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Human SMAD2 Protein expressed in HEK-293 Cells - ABIN2732219
Atanelishvili, Shirai, Akter, Buckner, Noguchi, Silver, Bogatkevich: M10, a caspase cleavage product of the hepatocyte growth factor receptor, interacts with Smad2 and demonstrates antifibrotic properties in vitro and in vivo. in Translational research : the journal of laboratory and clinical medicine 2016
the results of the present study indicated that miR4865p was upregulated in Osteoarthritis and may inhibit chondrocyte proliferation and migration by suppressing SMAD2.
relevance of the discovered Sirt1 (zeige SIRT1 Proteine)-Smad2 interaction for the regulation of TGFbeta (zeige TGFB1 Proteine)-dependent gene transcription
Our present study indicated that S100A11 (zeige S100A11 Proteine) promotes EMT (zeige ITK Proteine) through accumulation of TGF-beta1 (zeige TGFB1 Proteine) expression, and TGF-beta1 (zeige TGFB1 Proteine)-induced upregulation of p-SMAD2 and 3.
Compared with the control, miR (zeige MLXIP Proteine)-340 was significantly lower in the serum of hepatocellular carcinoma patients (p<0.01). miR (zeige MLXIP Proteine)-340 was lower in HCC (zeige FAM126A Proteine) tissues than in adjacent; however, DcR3 (zeige TNFRSF6B Proteine), TGF-beta1 (zeige TGFB1 Proteine) and Smad2 were higher.
the results of the present study indicated that miR2145p may promote the adipogenic differentiation of BMSCs through regulation of the TGFbeta (zeige TGFB1 Proteine)/Smad2/COL4A1 (zeige COL4A1 Proteine) signaling pathway, and potentially may be used to develop a novel drug for postmenopausal osteoporosis.
High SMAD2 expression is associated with fibrosis in chronic pancreatitis and pancreatic cancer.
The results suggest that co-expression of active SMAD2/3 could enhance multiple types of transcription factors (TF)-based cell identity conversion and therefore be a powerful tool for cellular engineering.
We found that ITZ treatment was efficient in suppressing EMT (zeige ITK Proteine) and that the effect of ITZ was partially mediated by impaired TGF-b/SMAD2/3 signaling. The role of TGF-b/SMAD2/3 signaling in mediating the effect of ITZ was confirmed based on the results that recombinant TGF-b induced, but the TGF-b neutralizing antibody inhibited EMT (zeige ITK Proteine) as well as the invasion and migration of pancreatic cancer cells
SMAD2/3 interactome reveals that TGFbeta (zeige TGFB1 Proteine) controls m(6)A mRNA methylation in pluripotency
This study's findings provide new insights into the mechanisms of how oscillatory shear stress regulates Smad2 signaling and pro-inflammatory genes through the complex signaling networks of integrins, transforming growth factor-beta receptors, and extracellular matrices, thus illustrating the molecular basis of regional pro-inflammatory activation within disturbed flow regions in the arterial tree.
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 (zeige TGFB1 Proteine) signalling that incorporates elements of previous models together with crosstalking between Smad1 (zeige SMAD1 Proteine)/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7 (zeige SMAD7 Proteine).
Activin A (zeige INHBA Proteine) and overexpression of SMAD2/3 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.
The non-Smad (zeige SMAD1 Proteine) JNK (zeige MAPK8 Proteine) signaling pathway, which is downstream of Nodal signaling, regulates nuclear movement independently of the Smad (zeige SMAD1 Proteine) pathway, and this nuclear movement is associated with Smad (zeige SMAD1 Proteine) signal transduction toward the nucleus.
The results of this study found that Bptf and TGF-beta (zeige TGFB1 Proteine)/Smad2 mediate nucleosome remodeling to regulate wnt8a (zeige WNT8A Proteine) expression and hence neural posteriorization.
Smad2 and Eomesodermin (zeige EOMES Proteine) a (Eomesa (zeige EOMES Proteine)) bind common genomic regions proximal to genes involved in mesoderm and endoderm formation, suggesting Eomesa (zeige EOMES Proteine) 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
Grg4 occupancy at the Xnr1 (zeige NODAL Proteine) enhancer significantly decreases with Smad2 overexpression.Nodal-activated Smad2 physically displaces Grg4 from FoxH1 (zeige FOXH1 Proteine) at the Xnr1 (zeige NODAL Proteine) enhancer, an essential feature of the transcriptional switch mechanism.
E2a (zeige TCF3 Proteine) is necessary to drive transcription of Smad2/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
GDF11 (zeige GDF11 Proteine) 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.
The expression of Toll (zeige TLR4 Proteine)-like receptor (TLR)4 (zeige TLR4 Proteine) and NF-kappaB p50 (zeige NFKB1 Proteine) was also inhibited by Andro. Additionally, in vitro data confirmed that Andro treatment not only attenuated the expression of profibrotic and proinflammatory factors but also blocked the TGF-beta1 (zeige TGFB1 Proteine)/Smad2 and TLR4 (zeige TLR4 Proteine)/NF-kappaB p50 (zeige NFKB1 Proteine) pathways.
both ERK (zeige EPHB2 Proteine) and Smad2 signal pathways are involved in the activation of macrophages induced by TGF-b1 and high-ambient glucose, while there is no crosstalk shown in the process.
Activin signaling through SMAD2/3 in retinal progenitor cells regulates expression of transcription factors involved in cell type determination and promotes photoreceptor lineage specification.
Kidney samples from patients with advanced stages of diabetic nephropathy showed elevated pSmad2 staining whereas db/db (zeige LEPR Proteine) mouse kidneys surprisingly showed a decrease in pSmad2 in the tubular compartment. These results indicate a lack of translation from type 2 diabetes patient kidneys to the db/db (zeige LEPR Proteine) model with regards to Smad (zeige SMAD1 Proteine) signaling pathway.
Results suggest that Smad2/3 linker threonine phosphorylation is expressed during acinar-ductal metaplasia.
NODAL/Activin signaling induces dramatic chromatin landscape changes, and a dynamic transcriptional network regulated by SMAD2, acting via multiple mechanisms.
Blocking Smad2/3 signaling in pluripotent stem cells results in epigenetic changes that enhance the capacity for endoderm differentiation.
cells expressing mutant huntingtin (zeige HTT Proteine) have a dysregulated transcriptional response to epidermal growth factor (zeige EGF Proteine) stimulation
Smad2- and Smad3 (zeige SMAD3 Proteine)-deficient bone marrow (BM) cells display reduced sensitivity to transforming growth factor-beta (TGFbeta (zeige TGFB1 Proteine)) inhibition.
Data (including data from studies using knockout mice) suggest Garp/Lrrc32 (zeige LRRC32 Proteine) is involved in up-regulation of Tgfb3 (zeige TGFB3 Proteine) and is essential for embryogenesis of palate; Garp (zeige LRRC32 Proteine) knockout causes postnatal lethality, cleft palate, and decreased apoptosis and Smad2 phosphorylation in medial edge epithelial cells of palatal shelf of embryos. (Garp (zeige LRRC32 Proteine) = glycoprotein A repetitions predominant (zeige LRRC32 Proteine) protein; Tgfb3 (zeige TGFB3 Proteine) = transforming growth factor beta 3 (zeige TGFB3 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 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.
MAD homolog 2
, SMAD, mothers against DPP homolog 2
, Sma- and Mad-related protein 2
, mother against DPP homolog 2
, mothers against decapentaplegic homolog 2
, SMAD 2
, mothers against DPP homolog 2
, mothers against decapentaplegic-like 2
, MAD (mothers against decapentaplegic, Drosophila) homolog 2
, SMA- and MAD-related protein 2
, SMAD family member 2
, Smad 2
, mad-related protein 2
, LOW QUALITY PROTEIN: mothers against decapentaplegic homolog 2