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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.
Store-operated calcium entry via Orai1 (show ORAI1 ELISA Kits) in mesangial cells negatively regulates the TGF-beta1 (show TGFB1 ELISA Kits)/Smad3 signaling pathway.
SMAD2 (show SMAD2 ELISA Kits)/SMAD3 signaling by bone morphogenetic proteins causes disproportionate induction of HAS2 (show HAS2 ELISA Kits) expression and hyaluronan production in immortalized human granulosa cells.
TF-induced microvessel stabilization is regulated via PAR2 (show F2RL1 ELISA Kits)-SMAD3 that is indispensable for the maintenance of vascular integrity.
cPLA2alpha (show PLA2G4A ELISA Kits) activates PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits) and inhibits Smad2 (show SMAD2 ELISA Kits)/3 during epithelial-mesenchymal transition of hepatocellular carcinoma cells.
stablish PPM1A (show PPM1A ELISA Kits) as a novel repressor of the SMAD3 pathway in renal fibrosis
Methylation in SMAD3 was selectively increased in asthmatic children of asthmatic mothers and was associated with childhood asthma risk
a direct crosstalk between the STAT3 (show STAT3 ELISA Kits) and Smad3 signaling pathways that may contribute to tumor development and inflammation.
It is reported here that TGF-beta (show TGFB1 ELISA Kits) directly regulates alternative splicing of cancer stem cell marker CD44 (show CD44 ELISA Kits) through a phosphorylated threonine179 of SMAD3-mediated interaction with RNA-binding protein (show PTBP1 ELISA Kits) PCBP1 (show PCBP1 ELISA Kits).
Bcl-3 (show BCL3 ELISA Kits) knockdown enhanced the degradation of Smad3 but not Smad2 (show SMAD2 ELISA Kits) following TGFbeta (show TGFB1 ELISA Kits) treatment.
miR (show MLXIP ELISA Kits)-206 and miR (show MLXIP ELISA Kits)-140, as tumor suppressors, induced lung adenocarcinoma cell death and inhibited cell proliferation by modifying oncogenic TRIB2 (show TRIB2 ELISA Kits) promoter activity through p-Smad3.
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
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.
These findings implicate TGF-beta (show TGFB1 ELISA Kits)-Smad2 (show SMAD2 ELISA Kits)/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 (show NFKB1 ELISA Kits), Smad3, and Nrf2 (show NFE2L2 ELISA Kits) at Rev-erb (show NR1D2 ELISA Kits)-sensitive enhancers and drives expression of genes characteristic of multiple polarization states in the same cells.
Store-operated calcium entry via Orai1 (show TMEM132A ELISA Kits) in mesangial cells negatively regulates the TGF-beta1 (show TGFB1 ELISA Kits)/Smad3 signaling pathway.
The results uncover an important aspect of the cross-talk between TGFbeta (show TGFB1 ELISA Kits) and Hippo signaling, showing that TGFbeta (show TGFB1 ELISA Kits) induces TAZ (show TAZ ELISA Kits) via a Smad3-independent, p38 (show CRK ELISA Kits)- and MRTF-mediated and yet MRTF translocation-independent mechanism.
Data suggest that Gas5 suppresses Tgfb1 (show TGFB1 ELISA Kits)/Smad3 signaling in vascular smooth muscle cell differentiation from mesenchymal progenitor cells; Gas5 competitively binds Smad3 via multiple RNA Smad (show SMAD1 ELISA Kits)-binding elements. (Gas5 = growth arrest-specific 5 long non-coding RNA; Tgfb1 (show TGFB1 ELISA Kits) = transforming growth factor beta 1 (show TGFB1 ELISA Kits); 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 (show TGFB1 ELISA Kits).
Soluble epoxide hydrolase (show EPHX2 ELISA Kits) inhibitor AUDA decreases bleomycin-induced pulmonary toxicity in mice by inhibiting the p38 (show CRK ELISA Kits)/Smad3 signaling pathway.
A critical role for the Smad3-c-Jun (show JUN ELISA Kits) pathway in the regulation of Fstl1 (show FSTL1 ELISA Kits).
Mirtazapine suppressed 5-HT (show DDC ELISA Kits)-mediated TGF-beta1 (show TGFB1 ELISA Kits)/Smad3 and ERK1/2 (show MAPK1/3 ELISA Kits) signaling pathways as well as oxidative stress that contribute to the progression of liver fibrosis.
These results suggest that Nedd9 (show NEDD9 ELISA Kits) is a Smad2 (show SMAD2 ELISA Kits)/3 target gene implicated in RANKL (show TNFSF11 ELISA Kits)-induced osteoclastogenesis.
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