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Data suggest that Clock1a (zeige CLOCK Proteine) coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 signaling; Clock1a (zeige CLOCK Proteine) alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a (zeige CLOCK Proteine) activates Smad3a promoter via its E-box1 element. (Clock1a (zeige CLOCK Proteine) = clock circadian regulator (zeige CLOCK Proteine) a; Nodal = nodal modulator 1 (zeige NOMO1 Proteine); Smad3a = SMAD (zeige SMAD1 Proteine) family member 3a)
Smad3 is mainly active in post-mitotic, non-proliferating cells with a role in TGF-beta (zeige TGFB1 Proteine) control of zebrafish spinal cord development
Nodal signaling and mesendoderm induction depend on Smad2 (zeige SMAD2 Proteine)/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2 (zeige SMAD2 Proteine)/3 signaling and embryonic patterning.
although the role of Smad (zeige SMAD1 Proteine) proteins in mediating Nodal signaling is well-documented, the functional characterization of Ttrap (zeige TDP2 Proteine) provides insight into a novel Smad (zeige SMAD1 Proteine) partner that plays an essential role in the fine-tuning of this signal transduction cascade
Smad2 (zeige SMAD2 Proteine)/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 (zeige TGFB1 Proteine)/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 (zeige HSF1 Proteine) activity is decreased in fibrotic hearts. HSF1 (zeige HSF1 Proteine) inhibits phosphorylation and nuclear distribution of Smad3 via direct binding to Smad3. Active Smad3 blocks the anti-fibrotic effect of HSF1 (zeige HSF1 Proteine).
miR (zeige MLXIP Proteine)-142-5p plays as a negative regulator in TGF-beta (zeige TGFB1 Proteine) pathway by targeting SMAD3 and suppresses TGF-beta (zeige TGFB1 Proteine)-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 (zeige BEST1 Proteine), 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 (zeige MLXIP Proteine)-216b, and Smad3 expression was reduced by miR (zeige MLXIP Proteine)-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 (zeige NFkBP65 Proteine) activation in response to mechanical cues
Asiaticoside hindered the invasive growth of KFs (zeige GDF6 Proteine) by inhibiting the GDF-9 (zeige GDF9 Proteine)/MAPK (zeige MAPK1 Proteine)/Smad (zeige SMAD1 Proteine) 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 (zeige TGFB1 Proteine) superfamily signaling and genetic aberrations in human granulosa cell tumor development (review).
E2a (zeige TCF3 Proteine) is necessary to drive transcription of Smad2 (zeige SMAD2 Proteine)/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
HSP70 (zeige HSP70 Proteine) indirectly interacted with Smad3.
Activin A (zeige INHBA Proteine) and overexpression of SMAD2 (zeige SMAD2 Proteine)/3 significantly promoted expressions of porcine NANOG (zeige NANOG Proteine) and OCT4 (zeige POU5F1 Proteine),maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog (zeige NANOG Proteine)/OCT4 (zeige POU5F1 Proteine) expression.
Smad3 regulate the activity and stability of myocardin-related transcription factor during epithelial-myofibroblast transition
SP1 (zeige SP1 Proteine) and SMAD3 are required for high glucose-induced p21(WAF1 (zeige CDKN1A Proteine)) gene transcription in LLC-PK1 (zeige PKLR Proteine) cells.
The results provide the first evidence that upregulation of TGFb (zeige TGFB1 Proteine)/Smad3 in injured arteries induces local smooth muscle cells CXCR4 (zeige CXCR4 Proteine) expression and cell migration, and consequently intimal hyperplasia.
Blocking Smad2 (zeige SMAD2 Proteine)/3 signaling in pluripotent stem cells results in epigenetic changes that enhance the capacity for endoderm differentiation.
M1 macrophages with inhibited STAT3 (zeige STAT3 Proteine), STAT6 (zeige STAT6 Proteine) 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 (zeige TGFB1 Proteine)/Smad3 pathway is involved in autosomal recessive polycystic kidney disease.
The Smad3 and Bmal1 (zeige ARNTL Proteine) regulate p21 and S100A4 (zeige S100A4 Proteine) expression in myocardial stromal fibroblasts through TNF-alpha (zeige TNF Proteine).
cells expressing mutant huntingtin (zeige HTT Proteine) have a dysregulated transcriptional response to epidermal growth factor (zeige EGF Proteine) stimulation
Smad2 (zeige SMAD2 Proteine)- and Smad3-deficient bone marrow (BM) cells display reduced sensitivity to transforming growth factor-beta (TGFbeta (zeige TGFB1 Proteine)) 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 (zeige SMAD2 Proteine)/3 and promotes transcription of TGFbeta (zeige TGFB1 Proteine), Smad2 (zeige SMAD2 Proteine), Smad3, Notch2 (zeige NOTCH2 Proteine) and Notch3 (zeige NOTCH3 Proteine) which, in turn, results in TGFbeta (zeige TGFB1 Proteine) and Notch (zeige NOTCH1 Proteine) pathway activation.
the present work provides evidence supporting a functional role of SMAD2 (zeige SMAD2 Proteine)/3 in bovine early embryogenesis
Mechanical compression not only with physiological but also with excessive stress can activate Smad2 (zeige SMAD2 Proteine)/3P signaling, which is known to be protective for articular cartilage and to block chondrocyte terminal differentiation.
a detailed computational model for TGF-beta (zeige TGFB1 Proteine) signalling that incorporates elements of previous models together with crosstalking between Smad1 (zeige SMAD1 Proteine)/5/8 and Smad2 (zeige SMAD2 Proteine)/3 channels through a negative feedback loop dependent on Smad7 (zeige SMAD7 Proteine).
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