anti-SMAD2 (SMAD2) Antikörper

Human SMAD, Mothers Against DPP Homolog 2 (SMAD2) Interaktionspartner

1. the results of the present study indicated that miR4865p was upregulated in Osteoarthritis and may inhibit chondrocyte proliferation and migration by suppressing SMAD2.

2. relevance of the discovered Sirt1 (zeige SIRT1 Antikörper)-Smad2 interaction for the regulation of TGFbeta (zeige TGFB1 Antikörper)-dependent gene transcription

3. Our present study indicated that S100A11 (zeige S100A11 Antikörper) promotes EMT (zeige ITK Antikörper) through accumulation of TGF-beta1 (zeige TGFB1 Antikörper) expression, and TGF-beta1 (zeige TGFB1 Antikörper)-induced upregulation of p-SMAD2 and 3.

4. Compared with the control, miR (zeige MLXIP Antikörper)-340 was significantly lower in the serum of hepatocellular carcinoma patients (p<0.01). miR (zeige MLXIP Antikörper)-340 was lower in HCC (zeige FAM126A Antikörper) tissues than in adjacent; however, DcR3 (zeige TNFRSF6B Antikörper), TGF-beta1 (zeige TGFB1 Antikörper) and Smad2 were higher.

5. the results of the present study indicated that miR2145p may promote the adipogenic differentiation of BMSCs through regulation of the TGFbeta (zeige TGFB1 Antikörper)/Smad2/COL4A1 (zeige COL4A1 Antikörper) signaling pathway, and potentially may be used to develop a novel drug for postmenopausal osteoporosis.

6. High SMAD2 expression is associated with fibrosis in chronic pancreatitis and pancreatic cancer.

7. 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.

8. We found that ITZ treatment was efficient in suppressing EMT (zeige ITK Antikörper) 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 Antikörper) as well as the invasion and migration of pancreatic cancer cells

9. SMAD2/3 interactome reveals that TGFbeta (zeige TGFB1 Antikörper) controls m(6)A mRNA methylation in pluripotency

10. 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.

Cow (Bovine) SMAD, Mothers Against DPP Homolog 2 (SMAD2) Interaktionspartner

1. the present work provides evidence supporting a functional role of SMAD2/3 in bovine early embryogenesis

2. 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.

3. a detailed computational model for TGF-beta (zeige TGFB1 Antikörper) signalling that incorporates elements of previous models together with crosstalking between Smad1 (zeige SMAD1 Antikörper)/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7 (zeige SMAD7 Antikörper).

Pig (Porcine) SMAD, Mothers Against DPP Homolog 2 (SMAD2) Interaktionspartner

1. Activin A (zeige INHBA Antikörper) and overexpression of SMAD2/3 significantly promoted expressions of porcine NANOG (zeige NANOG Antikörper) and OCT4 (zeige POU5F1 Antikörper),maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog (zeige NANOG Antikörper)/OCT4 (zeige POU5F1 Antikörper) expression.

Zebrafish SMAD, Mothers Against DPP Homolog 2 (SMAD2) Interaktionspartner

1. The non-Smad (zeige SMAD1 Antikörper) JNK (zeige MAPK8 Antikörper) signaling pathway, which is downstream of Nodal signaling, regulates nuclear movement independently of the Smad (zeige SMAD1 Antikörper) pathway, and this nuclear movement is associated with Smad (zeige SMAD1 Antikörper) signal transduction toward the nucleus.

2. The results of this study found that Bptf (zeige BPTF Antikörper) and TGF-beta (zeige TGFB1 Antikörper)/Smad2 mediate nucleosome remodeling to regulate wnt8a (zeige WNT8A Antikörper) expression and hence neural posteriorization.

3. Smad2 and Eomesodermin (zeige EOMES Antikörper) a (Eomesa (zeige EOMES Antikörper)) bind common genomic regions proximal to genes involved in mesoderm and endoderm formation, suggesting Eomesa (zeige EOMES Antikörper) forms a general component of the Smad2 signalling complex in zebrafish.

4. These results reveal that kinesin-mediated transport of Smad2 along microtubules to the receptors is an essential step in ligand-induced Smad2 activation.

5. 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

6. 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.

7. Smad2/3 activities play important roles not only in mesendodermal development but also in neural development during early vertebrate embryogenesis

Xenopus laevis SMAD, Mothers Against DPP Homolog 2 (SMAD2) Interaktionspartner

1. Grg4 (zeige TLE4 Antikörper) occupancy at the Xnr1 (zeige NODAL Antikörper) enhancer significantly decreases with Smad2 overexpression.Nodal-activated Smad2 physically displaces Grg4 (zeige TLE4 Antikörper) from FoxH1 (zeige FOXH1 Antikörper) at the Xnr1 (zeige NODAL Antikörper) enhancer, an essential feature of the transcriptional switch mechanism.

2. E2a (zeige TCF3 Antikörper) is necessary to drive transcription of Smad2/3 target genes, including critical regulators of dorsal cell fate and morphogenesis

3. GDF11 (zeige GDF11 Antikörper) has a central role in the activation of Smad2 phosphorylation in tailbud stage Xenopus embryos.

4. 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.

Mouse (Murine) SMAD, Mothers Against DPP Homolog 2 (SMAD2) Interaktionspartner

1. The expression of Toll (zeige TLR4 Antikörper)-like receptor (TLR)4 (zeige TLR4 Antikörper) and NF-kappaB p50 (zeige NFKB1 Antikörper) 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 Antikörper)/Smad2 and TLR4 (zeige TLR4 Antikörper)/NF-kappaB p50 (zeige NFKB1 Antikörper) pathways.

2. both ERK (zeige EPHB2 Antikörper) 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.

3. Activin (zeige Actbeta Antikörper) signaling through SMAD2/3 in retinal progenitor cells regulates expression of transcription factors involved in cell type determination and promotes photoreceptor lineage specification.

4. Kidney samples from patients with advanced stages of diabetic nephropathy showed elevated pSmad2 staining whereas db/db (zeige LEPR Antikörper) 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 Antikörper) model with regards to Smad (zeige SMAD1 Antikörper) signaling pathway.

5. Results suggest that Smad2/3 linker threonine phosphorylation is expressed during acinar-ductal metaplasia.

6. NODAL/Activin (zeige Actbeta Antikörper) signaling induces dramatic chromatin landscape changes, and a dynamic transcriptional network regulated by SMAD2, acting via multiple mechanisms.

7. Blocking Smad2/3 signaling in pluripotent stem cells results in epigenetic changes that enhance the capacity for endoderm differentiation.

8. cells expressing mutant huntingtin (zeige HTT Antikörper) have a dysregulated transcriptional response to epidermal growth factor (zeige EGF Antikörper) stimulation

9. Smad2- and Smad3 (zeige SMAD3 Antikörper)-deficient bone marrow (BM) cells display reduced sensitivity to transforming growth factor-beta (TGFbeta (zeige TGFB1 Antikörper)) inhibition.

10. Data (including data from studies using knockout mice) suggest Garp/Lrrc32 (zeige LRRC32 Antikörper) is involved in up-regulation of Tgfb3 (zeige TGFB3 Antikörper) and is essential for embryogenesis of palate; Garp (zeige LRRC32 Antikörper) 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 Antikörper) = glycoprotein A repetitions predominant (zeige LRRC32 Antikörper) protein; Tgfb3 (zeige TGFB3 Antikörper) = transforming growth factor beta 3 (zeige TGFB3 Antikörper))