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Data suggest that Clock1a (show CLOCK Proteins) coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 signaling; Clock1a (show CLOCK Proteins) alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a (show CLOCK Proteins) activates Smad3a promoter via its E-box1 element. (Clock1a (show CLOCK Proteins) = clock circadian regulator (show CLOCK Proteins) a; Nodal = nodal modulator 1 (show NOMO1 Proteins); Smad3a = SMAD (show SMAD1 Proteins) family member 3a)
Smad3 is mainly active in post-mitotic, non-proliferating cells with a role in TGF-beta (show TGFB1 Proteins) control of zebrafish spinal cord development
Nodal signaling and mesendoderm induction depend on Smad2 (show SMAD2 Proteins)/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2 (show SMAD2 Proteins)/3 signaling and embryonic patterning.
although the role of Smad (show SMAD1 Proteins) proteins in mediating Nodal signaling is well-documented, the functional characterization of Ttrap (show TDP2 Proteins) provides insight into a novel Smad (show SMAD1 Proteins) partner that plays an essential role in the fine-tuning of this signal transduction cascade
Smad2 (show SMAD2 Proteins)/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 (show TGFB1 Proteins)/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.
HSF1 (show HSF1 Proteins) activity is decreased in fibrotic hearts. HSF1 (show HSF1 Proteins) inhibits phosphorylation and nuclear distribution of Smad3 via direct binding to Smad3. Active Smad3 blocks the anti-fibrotic effect of HSF1 (show HSF1 Proteins).
miR (show MLXIP Proteins)-142-5p plays as a negative regulator in TGF-beta (show TGFB1 Proteins) pathway by targeting SMAD3 and suppresses TGF-beta (show TGFB1 Proteins)-induced growth inhibition in cancer cells.
Authors were able to confirm expression of SMAD3 in intact and degraded cartilage of the knee and hip. Our findings provide the first systematic evaluation of pleiotropy between OA and BMD (show BEST1 Proteins), highlight genes with biological relevance to both traits, and establish a robust new OA genetic risk locus at SMAD3.
A bioinformatics analysis and luciferase reporter assay identified Smad3 as a direct target gene of miR (show MLXIP Proteins)-216b, and Smad3 expression was reduced by miR (show MLXIP Proteins)-216b overexpression at both the mRNA and protein levels.
Because the expression of these genes correlates with cell shape, these are likely mechanosensitive genes that regulate SMAD3 and/or RELA (show NFkBP65 Proteins) activation in response to mechanical cues
Asiaticoside hindered the invasive growth of KFs (show GDF6 Proteins) by inhibiting the GDF-9 (show GDF9 Proteins)/MAPK (show MAPK1 Proteins)/Smad (show SMAD1 Proteins) pathway.
SMAD3 transcription facttor binds RNA with large internal loops or bulges with high apparent affinity, suggesting a biological role for RNA binding by SMAD3.
Case Report: internal mammary artery aneurysms in sisters with SMAD3 mutation.
High Smad3 expression is associated with invasion and metastasis in pancreatic ductal adenocarcinoma.
New evidence suggests that SMAD3 activation may serve as a critical converging point of dysregulated TGFB (show TGFB1 Proteins) superfamily signaling and genetic aberrations in human granulosa cell tumor development (review).
E2a (show TCF3 Proteins) is necessary to drive transcription of Smad2 (show SMAD2 Proteins)/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
HSP70 (show HSP70 Proteins) indirectly interacted with Smad3.
Activin A (show INHBA Proteins) and overexpression of SMAD2 (show SMAD2 Proteins)/3 significantly promoted expressions of porcine NANOG (show NANOG Proteins) and OCT4 (show POU5F1 Proteins),maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog (show NANOG Proteins)/OCT4 (show POU5F1 Proteins) expression.
Smad3 regulate the activity and stability of myocardin-related transcription factor during epithelial-myofibroblast transition
SP1 (show SP1 Proteins) and SMAD3 are required for high glucose-induced p21(WAF1 (show CDKN1A Proteins)) gene transcription in LLC-PK1 (show PKLR Proteins) cells.
The results provide the first evidence that upregulation of TGFb (show TGFB1 Proteins)/Smad3 in injured arteries induces local smooth muscle cells CXCR4 (show CXCR4 Proteins) expression and cell migration, and consequently intimal hyperplasia.
Blocking Smad2 (show SMAD2 Proteins)/3 signaling in pluripotent stem cells results in epigenetic changes that enhance the capacity for endoderm differentiation.
M1 macrophages with inhibited STAT3 (show STAT3 Proteins), STAT6 (show STAT6 Proteins) and/or SMAD3 effectively restrict tumor growth. The findings justify the development of new anti-tumor cell therapy technology.
Aberrant Smad3 phosphoisoforms in cyst-lining epithelial cells in the cpk mouse suggest a qualitative rather than a quantitative abnormality of the TGF-beta (show TGFB1 Proteins)/Smad3 pathway is involved in autosomal recessive polycystic kidney disease.
The Smad3 and Bmal1 (show ARNTL Proteins) regulate p21 and S100A4 (show S100A4 Proteins) expression in myocardial stromal fibroblasts through TNF-alpha (show TNF Proteins).
cells expressing mutant huntingtin (show HTT Proteins) have a dysregulated transcriptional response to epidermal growth factor (show EGF Proteins) stimulation
Smad2 (show SMAD2 Proteins)- and Smad3-deficient bone marrow (BM) cells display reduced sensitivity to transforming growth factor-beta (TGFbeta (show TGFB1 Proteins)) inhibition.
conclude that the cardiovascular manifestations of Smad3 deficient mice are strain-specific, with myocyte necrosis in 129 mice and aortic rupture in C57BL/6J mice
Lnc-LFAR1 binds directly to Smad2 (show SMAD2 Proteins)/3 and promotes transcription of TGFbeta (show TGFB1 Proteins), Smad2 (show SMAD2 Proteins), Smad3, Notch2 (show NOTCH2 Proteins) and Notch3 (show NOTCH3 Proteins) which, in turn, results in TGFbeta (show TGFB1 Proteins) and Notch (show NOTCH1 Proteins) pathway activation.
the present work provides evidence supporting a functional role of SMAD2 (show SMAD2 Proteins)/3 in bovine early embryogenesis
Mechanical compression not only with physiological but also with excessive stress can activate Smad2 (show SMAD2 Proteins)/3P signaling, which is known to be protective for articular cartilage and to block chondrocyte terminal differentiation.
a detailed computational model for TGF-beta (show TGFB1 Proteins) signalling that incorporates elements of previous models together with crosstalking between Smad1 (show SMAD1 Proteins)/5/8 and Smad2 (show SMAD2 Proteins)/3 channels through a negative feedback loop dependent on Smad7 (show SMAD7 Proteins).
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