|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for SMAD3(NM_005902.3) Search again
Product ID:
HQP010960
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HSPC193, HsT17436, JV15-2, LDS1C, LDS3, MADH3, hMAD-3, hSMAD3, mad3
Gene Description:
SMAD family member 3
Target Gene Accession:
NM_005902.3(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:
|
|
| A | B |
|
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. |
|
Gene References into function
- repression of transactivating activity by association with a novel splice variant of CCAAT-binding factor C subunit
- HTLV-1 tax represses Smad-mediated TGF-beta signaling.
- Smad3 trimerization, induced by phosphorylation, activates the TGF-beta signal by driving Smad3 dissociation from SARA & sets up the negative feedback mechanism by Ski.
- Data suggest that SMAD3 interactions with the positive regulators NKX2.1 and HNF-3 underlie the molecular basis for TGF-beta-induced repression of surfactant protein B gene transcription.
- Smad3 is unlikely to function as a classical tumor suppressor gene in the pathogenesis of sporadic parathyroid or enteropancreatic endocrine tumors.
- Nucleocytoplasmic shuttling of Smads 2, 3, and 4 permits sensing of TGF-beta receptor activity.
- interactions between AR, Smad3, and Smad4 may result in the differential regulation of the AR transactivation, which further strengthens their roles in the prostate cancer progression
- adenovirally-expressed Smad3 augmented the TGF-beta-elicited induction of MMP-13 expression
- Levels of phosphorylated Smad2/3 are sensors of the interplay between effects of retinoic acid and TGF-beta or vitamin D3 on monocytic and granulocytic differentiation of HL-60 cells.
- HTLV1 Tax inhibits TGF-beta1 signaling by reducing the Smad3 DNA binding activity
- autocrine regulation of TGF-beta2 production in endothelial cell hypoxia may involve cross-talk between Smad3 and hypoxia inducible factor-1alpha signaling pathways
- Phenotypic and functional changes associated with TGF-beta1-induced fibroblast terminal differentiation are differentially regulated by Smad2, Smad3, and Smad4.
- TGF-beta1 inhibited IFN-gamma and TNF-alpha-induced TARC production in HaCaT cells via Smad2/3. Modulation of TGF-beta/Smad signaling pathway may be beneficial for treatment of atopic dermatitis.
- In SMAD4-negative cell lines, TGF-beta caused Smad3 to move to the nucleus in a Smad4-independent fashion. Nuclear translocation of Smad3 was not sufficient to activate reporters for TGF-beta-induced transcriptional responses.
- Results suggest that the transcriptional cross talk between the TGFbeta-regulated Smads 3 and 4 and hepatocyte nuclear factor-4 is mediated by specific functional domains in the two types of transcription factors.
- stimulates basal and Tat-mediated transcription of MCP-1 in human astrocytic cells
- Mediation of tumor growth factor beta-1 induced collagen I expression in glomerular mesangial cells.
- Down-regulation of Smad 3 expression by TGF-beta(1) at later stage is involved in negative modulation of TGF-beta(1) signaling.
- SMAD3 has a role in regulating TGF-beta expression along with PIASy
- Protein and mRNA levels of SMAD3, but not of SMAD4 or SMAD7, were variably elevated in scleroderma fibroblasts
- A surface hydrophobic corridor within the MH2 domain of Smad3 is critical for association with CAN/Nup214 and nuclear import; Smad3 and Smad4 have different susceptibility to inhibition of import by cytoplasmic retention factor SARA
- smad3 interacts directly with YB1 during TGFbeta signal inhibition by interferon gamma
- Smad3 gene mutations could be associated with the pathogenesis of human osteoarthritis
- a signal transduction cascade of the TGF-beta/Smad signaling pathway, which is activated in the GEC, appears to be involved in the development of focal segmental glomerulosclerosis
- Smad2, Smad3 and Smad4 contribute to the regulation of TGF-beta responses to varying extents, and exhibit distinct roles in different cell types
- TGF-beta in a dose- and time-dependent manner increased the expression of Smads mRNA and protein, the rate of pSmad3 activation, and Smad3 translocation into the nucleus
- SMAD3 and SMAD4 activate gadd45beta through its third intron to facilitate G2 progression following TGFbeta treatment
- TGF-beta and Smad3 mediate beta-hydroxybutyrate(HB)-induced cell cycle-dependent growth inhibition while Smad3 mediates beta-HB-induced collagen production and p21WAF1/p27kip1 protein expression in human proximal tubule (HK-2) cells.
- Smad3 expression may have a critical role in tumor suppression in the early stages of gastric carcinogenesis.
- PIAS3 and Smad3 interact with each other at the endogenous protein level in mammalian cells and also in vitro, and the association occurs through the C-terminal domain of Smad3.
- a novel, functional binding element in the proximal region of the TN-C promoter mediating responsiveness to TGF-beta involving Smad3/4, Sp1, Ets1, and CBP/p300
- Analysis of the human SMAD3 promoter demonstrates that isoprenoid regulation of SMAD3 expression is dependent on Sp1/Sp3 activity
- Tuberin (TSC2) interact with smad2/smad3 during TGF-beta1 growth regulation.
- Smad3 has a role in Activin receptor-like kinase-7 induces apoptosis through activation of MAPKs
- menin and TGF-beta/Smad3 negatively regulate the BMP-2/Smad1/5- and Runx2-induced transcriptional activities leading to inhibition of cell differentiation
- The most transcriptionally active splice variants of Smad3 are made in macrophages (but not SMCs) of fibrofatty lesions and are upregulated after cell differentiation from monocytes. Cyclin inhibitors are induced by Smads. Fibrous plaque SMCs make Smad3.
- Gly-BSA increases DNA binding activity of Smad3 and that it stimulates PAI-1 transcription through Smad-binding CAGA sequences in the PAI-1 promoter in human mesangial cells
- Our findings suggest that BAMBI transcription is regulated by TGF-beta signaling through direct binding of SMAD3 and SMAD4 to the BAMBI promoter.
- sphingosine 1-phosphate receptors and the transforming growth factor beta-type I receptor serine/threonine kinase are essential for activation of Smad3 by lysophospholipids
- Smad2/3 is activated in undifferentiated human embryonic stem cells and required for the expression of genes controlling Nodal signaling
- HCV viral proteins interact with the TGF-beta signaling mediator Smad3 and differentially impair TGF-beta/Smad3-mediated transactivation and growth inhibition.
- TGF-beta-stimulation of transcription of PAI-1 is inhibited by VEGF, and TGF-beta phosphorylation of Smad2/3, an obligatory step of intracellular TGF-beta signaling, is suppressed by VEGF
- p38 MAP kinase and Rho/ROCK pathways together with Smad2 and Smad3 are necessary for TGF-beta-mediated growth inhibition
- Smad3 induces chondrogenesis through the activation of SOX9 via CREB-binding protein/p300 recruitment
- Transforming growth factor-beta1 stimulation of vascular endothelial growth factor production by fibroblasts is regulated by Smad3 but not by Smad2 signaling
- c-Jun NH(2)-terminal kinase tended to induce the phosphorylation of Smad2/3L in human colorectal adenoma-carcinoma sequence.
- TGFbeta1/Smad3 suppresses BRCA1-dependent DNA repair in response to a DNA damaging agent
- TGF-beta signaling suppresses nuclear export of Smad4 by chromosome region maintenance 1 and targets Smad4 into the nucleus; mutations in Smad4 that affect its interaction with Smad2 or Smad3 impair nuclear accumulation of Smad4 in response to TGF-beta
- TGF-beta/Smad3 signaling is required for hypoxia-mediated inhibition of adipocyte differentiation in marrow stromal cells
- Tsc-22 binds to and modulate the transcriptional activity of Smad3 and Smad4
- lysine residues of Smad3 MH2 domain play important roles in the transcriptional regulation of TGF-beta signals through TbetaR-I
- interleukin-1beta and its downstream mediator mitogen-activated protein kinase kinase kinase 7 inhibit SMAD3-mediated TGFbeta target gene activation
- TGF-beta1 and bleomycin intracellular signaling through autocrine regulation of Smad 3 binding to the proximal promoter of the Smad 7 gene
- deletion constructs of the promoter and mutational deletion of specific transcription factor binding sites indicated that Smad3/4 and AP-1 binding sites mediated the TGF-beta1 response on LTBP-3
- Distinct roles for Smad2 and Smad3 in TGFbeta1-induced CTGF expression and markers of EMT in human PTECs are reported.
- TGF-beta1 acts on adjacent stromal cells to turn on Smad3 signalling that could lead to stromal decidualization.
- These observations, together with the finding that CILP protein binds and inhibits TGF-beta1, suggest that CILP and TGF-beta1 may form a functional feedback loop that controls chondrocyte metabolism.
- A short peptide representing the minimal interaction domain in Smad3 effectively competes with Smad3 association to exportin 4 and blocks nuclear export of Smad3 in vivo.
- summary of the recent understanding of Smad3 phosphoisoform-mediated signaling, particularly 'cross-talk' between Smad3 and JNK pathways that cooperatively promote oncogenic activities in colorectal carcinogenesis [review]
- role in nuclear translocation of beta-catenin
- Activation of Smad3 but not Smad2 is a key mechanism by which Angioteinsin ii mediates artriosclerosis.
- One mechanism for positive regulation of TLR2 induction involves functional cooperation between the TGF-betaR-Smad3/4 pathway and NF-kappaB pathway. Another involves (MKP-1)-dependent inhibition of p38 MAPK, a known negative regulator for TLR2 induction
- TGFbeta suppresses TERT by Smad3 interactions with c-Myc and the hTERT gene
- a novel mutation was found to result in the inhibition of translocation of Smad3 protein to the nucleus and a reduction in the activity of Smad3 during TGF-beta-induced transcriptional activation
- These results suggest that RACK1 modulates transcription of alpha2(I) collagen by TGF-beta1 through interference with Smad3 binding to the gene promoter.
- These results suggest that p38 affects the phosphorylation of Smad2 and Smad3 differentially during TGF-beta signaling in human dental pulp cells and ERK1/2 might be involved in the process.
- identified the small C-terminal domain phosphatase 1 (SCP1) as a specific phosphatase for Smad2/3 dephosphorylation in the linker and N terminus
- mRNA expressed in human granulosa-luteal cells at oocyte retrieval.
- SHP is a novel co-regulator of Smad3 that regulates TGF-beta signaling
- Leptin and TGF-beta1 synergistically augmented activation of signalling components of mitogen-activated protein kinase (MAPK), STAT3 and Smad but did not modulate the expression of LEPR-B.
- These data lead to the conclusion that MEK1 is an important regulator of SMAD3 expression.
- Smad3 appears to be important in colonic inflammation.
- Neurofibrillary tangles sequester pSmad3, preventing its translocation into the nucleus and the induction of gene transcription. Interference with the Smad signaling may adversely affect survival of tangle-bearing neurons in AD.
- The TGFB/SMAD3 signaling pathway is involved in butyrate-mediated vitamin D receptor expression.
- examined the possible deterioration in the pathway in human squamous cancer cell lines, focusing on intracellular localization of S100C/A11 and its functional partners Smad3 and Smad4-
- Results show that Arkadia specifically activates transcription via Smad3/Smad4 binding sites by inducing degradation of the transcriptional repressor SnoN.
- Results define Erbin as a novel negative modulator of Smad2/Smad3 functions and expand the physiological role of Erbin to the regulation of TGFbeta signaling.
- These results suggest an important role for cross talk among Smad, p38 MAPK, JNK, and PI3K pathways in mediating the augmented expression of hAT(1)R following TGF-beta1 treatment in human fetal pulmonary fibroblasts.
- Inhibition of beta-catenin resulted in increased TGF-beta1-dependent Smad3 phosphorylation and restoration of TGF-beta1 anti-proliferative effects.
- transforming growth factor-beta has a role in Smad3-dependent activation of Gli2 and Gli1 expression
- findings suggest that CEA (CEACAM5) and CEACAM6 are major target genes for Smad3-mediated TGF-beta signaling.
- ALK5-dependent Smad3 signaling is the responsible pathway inducing CTGF expression.
- SMAD3 dependent inactivation of CYP17 promoter activity and repression of SF-1 expression.
- 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.
- Smad3, through regulating angiogenic molecule expression in tumor cells, is critical for progression of prostate cancer
- TGFbeta1 represses CYP7A1 gene transcription in human hepatocytes by a mechanism involving Smad3-dependent inhibition of HNF4alpha and histone deacetylase remodeling of CYP7A1 chromatin.
- Recent studies highlighted in this review suggest that TGF-beta suppresses neoplastic cell development by employing Smad3 protein to repress the human telomerase reverse transcriptase gene.
- functional characterization of a tumorigenic mutation in Smad4(E330A); findings show this mutant & a Smad3 mutant (Smad3 E239A) failed to activate transcription in response to TGFbeta stimulation because of defects in oligomerization
- SARS coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-beta signaling
- Thus, SMCX is a novel Smad3 corepressor that may antagonize the tumor suppressing activity of the TGF-beta/Smad3 signaling pathway and thereby contribute to tumorigenesis.
- These findings suggest that CLU regulates TGF-beta signaling pathway by modulating the stability of Smad2/3 proteins.
- Activin A increased and follistatin decreased phosphorylation of SMAD2/3 in vitro, and activin increased SMAD2 and decreased KITLG mRNA expression.
- TGF-beta(1) regulates proliferation through Smad3 signaling in both fibroblast populations; however, it is the levels of HA generated by the cells that influence the outcome of this response.
- TGF-beta-mediated activation of the ALK5-Smad 3 pathway plays a role in SHH promoted motility and invasiveness of gastric cancer cells
- myostatin enhanced nuclear translocation of beta-catenin and formation of the Smad3-beta-catenin-TCF4 complex, together with the altered expression of a number of Wnt/beta-catenin pathway genes in hMSCs
- increased TGF-beta-Smad signaling in sporadic and familial ALS and impaired TGF-beta signal transduction in neurons of sporadic ALS patients, presumably at the step of pSmad2/3 translocation into the nucleus
- 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.
- tagln is a novel target of TGF-beta/Smad3-dependent gene expression in alveolar epithelial type II cells
- AMPK inhibits TGFbeta-induced transcription downstream of Smad3 COOH-terminal phosphorylation and nuclear translocation
- interaction between RAP250, Smad2, and Smad3 constitutes an important bridging mechanism linking LXR and TGF-beta signaling pathways.
- 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
- Coexpression of Smad3 with PIASy and SUMO1 stimulated the nuclear export of Smad3.
- SMAD 2/3 signaling directly supports NANOG expression, while SMAD 1/5/8 activation moderately represses SOX2.
- A case-control study in Afro-Caribbeans found SMAD3 SNPs were not strongly associated with increased risk of developing keloids.
- PTEN abrogates TGF-beta-induced Smad2/3 phosphorylation. This study establishes a novel role for nuclear PTEN in the stabilization of PPM1A.
- the TGF-beta1-2-3/Smad3 pathway has a role in mediating ovarian oncogenesis by enhancing metastatic potential
- Data demonstrate that in response to TGFbeta stimulation the transcriptional regulator TAZ binds heteromeric Smad2/3-4 complexes and is recruited to TGFbeta response elements.
- a number of putative novel Smad2 and Smad3 associated proteins in TGF-beta1 signaling were identified that have functions in cell proliferation, apoptosis, actin cytoskeleton regulation, cell motility, transcription, and Ras or insulin signaling
- SMAD3 is one important transcription factor mediating transforming growth factor beta's- inhibitory effects on IFN-gamma production and antibody-dependent cellular cytotoxicity following CD16 activation of natural killer cells.
- TGF-beta1 and SMAD3 may be involved in the pathology of corneal diseases associated with herpes simplex virus type 1 infection.
- Galectin-1 decreases Smad3-complex from binding to the SBE, down-regulating transcription of COL1A2 in TGF-beta1-stimulated renal epithelial cells.
- Ligand-dependent ubiquitination of Smad3 is regulated by CK1g2, an inhibitor of TGF-beta signaling.
- Activin stimulates endogenous inhibin alpha- and betaB-subunit mRNA, protein, and proteolytic processing. Simultaneously, activin stimulated the proconvertase furin through a Smad2/3-dependent process.
- Binding elements for ETS and transcription factor AP-2 (TFAP2) were significantly enriched in Smad2/3 binding sites, and knockdown of either ETS1 or TFAP2A resulted in overall alteration of TGF-beta-induced transcription.
- Arginine 279, glutamic acid 246 in Smad3 and glutamic acid 1321 in Erbin are important for these proteins binding.
- These data indicate that the intracellular glutathione redox status regulates TGF-beta-induced fibrogenic effects through Smad3 activation.