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Validated All-in-One™ qPCR Primer for SMAD7(NM_005904.3) Search again
Product ID:
HQP010966
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CRCS3, MADH7, MADH8
Gene Description:
SMAD family member 7
Target Gene Accession:
NM_005904.3(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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Gene References into function
- results suggest that alterations in the Smad pathway, including marked Smad7 deficiency and Smad3 up-regulation, may be responsible for TGF-beta hyperresponsiveness observed in scleroderma
- plasma membrane localization of Smad7 by Smurf1 requires the C2 domain of Smurf1 and is essential for the inhibitory effect of Smad7 in the transforming growth factor-beta signaling pathway
- Smad7 is activated in injured podocytes in vitro and in human glomerular disease and participates in negative control of TGF-beta/Smad signaling in addition to its pro-apoptotic activity.
- Smad6 and Smad7 regulate thrombomodulin-dependent activation of protein C
- CRM1-dependent nuclear export of Smurf1 is essential for the negative regulation of TGF-beta signaling by Smad7.
- Smad7 may act as a scaffolding protein and facilitate TAK1- and MKK3-mediated activation of p38
- attenuation of transforming growth factor-beta signaling by activating Smad7 transcription may proceed not only through TGF-beta receptor-regulated Smad proteins but also an independent pathway involving transcription factor ER81 and TAK1 protein kinase
- Smad7 was overexpressed in ARO anaplastic cell line, the most malignant follicular thyroid carcinoma.
- endometrium, stromal cells and epithelial cells express Smad3, -4, and -7 mRNA and protein
- GADD34-PP1c recruited by Smad7 inhibits TGFbeta-induced cell cycle arrest.
- Smad7 and Smurf1 have roles in regulation of TGF-beta signaling in scleroderma fibroblasts
- In Helicobacter pylori-infected gastric mucosa, interferon-gamma induces expression of Smad7, which then prevents endogenous TGF-beta 1 from down-regulating ongoing tissue-damaging Th1 response.
- Jab1/CSN5 as an adapter that targets Smad7 for degradation, thus releasing Smad7-mediated suppression of TGF-beta1 signaling.
- Overexpression of SMAD7 inhibited the activity of the proliferation-specific promoters for the keratin 14 and cdc2 genes and reduced the expression of the mRNA for the proliferation-specific genes cdc2 and E2F1.
- tetradecanoylphorbol-13-acetate down-regulates Smad6 expression presumably via PKCmu-ERK-dependent pathway and up-regulates Smad7 expression via PKCmu-dependent mechanism(s) which need no MAPK and NF-kappaB activation
- Enhanced expression of the TGF-beta signaling inhibitor Smad7 may present one of the novel mechanisms of TGF-beta resistance in human gastric carcinomas.
- novel role for Smad7 in TGF-beta-dependent activation of Rho GTPases
- Smad7 is repressed by ski
- dual signaling pathways involving TGF-beta1, an antiapoptotic pathway mediated by the Smad pathway involving p21, and an apoptosis-permissive pathway mediated in part by p38 MAPK.
- WWP1 negatively regulates TGF-beta signaling in cooperation with Smad7.
- identified target genes regulated by Smad7 in primitive hematopoietic cells that may control process of modulating the cell fate decisions of primary multipotent human repopulating cells
- The regulation in chondrocytes of Smad6 and Smad7 expression by IL-1beta suggests a potentially important role of IL-1beta signaling in chondrocytes, via indirect influencing of the bone morphogenetic protein/TGFbeta signaling cascade.
- induction of Smad7 gene expression by UV irradiation is mediated via induction of the transcription factor AP-1 in human skin fibroblasts
- Abeta1-42 may play an important role in the negative regulation of TGF-beta1-induced MMP-2 production via Smad7 expression
- Smad7 appears to be upregulated in endometrial cancers compared to normal endometrium.
- Physical association of Smad7 and beta-catenin was found to be important for TGF-beta-induced apoptosis.
- expression of Smad7 is crucial for 2-ME-induced apoptosis in human prostate cancer cells
- Smad6 and Smad7 expression affects the progression of early lesions of esophageal SCC and indicates a poor prognosis.
- autocrine TGF-beta/Smad signaling is involved in contractility and matrix gene expression of fibroblasts from normal and hypertrophic scars; Smad7 inhibits these processes and may exert beneficial effects on excessive scar formation
- 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.
- Smad7 acts to functionally inactivate RB and de-repress E2F without blocking the activation of TbetaRI and the nuclear translocation of Smad2/3, allowing TGF-beta1 to exert effects in a cancer cell that is resistant to TGF-beta1-mediated growth inhibitio
- the degradation of Smad7 is regulated by the balance between acetylation, deacetylation and ubiquitination
- In mature human B cells, BMP-6 inhibited cell growth, and rapidly induced phosphorylation of Smad8.
- SMAD7 induces tumorigenicity by blocking TGF-beta-induced growth inhibition and apoptosis.
- Various cellular functions implicated in melanoma development may be under control of autocrine TGF-beta and may be inhibited by Smad7 expression
- TGF-beta1 and bleomycin intracellular signaling through autocrine regulation of Smad 3 binding to the proximal promoter of the Smad 7 gene
- TGF-beta is involved in the physiological loss of gastric epithelial cells by activating apoptosis mediated by Smad7, Bim, and caspase-9
- Smad7 is not transcriptionally regulated in gut but its increase in inflammatory bowel disease is due to posttranscriptional acetylation and stabilization by p300, which prevents Smad7 ubiquitination and degradation in the proteasome
- TGFbeta-mediated phosphorylation of IkappaB-alpha and NF-kappaB nuclear translocation and DNA binding activity are inhibited by Smad7
- SnoN also seems to regulate negatively the TGF-beta-responsive smad7 gene by binding and repressing its promoter in a similar way to Ski
- Axin and Arkadia cooperate with each other in promoting Smad7 ubiquitination.
- analysis of the WW domain recognition motif for the interaction of Smad7 and the E3 ubiquitin ligase Smurf2
- TGFbeta rapidly induces nuclear translocation of Smad proteins and subsequently stimulates Smad-Sp1 complex formation which increases Sp1 binding to promoter boxes in a pancreatic cancer cell line.
- results suggest that inhibition of cell growth by activin is regulated by the negative feedback effect of Smad7 on the activin signaling pathway, and is mediated through p21(CIP1/WAF1) activation in SNU-16 cells
- These findings indicate a new inhibitory function of FKBP12 as an adaptor molecule for the Smad7-Smurf1 complex to regulate the duration of the activin signal through activin type I receptors.
- UVA1 phototherapy demonstrated the alteration of SMAD7 gene expression in localized scleroderma, as SMAD7 mRNA levels normalized after UVA1. The pathogenetic relevance of SMAD7 levels with respect to clinical improvement needs further investigation.
- Smad7 plays a crucial role upstream of ATM and p53 to protect the genome from insults evoked by extracellular stress.
- Smad7 appears to be important in colonic inflammation.
- Stable overexpression of Smad7 in human melanoma cells impairs bone metastasis.
- Smad7 expression was upregulated by IL-10 plus either IL-5 or GM-CSF. IL-10 inhibited the expression of TGF-beta-inducible early gene, which is known to downregulate Smad7 expression.
- SMAD7 antagonizes TGFB1 signaling in the nucleus by interfering with functional Smad-DNA complex formation.
- Arkadia induces degradation of SnoN and c-Ski in addition to Smad7.
- Smad7 overexpression in cultured hepatocytes abrogated TGF-beta-dependent and intrinsic CTGF expression.
- In this review, Smad7 inhibits the signaling response to transforming growth factor (TGF)-beta by a variety of mechanisms associated with peritoneal membrane failure during chronic peritoneal dialysis.
- the up-regulation of TCF11/MafG binding could be suppressed by overexpression of the TGF-beta inhibitor Smad7, and a small interfering RNA to TCF11 blocked the suppression of iNOS by TGF-beta.
- Gene variants may weakly contribute to a particular genetic background that increases the susceptibility to development of type 2 diabetes.
- Single nucleotide polymorphism in SMAD7 is associated with colorectal cancer
- high levels of Smad7 interferes with TGF-beta/activin-induced Smad/MAPK signaling and erythro-differentiation and promotes megakaryocytic differentiation, possibly by blocking autocrine TGF-beta.
- up-regulation of Smad7 by IL-1beta is mediated through the NF-kappaB pathway, especially the p65 subunit in chondrocytes
- variation at SMAD7 does not significantly contribute to an inherited susceptibility to CLL
- A case-control study in Afro-Caribbeans found SMAD7 SNPs were not strongly associated with increased risk of developing keloids.
- rather than being translocated to the nucleus for regulating the target gene transcription, Smad7-stabilized-beta-catenin is shunted to the E-cadherin complex to modulate cell-cell adhesion.
- The level of Smad7 is modulated by its physical interaction with Hic-5 and targeted to a degradation pathway not likely to be proteasomal