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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 present study highlights possible new molecular mechanisms involving progesterone, including inhibition of TGF-beta1-activated Smad signaling and TGF-beta1-regulated genes involved in bronchopulmonary dysplasia pathogenesis, which are likely to attenuate the development of BPD by inhibiting TGF-beta1-mediated airway remodeling.
Overall, these findings suggest a more dominant role for SMAD3 and SMAD4 than SMAD2 in TGFbeta-induced chondrogenesis of human bone marrow-derived mesenchymal stem cells.
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-Smad2 interaction for the regulation of TGFbeta-dependent gene transcription
Our present study indicated that S100A11 promotes EMT through accumulation of TGF-beta1 expression, and TGF-beta1-induced upregulation of p-SMAD2 and 3.
Compared with the control, miR-340 was significantly lower in the serum of hepatocellular carcinoma patients (p<0.01). miR-340 was lower in HCC tissues than in adjacent; however, DcR3, TGF-beta1 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/Smad2/COL4A1 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 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 as well as the invasion and migration of pancreatic cancer cells
It is a protein that promotes renal fibrosis in diabetic nephropathy.
SMAD2/3 interactome reveals that TGFbeta 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.
our findings demonstrated that thymoquinone suppressed the metastatic phenotype and reversed EMT of prostate cancer cells by negatively regulating the TGF-beta/Smad2/3 signaling pathway. These findings suggest that thymoquinone is a potential therapeutic agent against prostate cancer which functions by targeting TGF-beta
MicroRNA-486-5p suppresses TGFB2-induced proliferation, invasion and epithelial-mesenchymal transition of lens epithelial cells by targeting Smad2.
was found that treatment with iPSC-CM markedly reduced the proliferation of TGF-beta1-exposed cells, and the activities of TGF-beta1, Smad-2 and Smad-3. Accompanied by alterations in the expression of the indicated molecules, the lung structure of mice with PF was also markedly ameliorated.
We found expression of pSmad2/3 and Smad4 in different liver tissues, with up-regulated expression of both antibodies in chronic hepatitis C with higher stage of fibrosis and higher grade of activity.
TGFbeta and IL1beta signaling interact at the SMAD2/3 level in human primary MSC. Down-stream TGFbeta target genes were repressed by IL1beta independent of C-terminal SMAD2 phosphorylation. We demonstrate that SMAD2/3 linker modifications are required for this interplay and identified TAK1 as a crucial mediator of IL1beta-induced TGFbeta signal modulation.
Our studies provide a molecular mechanism by which UCHL5 mitigates TGFbeta-1 signaling by stabilizing Smad2/Smad3. These data indicate that UCHL5 may contribute to the pathogenesis of idiopathic pulmonary fibrosis and may be a potential therapeutic target.
we demonstrated that the downregulation of CLDN6 is regulated through promoter methylation by DNMT1, which depends on the SMAD2 pathway, and that CLDN6 is a key regulator in the SMAD2/DNMT1/CLDN6 pathway to inhibit EMT, migration and invasion of breast cancer cells
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 signalling that incorporates elements of previous models together with crosstalking between Smad1/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7.
Activin A and overexpression of SMAD2/3 significantly promoted expressions of porcine NANOG and OCT4,maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog/OCT4 expression.
The non-Smad JNK signaling pathway, which is downstream of Nodal signaling, regulates nuclear movement independently of the Smad pathway, and this nuclear movement is associated with Smad signal transduction toward the nucleus.
The results of this study found that Bptf and TGF-beta/Smad2 mediate nucleosome remodeling to regulate wnt8a expression and hence neural posteriorization.
Smad2 and Eomesodermin a (Eomesa) bind common genomic regions proximal to genes involved in mesoderm and endoderm formation, suggesting Eomesa 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 enhancer significantly decreases with Smad2 overexpression.Nodal-activated Smad2 physically displaces Grg4 from FoxH1 at the Xnr1 enhancer, an essential feature of the transcriptional switch mechanism.
E2a is necessary to drive transcription of Smad2/3 target genes, including critical regulators of dorsal cell fate and morphogenesis
GDF11 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 role of renal Smad2 in the development of tubulointerstitial fibrosis and epithelial-to-mesenchymal transition during streptozotocin-induced diabetic nephropathy by using a fibroblast-specific protein 1 (FSP1)-promotor-driven SMAD2 knockout mouse model, is reported.
The expression of Toll-like receptor (TLR)4 and NF-kappaB p50 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/Smad2 and TLR4/NF-kappaB p50 pathways.
both ERK 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 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 model with regards to Smad 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 have a dysregulated transcriptional response to epidermal growth factor stimulation
Smad2- and Smad3-deficient bone marrow (BM) cells display reduced sensitivity to transforming growth factor-beta (TGFbeta) inhibition.
Data (including data from studies using knockout mice) suggest Garp/Lrrc32 is involved in up-regulation of Tgfb3 and is essential for embryogenesis of palate; Garp knockout causes postnatal lethality, cleft palate, and decreased apoptosis and Smad2 phosphorylation in medial edge epithelial cells of palatal shelf of embryos. (Garp = glycoprotein A repetitions predominant protein; Tgfb3 = transforming growth factor beta 3)
This study tested the hypothesis that inhibins act in an autocrine manner on Leydig cells using a pre-pubertal Leydig cell line, TM3, as a model of immature Leydig cells.
Lnc-LFAR1 binds directly to Smad2/3 and promotes transcription of TGFbeta, Smad2, Smad3, Notch2 and Notch3 which, in turn, results in TGFbeta and Notch pathway activation.
P311 is a novel TGFbeta1/Smad signaling-mediated regulator of transdifferentiation in epidermal stem cells during cutaneous wound healing.
the levels of Smad2/3, P-Smad2/3 expressions were decreased, while the level of Smad7 expression was increased after treatment with osthole.
These findings implicate TGF-beta-Smad2/3 signaling in activated tissue-resident cardiac fibroblasts as principal mediators of the fibrotic response.
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.
selective inhibition of SMAD3 or CCT6A efficiently suppresses TGF-beta-mediated metastasis. Findings provide a mechanism that directs TGF-beta signaling toward its prometastatic arm and may contribute to the development of therapeutic strategies targeting TGF-beta for non-small-cell lung carcinoma.
results demonstrate that TGF-beta1-induced autophagy links beta-catenin and Smad signaling to promote epithelial-mesenchymal transition in C1.1 cells through a novel pY654-beta-catenin/p-Smad2/ILK pathway.
These results suggest that Nedd9 is a Smad2/3 target gene implicated in RANKL-induced osteoclastogenesis.
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