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Data suggest that Clock1a coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 signaling; Clock1a alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a activates Smad3a promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1; Smad3a = SMAD family member 3a)
Smad3 is mainly active in post-mitotic, non-proliferating cells with a role in TGF-beta control of zebrafish spinal cord development
Nodal signaling and mesendoderm induction depend on Smad2/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2/3 signaling and embryonic patterning.
although the role of Smad proteins in mediating Nodal signaling is well-documented, the functional characterization of Ttrap provides insight into a novel Smad partner that plays an essential role in the fine-tuning of this signal transduction cascade
Smad2/3 activities play important roles not only in mesendodermal development but also in neural development during early vertebrate embryogenesis
Data indicate that cardiac contractility modulation (CCM) therapy exerted protective effects against myocardial fibrosis potentially by inhibiting TGF-beta1/Smad3 signaling pathway in chronic heart failure .
study suggested that TGF-beta1/Smad3/smad7 is a major pathway which plays an important role in the regulation of the IUA and specific inhibitor of Smad3 (SIS3) may provide a new therapeutic strategy for IUA.
Study established a relationship between OCT4 and SMAD3 heterodimers formation and Snail, Slug, and CXCL13 transcription promotion mediating breast cancer progression.
Study results using gene editing indicate the cancer-promoting role of Smad3 T179 phosphorylation in the human triple-negative breast cancer cells.
Overall, these findings suggest a more dominant role for SMAD3 and SMAD4 than SMAD2 in TGFbeta-induced chondrogenesis of human bone marrow-derived mesenchymal stem cells.
Downregulation of miR-637 promotes proliferation and migration of fibroblasts by targeting Smad3 in keloids.
The findings of the present study indicated that miR326 inhibited endometrial fibrosis by suppressing the TGFbeta1/Smad3 signaling pathway, suggesting that miR326 may be a prognostic biomarker and therapeutic target for Intrauterine adhesion (IUA).
Study validated a specific model prediction that SMAD3 regulates Huntington's disease (HD)-related gene expression changes. Also, results found CAG repeat length-dependent changes in the genomic occupancy of SMAD3 and confirmed the model's prediction that many SMAD3 target genes are downregulated early in HD.
The SMAD3 rs12901499 polymorphism may be involved in the development of knee osteoarthritis. Larger studies with more diverse ethnic populations are needed to confirm these result.
NLRC5 may act as a key mediator in renal fibroblast activation and fibrogenesis
The results suggest that co-expression of active SMAD2/3 could enhance multiple types of transcription factors (TF)-based cell identity conversion and therefore be a powerful tool for cellular engineering.
The SMAD3 SNP rs12901499 GA genotype and G variant may increase the risk of hip osteoarthritis in Chinese Han patients.
We found that ITZ treatment was efficient in suppressing EMT and that the effect of ITZ was partially mediated by impaired TGF-b/SMAD2/3 signaling. The role of TGF-b/SMAD2/3 signaling in mediating the effect of ITZ was confirmed based on the results that recombinant TGF-b induced, but the TGF-b neutralizing antibody inhibited EMT as well as the invasion and migration of pancreatic cancer cells
Positive cooperativity of Smad3 and STAT3 during epithelial-mesenchymal transition [Review].
CXCL12 activates the MEKK1/JNK signaling pathway, which in turn initiates SMAD3 phosphorylation, its translocation to nuclei, and recruitment of SMAD3 to the CTGF promoter, which ultimately induces CTGF expression in human lung fibroblasts.
SMAD2/3 interactome reveals that TGFbeta controls m(6)A mRNA methylation in pluripotency
these results indicated that Bone marrow-derived mesenchymal stem cells -conditioned medium suppressed the epithelial-mesenchymal transition which might be associated with TGF-B1/Smad3. This study provides the theoretical basis for the research of the mechanisms responsible for pulmonary disease.
our findings demonstrated that thymoquinone suppressed the metastatic phenotype and reversed EMT of prostate cancer cells by negatively regulating the TGF-beta/Smad2/3 signaling pathway. These findings suggest that thymoquinone is a potential therapeutic agent against prostate cancer which functions by targeting TGF-beta
The present findings indicate that RACK1 silencing attenuates renal fibrosis by suppressing the activation of TGF-beta1/Smad3 signaling pathway in HK-2 cells. Thus, RACK1 may serve as a novel regulator of renal fibrosis.
was found that treatment with iPSC-CM markedly reduced the proliferation of TGF-beta1-exposed cells, and the activities of TGF-beta1, Smad-2 and Smad-3. Accompanied by alterations in the expression of the indicated molecules, the lung structure of mice with PF was also markedly ameliorated.
MSP analysis from 81 Acute coronary syndrome (ACS)samples, 74 SCAD samples and 53 healthy samples, and Sequenom MassARRAY analysis, confirmed that differential CpG methylation of SMAD3 was significantly corrected with the reference results of the HumanMethylation450 array.
Smad3 knockdown could restore the inhibition of cell proliferation induced by FSTL1 overexpression in MDAMB231FSTL1 cells, indicating that the antiproliferative effect of FSTL1 overexpression may be associated with Smad3 involved TGFbeta signaling pathway regulation. This study identified FSTL1 as an inhibitor of cell proliferation in MDAMB231 and 231BR cell lines
E2a is necessary to drive transcription of Smad2/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
TAZ confers SMAD3 sensitivity to the smooth muscle actin promoter.
HSP70 indirectly interacted with Smad3.
Activin A and overexpression of SMAD2/3 significantly promoted expressions of porcine NANOG and OCT4,maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog/OCT4 expression.
Smad3 regulate the activity and stability of myocardin-related transcription factor during epithelial-myofibroblast transition
SP1 and SMAD3 are required for high glucose-induced p21(WAF1) gene transcription in LLC-PK1 cells.
Data indicate E4BP4/NFIL3 as a direct Smad3 target gene critical for NK cell differentiation.
Data suggest that Smad-specific E3 ubiquitin ligase 2 (SMURF2)-mediated SMAD3 protein (SMAD3) monoubiquitination interferes with the formation of a SMAD3-vitamin D receptor (VDR) complex.
These data indicate that SMAD3- and beta-catenin-dependent induction occurs in the taurine transporter knockout mouse
Cav-3 and Smad3 may be involved in the occurrence and development of viral myocarditis.
In pancreata of mice and rats, TGFB promotes peripheral nociceptive sensitization via a direct effect on primary sensory neurons mediated by intra-neuronal SMAD3.
We provide the evidence that over-expression of miR-145 could inhibit osteoclast differentiation, at least partially, by decreasing Smad3 expression
Activin signaling through SMAD2/3 in retinal progenitor cells regulates expression of transcription factors involved in cell type determination and promotes photoreceptor lineage specification.
conclude that VDD promotes tumor growth in the context of Smad3 disruption, potentially through regulation of TLR7 expression and beta-catenin activation
SMAD3 is regulated by miR-489 in pulmonary fibrosis.miR-489 suppresses fibroblast differentiation by targeting Smad3.
Alendronate (ALN)-augmented IL-1beta production and cell death require Smad3 and ASC activation, and SIS3 and anti-ASC antibodies may serve as palliative agents for necrotizing inflammatory diseases caused by ALN
CRP is pathogenic in type-2 diabetes (T2DN). CRP may promote CD32b- NF-kappaB signaling to mediate renal inflammation; whereas, CRP may enhance renal fibrosis in T2DN via CD32b-Smad3-mTOR signaling.
A Smad3-PTEN regulatory loop controls proliferation and apoptotic responses to TGF-beta in mouse endometrium.
These findings indicate that both systemic factors and intrinsic properties of skin cells contribute to enhanced wound healing and less inflammatory reaction observed in Smad3 knock-out mice.
Data show that Smad3 knockdown attenuated the effect of activin A on IL-6 release
Results suggest that Smad2/3 linker threonine phosphorylation is expressed during acinar-ductal metaplasia.
Sirt1 reduced endoplasmic reticulum stress and apoptosis of brown adipocytes in vivo/in vitro by inhibiting Smad3/ATF4 signaling pathway.
these findings support the notion that Smad3 has important tumor suppressor function for breast cancer
Treatment with metformin suppressed CCl4-induced expression of transforming growth factor beta 1 (TGF-beta1) and phosphorylation of Smad3.
HSF1 activity is decreased in fibrotic hearts. HSF1 inhibits phosphorylation and nuclear distribution of Smad3 via direct binding to Smad3. Active Smad3 blocks the anti-fibrotic effect of HSF1.
The results provide the first evidence that upregulation of TGFb/Smad3 in injured arteries induces local smooth muscle cells CXCR4 expression and cell migration, and consequently intimal hyperplasia.
Data show that the transcription factor Smad3 (Smad3) gene was expressed ubiquitously in 11 bovine tissues and displayed different expression patterns between muscle and adipose tissue.
the present work provides evidence supporting a functional role of SMAD2/3 in bovine early embryogenesis
Mechanical compression not only with physiological but also with excessive stress can activate Smad2/3P signaling, which is known to be protective for articular cartilage and to block chondrocyte terminal differentiation.
a detailed computational model for TGF-beta signalling that incorporates elements of previous models together with crosstalking between Smad1/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7.
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 functions as a transcriptional modulator activated by transforming growth factor-beta and is thought to play a role in the regulation of carcinogenesis.
MAD homolog 3
, MAD homolog 3a
, MAD, mothers against decapentaplegic homolog 3
, SMA- and MAD-related protein 3
, SMAD, mothers against DPP homolog 3
, mad homolog JV15-2
, mad protein homolog
, mothers against DPP homolog 3
, mothers against decapentaplegic homolog 3
, SMAD 3
, TGF beta response effector Smad3
, TGF-beta response effector Smad3
, Smad 3
, MAD (mothers against decapentaplegic, Drosophila) homolog 3
, SMAD family member 3