated with a significantly decreased risk of gastric cancer.
- These results also indicate that the CSF level assay of TGF-beta1, TbetaR-II and LRG is useful for the diagnosis of patients with INPH, and TGF-beta1, TbetaR-II and LRG may be involved in the pathogenesis of the disease.
- TGFBR2 mutation is associated with CpG island methylator phenotype-high colorectal cancer and indirectly with RUNX3 methylation
- common variants in TGFBR2 gene do not strongly influence genetic susceptibility to diabetic nephropathy in an Irish Caucasian population.
- Genetic testing revealed in patient with diffuse and rapidly progressing vascular disease a de novo mutation in transforming growth factor receptor 2.
- data suggest that promoter methylation plays an important role in T beta RII gene silencing and subsequent development of a TGF-beta1-resistant phenotype by some B-cell lymphoma cells
- TGF-beta receptor type II and its mRNA were found in platelets.
- High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC.
- This review of 5 cases describes patients with musculoskeletal abnormalities and a TGFBR2 mutation in the neonatal period who are subsequently diagnosed with Loeys-Dietz syndrome.
- TGFBR2 gene is reported to be linked to schizophrenia.
- the defective TGFBR2 expression might contribute to the carcinogenesis and/or development of large cell carcinoma
- Sequential cytoplasmic truncations resulted in receptor missorting to apical surfaces, and they indicated an essential targeting element(s) near the receptor's C terminus.
- TGF-beta signaling in reactive stroma is angiogenic and tumor promoting and is mediated in part through a TbetaRII/Smad3-dependent upregulation of FGF-2 expression and release.
- mutations in the TGFBR1,2 gene may be associated with greater phenotypic heterogeneity than previously reported
- RANTES signaling is required for invasion in TGFbetaRII-deficient neoplastic cells.
- Alterations in TGF-betaRII, BAX, IGFIIR, caspase-5, hMSH3 and hMSH6 genes of microsatellite instability are rare in urinary bladder carcinoma and they are not associated with microsatellite instability or the presence of p53 mutations.
- it was observed the progression of premalignant lung lesions toward carcinoma in situ is accompanied by a decrease in TBR II expression and apoptosis and an increase in the expression of Ki-67 and MC
- genetic variants in transforming growth factor beta receptor II may modulate the risk of esophageal squamous cell carcinoma
- TGF-beta receptor 2 downregulation in tumor-associated stroma is associated with colon carcinoma
- 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.
- Mutant p53 attenuates TGF-beta1 signaling. This was exhibited by a reduction in SMAD2/3 phosphorylation and an inhibition of both the formation of SMAD2/SMAD4 complexes and the translocation of SMAD4 to the cell nucleus.
- Mutations at the mononucleotide repeats within the TGF-betaRII gene occurred in certain basal cell carcinomas, not always in association with microsatellite instability .
- Both genomic instability and clonal selection of transforming growth factor beta resistant cells contribute to the high frequency of TGFBR2 mutations in microsatellite unstable colon cancer.
- TGFbeta2 and TbetaRII have roles in the antiestrogenic activity of tamoxifen metabolites in breast cancer
- IL-1beta decreases TbetaRII expression by inducing Sp3 via NFkappaB
- Molecular genetic analysis demonstrated a heterozygous missense mutation of the transforming growth factor-beta receptor II gene in both the patient and his father, which thus caused Loeys-Dietz syndrome.
- 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].
- KSHV evades both the antiproliferative effects of TGF-beta signaling by silencing TbetaRII gene expression and immune recognition by suppressing TGF-beta-responsive immune cells through the elevated secretion of TGF-beta1
- TGF-beta1, TbetaRI, and TbetaRII loss of expression correlates with differentiation in human oral squamous cell carcinomas
- TGF-beta complexes assemble cooperatively through recruitment of the low-affinity (type I) receptor by the ligand-bound high-affinity (type II) pair.
- TGFBR2 mutations are not a major factor in spontaneous spinal CSF leaks.
- Filtering bleb scarring is associated with an abundant expression of TGF-beta receptors in activated fibroblasts and the deposition of the fibrogenic ED-A fibronectin splice-variant.
- Cancer-associated missense mutations of the T beta RII gene (TGFBR2) are associated with at least two different phenotypes.
- The exogenous tTGFbetaRII can efficiently trap TGF-beta I from access to wild-type receptors and can suppress TGF-beta I triggered signals. Thus it may potentially be clinically applied to scar therapy.
- Mesenchymal stem cells from patients with osteoarthritis showed significantly increased total TGF-beta, TGF-beta1 isoform, TBR-II, and TBR-III mRNA expression compared to controls.
- mature human M2 macrophages made permissive to TGF-beta by glucocorticoid-induced surface expression of TGF-betaRII activate in response to TGF-beta1
- A significant elevation in expression of TGFBR2 in oral squamous cell carcinoma cells was seen in carbon and neon-irradiated cells.
- 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
- The roles played by the ecto/transmembrane (ecto/TM) domains and endodomains of RI and RII TGF-beta receptors in these processes by transfecting 293 or HeLa cells with different combinations of receptor mutants, was analysed.
- Mutations in TGFBR1 and TGFBR2 rarely cause sporadic BAV.
- the frequent loss of stromal TGF-beta type II receptor expression in prostate cancer can relieve the paracrine suppression of Wnt3a expression
- Mutations and polymorphisms in TGFBR1 and TGFBR2 in patients with Marfan syndrome, Loeys-Dietz syndrome and related disorders are described.
- DHT decreases the level of TGF-beta receptor II (TbetaRII) through a transcriptional mechanism.
- The -1 bp frameshift mutation rates of TGFBR2 and ACVR2 microsatellite sequences are dependent upon the human DNA Mismatch repair background
- report of somatic mosaicism of a TGFBR2 missense mutation, c.1336G>A (D446N)in a patient with Loeys-Dietz syndrome; DNA from leukocytes, buccal cells, hair root cells, & nails in the father indicated 52%, 25%, 0%, & 35% of cells harbored the mutation
- sTbetaRII attenuates the biological activities of TGF-beta in colorectal cancer