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Human SMAD2 Kit ELISA pour Sandwich ELISA - ABIN417849
Piotrowski, Kiszałkiewicz, Górski, Antczak, Górski, Pastuszak-Lewandoska, Migdalska-Sęk, Domańska-Senderowska, Nawrot, Czarnecka, Kurmanowska, Brzeziańska-Lasota: Immunoexpression of TGF-β/Smad and VEGF-A proteins in serum and BAL fluid of sarcoidosis patients. dans BMC immunology 2015
Rat (Rattus) SMAD2 Kit ELISA pour Sandwich ELISA - ABIN432538
Kabel, Abd Elmaaboud, Albarraq: Ameliorative potential of omega 3 fatty acids and HMG-CoA reductase inhibitors on experimentally-induced non-alcoholic steatohepatitis. dans Prostaglandins, leukotrienes, and essential fatty acids 2015
The results of this study found that Bptf and TGF-beta (Montrer TGFB1 Kits ELISA)/Smad2 mediate nucleosome remodeling to regulate wnt8a (Montrer WNT8A Kits ELISA) expression and hence neural posteriorization.
Smad2 and Eomesodermin (Montrer EOMES Kits ELISA) a (Eomesa (Montrer EOMES Kits ELISA)) bind common genomic regions proximal to genes involved in mesoderm and endoderm formation, suggesting Eomesa (Montrer EOMES Kits ELISA) forms a general component of the Smad2 signalling complex in zebrafish.
These results reveal that kinesin-mediated transport of Smad2 along microtubules to the receptors is an essential step in ligand-induced Smad2 activation.
study systemically uncovers a large number of Smad2 targets in early gastrulas and suggests cooperative roles of Smad2 and other transcription factors in controlling target gene transcription
Nodal signaling and mesendoderm induction depend on Smad2/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2/3 signaling and embryonic patterning.
Smad2/3 activities play important roles not only in mesendodermal development but also in neural development during early vertebrate embryogenesis
Low SMAD2 expression is associated with progression of hepatic fibrosis.
In order to study the translation between mouse model and patients, we evaluated the signature of phosphorylated Sma- and Mad-related protein 2 (pSmad2), as molecular marker of TGF-beta/activin activity, in the kidneys of streptozotocin (STZ)-treated mice compared to that of type 1 diabetes (T1D) patients.
SMAD2/SMAD3 (Montrer SMAD3 Kits ELISA) signaling by bone morphogenetic proteins causes disproportionate induction of HAS2 (Montrer HAS2 Kits ELISA) expression and hyaluronan production in immortalized human granulosa cells.
miR (Montrer MLXIP Kits ELISA)-27a contributed to cell proliferation and invasion by inhibiting TGF-beta (Montrer TGFB1 Kits ELISA)-induced cell cycle arrest. These results suggest that miR (Montrer MLXIP Kits ELISA)-27a may function as an oncogene (Montrer RAB1A Kits ELISA) by regulating SMAD2 and SMAD4 (Montrer SMAD4 Kits ELISA) in lung cancer.
cPLA2alpha (Montrer PLA2G4A Kits ELISA) activates PI3K (Montrer PIK3CA Kits ELISA)/AKT (Montrer AKT1 Kits ELISA) and inhibits Smad2/3 during epithelial-mesenchymal transition of hepatocellular carcinoma cells.
selective inhibition of SMAD3 (Montrer SMAD3 Kits ELISA) or CCT6A (Montrer CCT6A Kits ELISA) efficiently suppresses TGF-beta (Montrer TGFB1 Kits ELISA)-mediated metastasis. Findings provide a mechanism that directs TGF-beta (Montrer TGFB1 Kits ELISA) signaling toward its prometastatic arm and may contribute to the development of therapeutic strategies targeting TGF-beta (Montrer TGFB1 Kits ELISA) for non-small-cell lung carcinoma.
In response to TGF-beta (Montrer TGFB1 Kits ELISA), RASSF1A (Montrer RASSF1 Kits ELISA) is recruited to TGF-beta (Montrer TGFB1 Kits ELISA) receptor I and targeted for degradation by the co-recruited E3 ubiquitin ligase ITCH. RASSF1A (Montrer RASSF1 Kits ELISA) degradation is necessary to permit Hippo pathway effector YAP1 (Montrer YAP1 Kits ELISA) association with SMADs and subsequent nuclear translocation of receptor-activated SMAD2.
Smad2 is a key scaffold, allowing RIN1 (Montrer RIN1 Kits ELISA) to act as a GTP (Montrer AK3 Kits ELISA) exchange factor for MFN2 (Montrer MFN2 Kits ELISA)-GTPase (Montrer RACGAP1 Kits ELISA) activation to promote mitochondrial ATP synthesis and suppress superoxide production during mitochondrial fusion.
Ang (Montrer ANG Kits ELISA) down-regulate the expression of Col (Montrer HDAC1 Kits ELISA)-I, alpha-SMA (Montrer SMN1 Kits ELISA) and TGF-beta1 (Montrer TGFB1 Kits ELISA)/Smad2/3 and subsequently inhibits fibroblast-myofibroblast transition.
The nuclear importin IPO5 (Montrer IPO5 Kits ELISA) was identified as a novel interacting protein of SMAD1 (Montrer GARS Kits ELISA). Overexpression of IPO5 (Montrer IPO5 Kits ELISA) in various cell lines specifically increases nuclear localization of BMP receptor (Montrer BMPR1A Kits ELISA)-activated SMADs (R-SMADs) confirming a functional relationship between IPO5 (Montrer IPO5 Kits ELISA) and BMP but not TGF-beta (Montrer TGFB1 Kits ELISA) R-SMADs.
Grg4 occupancy at the Xnr1 (Montrer NODAL Kits ELISA) enhancer significantly decreases with Smad2 overexpression.Nodal-activated Smad2 physically displaces Grg4 from FoxH1 (Montrer FOXH1 Kits ELISA) at the Xnr1 (Montrer NODAL Kits ELISA) enhancer, an essential feature of the transcriptional switch mechanism.
E2a (Montrer TCF3 Kits ELISA) is necessary to drive transcription of Smad2/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
GDF11 (Montrer GDF11 Kits ELISA) has a central role in the activation of Smad2 phosphorylation in tailbud stage Xenopus embryos.
XPIASy functions as an essential negative regulator of the XSmad2 pathway to ensure proper mesoderm induction at the appropriate time and in the appropriate region.
Activin A (Montrer INHBA Kits ELISA) and overexpression of SMAD2/3 significantly promoted expressions of porcine NANOG (Montrer NANOG Kits ELISA) and OCT4 (Montrer POU5F1 Kits ELISA),maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog (Montrer NANOG Kits ELISA)/OCT4 (Montrer POU5F1 Kits ELISA) expression.
the present work provides evidence supporting a functional role of SMAD2/3 in bovine early embryogenesis
Mechanical compression not only with physiological but also with excessive stress can activate Smad2/3P signaling, which is known to be protective for articular cartilage and to block chondrocyte terminal differentiation.
a detailed computational model for TGF-beta (Montrer TGFB1 Kits ELISA) signalling that incorporates elements of previous models together with crosstalking between Smad1 (Montrer SMAD1 Kits ELISA)/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7 (Montrer SMAD7 Kits ELISA).
These findings implicate TGF-beta (Montrer TGFB1 Kits ELISA)-Smad2/3 signaling in activated tissue-resident cardiac fibroblasts as principal mediators of the fibrotic response.
results demonstrate that TGF-beta1 (Montrer TGFB1 Kits ELISA)-induced autophagy links beta-catenin (Montrer CTNNB1 Kits ELISA) and Smad (Montrer SMAD1 Kits ELISA) signaling to promote epithelial-mesenchymal transition in C1.1 cells through a novel pY654-beta-catenin (Montrer CTNNB1 Kits ELISA)/p-Smad2/ILK (Montrer ILK Kits ELISA) pathway.
These results suggest that Nedd9 (Montrer NEDD9 Kits ELISA) is a Smad2/3 target gene implicated in RANKL (Montrer TNFSF11 Kits ELISA)-induced osteoclastogenesis.
In conclusion, TGF-beta (Montrer TGFB1 Kits ELISA) signaling pathway may influence liver fibrosis by incorporating with YB-1 (Montrer YBX1 Kits ELISA), indicating that YB-1 (Montrer YBX1 Kits ELISA) could be a potential target for therapies against liver fibrosis.
miR (Montrer MLXIP Kits ELISA)-27b is an anti-fibrotic microRNA that inhibits fibroblast activation by targeting TGFbeta (Montrer TGFB1 Kits ELISA) receptor 1 and SMAD2.
hese studies revealed that Smad2 plays an essential role in the development of the growth plate, that both Smads 2 and 3 inhibit Ihh (Montrer IHH Kits ELISA) expression in the neonatal growth plate, and suggested they accomplish this by binding to distinct SBEs, mediating assembly of distinct repressive complexes.
This study found evidence of increased leukocyte phosphorylated-Smad2/3 staining in both single leukocytes and platelet-leukocyte aggregates in mice that developed aortic valve stenosis, suggesting the presence of increased circulating active TGF-beta1 (Montrer TGFB1 Kits ELISA).
Data show that muscle-specific (Montrer EIF3K Kits ELISA) Smad (Montrer SMAD1 Kits ELISA) proteins Smad2/3-deficient mice exhibited significant resistance to denervation-induced muscle atrophy.
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 mediates the signal of the transforming growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation. This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4. The association with SMAD4 is important for the translocation of this protein into the nucleus, where it binds to target promoters and forms a transcription repressor complex with other cofactors. This protein can also be phosphorylated by activin type 1 receptor kinase, and mediates the signal from the activin. Alternatively spliced transcript variants have been observed for this gene.
SMAD, mothers against DPP homolog 2
, MAD (mothers against decapentaplegic, Drosophila) homolog 2
, SMA- and MAD-related protein 2
, SMAD 2
, SMAD family member 2
, mothers against DPP homolog 2
, mothers against decapentaplegic homolog 2
, MAD homolog 2
, Sma- and Mad-related protein 2
, mother against DPP homolog 2
, mothers against decapentaplegic-like 2
, Smad 2
, mad-related protein 2