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Data suggest that Clock1a (show CLOCK ELISA Kits) coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 signaling; Clock1a (show CLOCK ELISA Kits) alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a (show CLOCK ELISA Kits) activates Smad3a promoter via its E-box1 element. (Clock1a (show CLOCK ELISA Kits) = clock circadian regulator (show CLOCK ELISA Kits) a; Nodal = nodal modulator 1 (show NOMO1 ELISA Kits); Smad3a = SMAD (show SMAD1 ELISA Kits) family member 3a)
Smad3 is mainly active in post-mitotic, non-proliferating cells with a role in TGF-beta (show TGFB1 ELISA Kits) control of zebrafish spinal cord development
Nodal signaling and mesendoderm induction depend on Smad2 (show SMAD2 ELISA Kits)/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2 (show SMAD2 ELISA Kits)/3 signaling and embryonic patterning.
although the role of Smad (show SMAD1 ELISA Kits) proteins in mediating Nodal signaling is well-documented, the functional characterization of Ttrap (show TDP2 ELISA Kits) provides insight into a novel Smad (show SMAD1 ELISA Kits) partner that plays an essential role in the fine-tuning of this signal transduction cascade
Smad2 (show SMAD2 ELISA Kits)/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 ELISA Kits)/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.
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 ELISA Kits), 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 ELISA Kits)-216b, and Smad3 expression was reduced by miR (show MLXIP ELISA Kits)-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 ELISA Kits) activation in response to mechanical cues
Asiaticoside hindered the invasive growth of KFs (show GDF6 ELISA Kits) by inhibiting the GDF-9 (show GDF9 ELISA Kits)/MAPK (show MAPK1 ELISA Kits)/Smad (show SMAD1 ELISA Kits) 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 ELISA Kits) superfamily signaling and genetic aberrations in human granulosa cell tumor development (review).
CytoD modified MKL1, a coactivator of serum response factor (SRF) regulating CTGF induction, and promoted its nuclear localization.
We find that DIGIT is divergent to Goosecoid (GSC (show GSC ELISA Kits)) and expressed during endoderm differentiation. Deletion of the SMAD3-occupied enhancer proximal to DIGIT inhibits DIGIT and GSC (show GSC ELISA Kits) expression and definitive endoderm differentiation.
E2a (show TCF3 ELISA Kits) is necessary to drive transcription of Smad2 (show SMAD2 ELISA Kits)/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
HSP70 (show HSP70 ELISA Kits) indirectly interacted with Smad3.
Activin A (show INHBA ELISA Kits) and overexpression of SMAD2 (show SMAD2 ELISA Kits)/3 significantly promoted expressions of porcine NANOG (show NANOG ELISA Kits) and OCT4 (show POU5F1 ELISA Kits),maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog (show NANOG ELISA Kits)/OCT4 (show POU5F1 ELISA Kits) expression.
Smad3 regulate the activity and stability of myocardin (show MYOCD ELISA Kits)-related transcription factor during epithelial-myofibroblast transition
SP1 (show SP1 ELISA Kits) and SMAD3 are required for high glucose-induced p21(WAF1 (show CDKN1A ELISA Kits)) gene transcription in LLC-PK1 (show PKLR ELISA Kits) cells.
The results provide the first evidence that upregulation of TGFb (show TGFB1 ELISA Kits)/Smad3 in injured arteries induces local smooth muscle cells CXCR4 (show CXCR4 ELISA Kits) expression and cell migration, and consequently intimal hyperplasia.
Blocking Smad2 (show SMAD2 ELISA Kits)/3 signaling in pluripotent stem cells results in epigenetic changes that enhance the capacity for endoderm differentiation.
M1 macrophages with inhibited STAT3 (show STAT3 ELISA Kits), STAT6 (show STAT6 ELISA Kits) 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 ELISA Kits)/Smad3 pathway is involved in autosomal recessive polycystic kidney disease.
The Smad3 and Bmal1 (show ARNTL ELISA Kits) regulate p21 and S100A4 (show S100A4 ELISA Kits) expression in myocardial stromal fibroblasts through TNF-alpha (show TNF ELISA Kits).
cells expressing mutant huntingtin (show HTT ELISA Kits) have a dysregulated transcriptional response to epidermal growth factor (show EGF ELISA Kits) stimulation
Smad2 (show SMAD2 ELISA Kits)- and Smad3-deficient bone marrow (BM) cells display reduced sensitivity to transforming growth factor-beta (TGFbeta (show TGFB1 ELISA Kits)) 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 ELISA Kits)/3 and promotes transcription of TGFbeta (show TGFB1 ELISA Kits), Smad2 (show SMAD2 ELISA Kits), Smad3, Notch2 (show NOTCH2 ELISA Kits) and Notch3 (show NOTCH3 ELISA Kits) which, in turn, results in TGFbeta (show TGFB1 ELISA Kits) and Notch (show NOTCH1 ELISA Kits) pathway activation.
Smad3 binding to the -335 hypoxia-responsive element of the COL1A2 (show COL1A2 ELISA Kits) promoter required HIF-1alpha (show HIF1A ELISA Kits) both in vitro and in kidney lysate from the disease model, suggesting formation of an HIF-1alpha (show HIF1A ELISA Kits)-Smad3 transcriptional complex. Thus, HIF-1alpha (show HIF1A ELISA Kits)-Smad3 has a novel interaction in glomerulosclerosis.
the present work provides evidence supporting a functional role of SMAD2 (show SMAD2 ELISA Kits)/3 in bovine early embryogenesis
Mechanical compression not only with physiological but also with excessive stress can activate Smad2 (show SMAD2 ELISA Kits)/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 ELISA Kits) signalling that incorporates elements of previous models together with crosstalking between Smad1 (show SMAD1 ELISA Kits)/5/8 and Smad2 (show SMAD2 ELISA Kits)/3 channels through a negative feedback loop dependent on Smad7 (show SMAD7 ELISA Kits).
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