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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.
Smad3 knockdown could restore the inhibition of cell proliferation induced by FSTL1 (show FSTL1 Proteins) overexpression in MDAMB231FSTL1 cells, indicating that the antiproliferative effect of FSTL1 (show FSTL1 Proteins) overexpression may be associated with Smad3 involved TGFbeta (show TGFB1 Proteins) signaling pathway regulation. This study identified FSTL1 (show FSTL1 Proteins) as an inhibitor of cell proliferation in MDAMB231 and 231BR cell lines
miR (show MLXIP Proteins)-195 inhibited proliferation and induced apoptosis of vascular smooth muscle cells, which was abated by Smad3 overexpression
We found expression of pSmad2/3 and Smad4 (show SMAD4 Proteins) in different liver tissues, with up-regulated expression of both antibodies in chronic hepatitis C with higher stage of fibrosis and higher grade of activity.
SMAD3 SNP rs422342 is statistically associated with intervertebral disc degeneration in Greek population.
we observed that SMAD3 rs1065080 single nucleotide gene polymorphisms were significantly associated with patient susceptibility to intracranial arterial aneurysms
TGFbeta (show TGFB1 Proteins) and IL1beta (show IL1B Proteins) signaling interact at the SMAD2 (show SMAD2 Proteins)/3 level in human primary MSC (show MSC Proteins). Down-stream TGFbeta (show TGFB1 Proteins) target genes were repressed by IL1beta (show IL1B Proteins) independent of C-terminal SMAD2 (show SMAD2 Proteins) phosphorylation. We demonstrate that SMAD2 (show SMAD2 Proteins)/3 linker modifications are required for this interplay and identified TAK1 (show MAP3K7 Proteins) as a crucial mediator of IL1beta (show IL1B Proteins)-induced TGFbeta (show TGFB1 Proteins) signal modulation.
Smad3 binds with type I TGF-beta (show TGFB1 Proteins) receptor (TRI (show VANGL2 Proteins)) even in unstimulated cells.
Our studies provide a molecular mechanism by which UCHL5 (show UCHL5 Proteins) mitigates TGFbeta (show TGFB1 Proteins)-1 signaling by stabilizing Smad2 (show SMAD2 Proteins)/Smad3. These data indicate that UCHL5 (show UCHL5 Proteins) may contribute to the pathogenesis of idiopathic pulmonary fibrosis and may be a potential therapeutic target.
This study demonstrates that Smad3 protein had low expression in ACTH (show POMC Proteins)-Pituitary Adenoma Development.
data suggest that TGF-beta (show TGFB1 Proteins) stimulated the expression of ChPF (show CHPF Proteins) and sGAG synthesis in nucleus pulposus cells through Smad3, RhoA (show RHOA Proteins)/ROCK1 (show ROCK1 Proteins) and the three MAPK (show MAPK1 Proteins) signaling pathways.
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.
We provide the evidence that over-expression of miR (show MLXIP Proteins)-145 could inhibit osteoclast differentiation, at least partially, by decreasing Smad3 expression
Activin signaling through SMAD2 (show SMAD2 Proteins)/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 (show TLR7 Proteins) expression and beta-catenin (show CTNNB1 Proteins) activation
SMAD3 is regulated by miR (show MLXIP Proteins)-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 (show CRP Proteins) is pathogenic in type-2 diabetes (T2DN). CRP (show CRP Proteins) may promote CD32b- NF-kappaB (show NFKB1 Proteins) signaling to mediate renal inflammation; whereas, CRP (show CRP Proteins) may enhance renal fibrosis in T2DN via CD32b-Smad3-mTOR (show FRAP1 Proteins) signaling.
A Smad3-PTEN regulatory loop controls proliferation and apoptotic responses to TGF-beta (show TGFB1 Proteins) 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 (show INHBA Proteins) on IL-6 (show IL6 Proteins) release
Results suggest that Smad2 (show SMAD2 Proteins)/3 linker threonine phosphorylation is expressed during acinar-ductal metaplasia.
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 (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