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Validated All-in-One™ qPCR Primer for SMAD2(NM_005901.5) Search again
Product ID:
HQP054007
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CHTD8, JV18, JV18-1, LDS6, MADH2, MADR2, hMAD-2, hSMAD2
Gene Description:
SMAD family member 2
Target Gene Accession:
NM_005901.5(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.
Summary
The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein mediates the signal of the transforming growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation. This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4.
Gene References into function
- Crystal structure of a phosphorylated Smad2. Recognition of phosphoserine by the MH2 domain and insights on Smad function in TGF-beta signaling
- repression of transactivating activity by association with a novel splice variant of CCAAT-binding factor C subunit
- c-Jun associates with the oncoprotein Ski and suppresses Smad2 transcriptional activity
- activation by transforming growth factor beta in absence of receptor endocytosis
- HTLV-1 tax represses Smad-mediated TGF-beta signaling.
- activation of TGF-beta1/Smad2 signaling is associated with airway remodeling in asthma
- Nucleocytoplasmic shuttling of Smads 2, 3, and 4 permits sensing of TGF-beta receptor activity.
- overexpression of adenoviral Smad1 and Smad2 proteins without exogenously added ligands induced inhibin B production
- 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.
- 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 Smad2 to move to the nucleus in a Smad4-independent fashion. Nuclear translocation of Smad2 was not sufficient to activate reporters for TGF-beta-induced transcriptional responses.
- Results suggest that the Smad 2 may be the downstream signal transducers of TGF-beta(1) in human dental pulp cells.
- A deletion of 'G' in the L3 loop (crucial in Smad-receptor interaction) & an insertion of 'A' in codon 122 (loss of MH2 domain) in cervical tumor cells caused frame shift & pretermination in Smad2, highlighting its important role in these tumors.
- 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
- Tuberin (TSC2) interact with smad2/smad3 during TGF-beta1 growth regulation.
- The most transcriptionally active splice variants of Smad2 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 Smad2.
- Differential gene expression of Smad2, a tumor suppressor gene, plays a significant role in the proliferation of breast cancer
- Regulated cytoplasmic and nuclear retention may play a role in determining the distribution of Smads between the cytoplasm and the nucleus in both uninduced cells and upon TGF-beta induction.
- Smad2/3 is activated in undifferentiated human embryonic stem cells and required for the expression of genes controlling Nodal signaling
- 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
- NEDD4-2 bound to TGF-beta-specific R-Smads, Smads 2 and 3, in a ligand-dependent manner, and induced degradation of Smad2, but not Smad3
- p38 MAP kinase and Rho/ROCK pathways together with Smad2 and Smad3 are necessary for TGF-beta-mediated growth inhibition
- caspase-3 is crucial for the differentiation of bone marrow stromal stem cells by influencing TGF-beta/Smad2 pathway and cell cycle progression
- internalization is important for transforming growth factor beta1-induced Smad2 association with Smad anchor for receptor activation (SARA) and Smad2-dependent signaling in human mesangial cells
- c-Jun NH(2)-terminal kinase tended to induce the phosphorylation of Smad2/3L in human colorectal adenoma-carcinoma sequence.
- 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
- 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.
- Smad4, but not Smad2, mediates TGF-beta1-induced MMP-2 expression in invasive extravillous trophoblasts
- Distinct roles for Smad2 and Smad3 in TGFbeta1-induced CTGF expression and markers of EMT in human PTECs are reported.
- TGF-beta-dependent nuclear accumulation of Smad2 is caused exclusively by selective nuclear trapping of phosphorylated, complexed Smad2
- TGF-beta1 acts on adjacent stromal cells to turn on Smad2 signalling that could lead to stromal decidualization.
- Babo/dSmad2 signaling prior to metamorphosis may be widely required to prepare neurons for the dynamic environment present during metamorphosis.
- A novel missense mutation of SMAD2, located in exon 8 at codon 276 TCG (ser) -->TTG (leu), was identified in head and neck squamous cell carcinoma cell line SCC-15.
- Activation of Smad3 but not Smad2 is a key mechanism by which Angioteinsin ii mediates artriosclerosis.
- Our data indicate that TGF-beta1 induces endothelial barrier dysfunction involving Smad2-dependent p38 activation, resulting in RhoA activation by possible transcriptional regulation.
- 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.
- 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.
- Disruption of the TGF-beta 1-Smad2 signaling pathway may lead to the resistance of TGF-beta 1 growth-inhibitory effect on oral squamous cell carcinoma.
- High Smad2 is associated with glioma
- Breast cancer wiwthw hight expression of cancerous phosphorylated Smad2 tended to have a better prognosis, although statistic significance was never reached.
- Platelets possess Smad2 protein and that its phosphorylation state is increased after exposure to TGF-beta1.
- High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC.
- 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.
- Aberrant location of expression/staining intensity of PTEN, PPM1A and P-Smad2 in hepatocellular carcinoma may impact disease progression.
- 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.
- 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.
- 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.
- interaction between RAP250, Smad2, and Smad3 constitutes an important bridging mechanism linking LXR and TGF-beta signaling pathways.
- SMAD 2/3 signaling directly supports NANOG expression, while SMAD 1/5/8 activation moderately represses SOX2.
- PTEN abrogates TGF-beta-induced Smad2/3 phosphorylation. This study establishes a novel role for nuclear PTEN in the stabilization of PPM1A.
- PCTA defines a new component of the TGF-beta signalling pathway that functions to facilitate Smad2 phosphorylation through controlling the accumulation of cPML into the cytoplasm, and consequently, the assembly of Smad2-receptor complex.
- 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.
- Keratinocyte-specific SMAD2 ablation results in increased epithelial-mesenchymal transition during skin cancer formation and progression.
- 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
- 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.
- SMAD2 is not shown to have a role in colorectal cancer with inflammatory bowel disease
- 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.
- This study has demonstrated that constant cyclic stretching inhibits adipogenic differentiation of human umbilical cord progenitor cells via autocrine/paracrine stimulation of the TGFbeta1/Smad2 signaling pathway.
- Data suggest that integrin alpha3beta1 is a critical coordinator of epithelial-mesenchyme transition signaling pathways involving beta-catenin and pSmad2.
- disruption of Smad2 function by CDK2 phosphorylation acts as a mechanism for TGF-beta resistance in multiple myeloma.