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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.
Particularly, galangin effectively inhibits phosphorylation of the Thr (zeige TRH Proteine)-179 site at Smad3 linker region through suppression of CDK4 (zeige CDK4 Proteine) phosphorylation. Thus, galangin can be a promising candidate as a selective inhibitor to suppress phosphorylation of Smad3 linker region.
CRT (zeige SLC6A8 Proteine) regulates TGF-beta1 (zeige TGFB1 Proteine)-induced-EMT (zeige ITK Proteine) through modulating Smad (zeige SMAD1 Proteine) signaling
Up-regulation of miR (zeige MLXIP Proteine)-195 suppressed cell migration and invasion in vitro. Smad3 was verified as a direct target of miR (zeige MLXIP Proteine)-195, which was further confirmed by the inverse expression of miR (zeige MLXIP Proteine)-195 and Smad3 in patients' specimens.
IL-17 can induce A549 alveolar epithelial cells to undergo epithelial-mesenchymal transition via the TGF-beta1 mediated Smad2/3 and ERK1/2 activation
In human primary tubular epithelial cells, inhibition of HIF sensing prolylhydroxylases by DMOG or exposure of the cells to hypoxia upregulated Smad3 expression and enhanced its translocation to the nucleus.
Findings demonstrate that TGFbeta1 (zeige TGFB1 Proteine) allows tumors to evade host immune responses in part through enhanced SMAD3-mediated PD-1 (zeige PDCD1 Proteine) expression on tumor infiltrating lymphocytes.
Store-operated calcium entry via Orai1 in mesangial cells negatively regulates the TGF-beta1 (zeige TGFB1 Proteine)/Smad3 signaling pathway.
SMAD2 (zeige SMAD2 Proteine)/SMAD3 signaling by bone morphogenetic proteins causes disproportionate induction of HAS2 (zeige HAS2 Proteine) expression and hyaluronan production in immortalized human granulosa cells.
TF-induced microvessel stabilization is regulated via PAR2 (zeige F2RL1 Proteine)-SMAD3 that is indispensable for the maintenance of vascular integrity.
cPLA2alpha (zeige PLA2G4A Proteine) activates PI3K (zeige PIK3CA Proteine)/AKT (zeige AKT1 Proteine) and inhibits Smad2 (zeige SMAD2 Proteine)/3 during epithelial-mesenchymal transition of hepatocellular carcinoma cells.
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
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.
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.
Smad3 binding to the -335 hypoxia-responsive element of the COL1A2 (zeige COL1A2 Proteine) promoter required HIF-1alpha (zeige HIF1A Proteine) both in vitro and in kidney lysate from the disease model, suggesting formation of an HIF-1alpha (zeige HIF1A Proteine)-Smad3 transcriptional complex. Thus, HIF-1alpha (zeige HIF1A Proteine)-Smad3 has a novel interaction in glomerulosclerosis.
These findings implicate TGF-beta (zeige TGFB1 Proteine)-Smad2 (zeige SMAD2 Proteine)/3 signaling in activated tissue-resident cardiac fibroblasts as principal mediators of the fibrotic response.
Unexpectedly, a complex damage signal promotes co-localization of NF-kappaB (zeige NFKB1 Proteine), Smad3, and Nrf2 (zeige NFE2L2 Proteine) at Rev-erb (zeige NR1D2 Proteine)-sensitive enhancers and drives expression of genes characteristic of multiple polarization states in the same cells.
Store-operated calcium entry via Orai1 (zeige TMEM132A Proteine) in mesangial cells negatively regulates the TGF-beta1 (zeige TGFB1 Proteine)/Smad3 signaling pathway.
The results uncover an important aspect of the cross-talk between TGFbeta (zeige TGFB1 Proteine) and Hippo signaling, showing that TGFbeta (zeige TGFB1 Proteine) induces TAZ (zeige TAZ Proteine) via a Smad3-independent, p38 (zeige CRK Proteine)- and MRTF-mediated and yet MRTF translocation-independent mechanism.
Data suggest that Gas5 suppresses Tgfb1 (zeige TGFB1 Proteine)/Smad3 signaling in vascular smooth muscle cell differentiation from mesenchymal progenitor cells; Gas5 competitively binds Smad3 via multiple RNA Smad (zeige SMAD1 Proteine)-binding elements. (Gas5 = growth arrest-specific 5 long non-coding RNA; Tgfb1 (zeige TGFB1 Proteine) = transforming growth factor beta 1 (zeige TGFB1 Proteine); Smad3 = MAD homolog 3 protein)
point mutant that was unable to bind pSMAD3 proved ineffective. These findings indicate that specifically targeting pSMAD3 can ameliorate both the direct and indirect fibroproliferative actions of TGF-beta (zeige TGFB1 Proteine).
Soluble epoxide hydrolase (zeige EPHX2 Proteine) inhibitor AUDA decreases bleomycin-induced pulmonary toxicity in mice by inhibiting the p38 (zeige CRK Proteine)/Smad3 signaling pathway.
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