Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Select your species
Data suggest that Clock1a (zeige CLOCK ELISA Kits) coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 signaling; Clock1a (zeige CLOCK ELISA Kits) alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a (zeige CLOCK ELISA Kits) activates Smad3a promoter via its E-box1 element. (Clock1a (zeige CLOCK ELISA Kits) = clock circadian regulator (zeige CLOCK ELISA Kits) a; Nodal = nodal modulator 1 (zeige NOMO1 ELISA Kits); Smad3a = SMAD (zeige SMAD1 ELISA Kits) family member 3a)
Smad3 is mainly active in post-mitotic, non-proliferating cells with a role in TGF-beta (zeige TGFB1 ELISA Kits) control of zebrafish spinal cord development
Nodal signaling and mesendoderm induction depend on Smad2 (zeige SMAD2 ELISA Kits)/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2 (zeige SMAD2 ELISA Kits)/3 signaling and embryonic patterning.
although the role of Smad (zeige SMAD1 ELISA Kits) proteins in mediating Nodal signaling is well-documented, the functional characterization of Ttrap (zeige TDP2 ELISA Kits) provides insight into a novel Smad (zeige SMAD1 ELISA Kits) partner that plays an essential role in the fine-tuning of this signal transduction cascade
Smad2 (zeige 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 (zeige 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.
CRT (zeige SLC6A8 ELISA Kits) regulates TGF-beta1 (zeige TGFB1 ELISA Kits)-induced-EMT (zeige ITK ELISA Kits) through modulating Smad (zeige SMAD1 ELISA Kits) signaling
Up-regulation of miR (zeige MLXIP ELISA Kits)-195 suppressed cell migration and invasion in vitro. Smad3 was verified as a direct target of miR (zeige MLXIP ELISA Kits)-195, which was further confirmed by the inverse expression of miR (zeige MLXIP ELISA Kits)-195 and Smad3 in patients' specimens.
IL-17 (zeige IL17A ELISA Kits) can induce A549 alveolar epithelial cells to undergo epithelial-mesenchymal transition via the TGF-beta1 (zeige TGFB1 ELISA Kits) mediated Smad2 (zeige SMAD2 ELISA Kits)/3 and ERK1/2 (zeige MAPK1/3 ELISA Kits) 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 ELISA Kits) allows tumors to evade host immune responses in part through enhanced SMAD3-mediated PD-1 (zeige PDCD1 ELISA Kits) expression on tumor infiltrating lymphocytes.
Store-operated calcium entry via Orai1 (zeige ORAI1 ELISA Kits) in mesangial cells negatively regulates the TGF-beta1 (zeige TGFB1 ELISA Kits)/Smad3 signaling pathway.
SMAD2 (zeige SMAD2 ELISA Kits)/SMAD3 signaling by bone morphogenetic proteins causes disproportionate induction of HAS2 (zeige HAS2 ELISA Kits) expression and hyaluronan production in immortalized human granulosa cells.
TF-induced microvessel stabilization is regulated via PAR2 (zeige F2RL1 ELISA Kits)-SMAD3 that is indispensable for the maintenance of vascular integrity.
cPLA2alpha (zeige PLA2G4A ELISA Kits) activates PI3K (zeige PIK3CA ELISA Kits)/AKT (zeige AKT1 ELISA Kits) and inhibits Smad2 (zeige SMAD2 ELISA Kits)/3 during epithelial-mesenchymal transition of hepatocellular carcinoma cells.
stablish PPM1A (zeige PPM1A ELISA Kits) as a novel repressor of the SMAD3 pathway in renal fibrosis
E2a (zeige TCF3 ELISA Kits) is necessary to drive transcription of Smad2 (zeige SMAD2 ELISA Kits)/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
Activin A (zeige INHBA ELISA Kits) and overexpression of SMAD2 (zeige SMAD2 ELISA Kits)/3 significantly promoted expressions of porcine NANOG (zeige NANOG ELISA Kits) and OCT4 (zeige POU5F1 ELISA Kits),maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog (zeige NANOG ELISA Kits)/OCT4 (zeige POU5F1 ELISA Kits) expression.
Smad3 regulate the activity and stability of myocardin (zeige MYOCD ELISA Kits)-related transcription factor during epithelial-myofibroblast transition
SP1 (zeige SP1 ELISA Kits) and SMAD3 are required for high glucose-induced p21(WAF1 (zeige CDKN1A ELISA Kits)) gene transcription in LLC-PK1 (zeige PKLR ELISA Kits) cells.
Lnc-LFAR1 binds directly to Smad2 (zeige SMAD2 ELISA Kits)/3 and promotes transcription of TGFbeta (zeige TGFB1 ELISA Kits), Smad2 (zeige SMAD2 ELISA Kits), Smad3, Notch2 (zeige NOTCH2 ELISA Kits) and Notch3 (zeige NOTCH3 ELISA Kits) which, in turn, results in TGFbeta (zeige TGFB1 ELISA Kits) and Notch (zeige NOTCH1 ELISA Kits) pathway activation.
Smad3 binding to the -335 hypoxia-responsive element of the COL1A2 (zeige COL1A2 ELISA Kits) promoter required HIF-1alpha (zeige HIF1A ELISA Kits) both in vitro and in kidney lysate from the disease model, suggesting formation of an HIF-1alpha (zeige HIF1A ELISA Kits)-Smad3 transcriptional complex. Thus, HIF-1alpha (zeige HIF1A ELISA Kits)-Smad3 has a novel interaction in glomerulosclerosis.
These findings implicate TGF-beta (zeige TGFB1 ELISA Kits)-Smad2 (zeige 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 (zeige NFKB1 ELISA Kits), Smad3, and Nrf2 (zeige NFE2L2 ELISA Kits) at Rev-erb (zeige 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 (zeige TMEM132A ELISA Kits) in mesangial cells negatively regulates the TGF-beta1 (zeige TGFB1 ELISA Kits)/Smad3 signaling pathway.
The results uncover an important aspect of the cross-talk between TGFbeta (zeige TGFB1 ELISA Kits) and Hippo signaling, showing that TGFbeta (zeige TGFB1 ELISA Kits) induces TAZ (zeige TAZ ELISA Kits) via a Smad3-independent, p38 (zeige CRK ELISA Kits)- and MRTF-mediated and yet MRTF translocation-independent mechanism.
Data suggest that Gas5 suppresses Tgfb1 (zeige TGFB1 ELISA Kits)/Smad3 signaling in vascular smooth muscle cell differentiation from mesenchymal progenitor cells; Gas5 competitively binds Smad3 via multiple RNA Smad (zeige SMAD1 ELISA Kits)-binding elements. (Gas5 = growth arrest-specific 5 long non-coding RNA; Tgfb1 (zeige TGFB1 ELISA Kits) = transforming growth factor beta 1 (zeige 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 (zeige TGFB1 ELISA Kits).
Soluble epoxide hydrolase (zeige EPHX2 ELISA Kits) inhibitor AUDA decreases bleomycin-induced pulmonary toxicity in mice by inhibiting the p38 (zeige CRK ELISA Kits)/Smad3 signaling pathway.
A critical role for the Smad3-c-Jun (zeige JUN ELISA Kits) pathway in the regulation of Fstl1 (zeige FSTL1 ELISA Kits).
the present work provides evidence supporting a functional role of SMAD2 (zeige SMAD2 ELISA Kits)/3 in bovine early embryogenesis
Mechanical compression not only with physiological but also with excessive stress can activate Smad2 (zeige 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 (zeige TGFB1 ELISA Kits) signalling that incorporates elements of previous models together with crosstalking between Smad1 (zeige SMAD1 ELISA Kits)/5/8 and Smad2 (zeige SMAD2 ELISA Kits)/3 channels through a negative feedback loop dependent on Smad7 (zeige 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