Aperçu des produits pour anti-SMAD2 (SMAD2) Anticorps

Human SMAD, Mothers Against DPP Homolog 2 (SMAD2) interaction partners

1. PIM1 could interact with Smad2 or Smad3 in the nucleus and subsequently phosphorylate Smad2 and Smad3 to induce the expression of transcription factors.

2. The associations between Golgi membrane protein 73 (GP73) /transforming growth factor beta 1 (TGF-beta1)/SMAD2 protein (Smad2) and the clinic pathological features of patients with bladder cancer were explored.

3. Results revealed two pathogenic truncating variants, a splice variant, and a predicted deleterious missense variant in SMAD2 in congenital heart disease (CHD) patients suggesting two distinct phenotypes: complex CHD with or without laterality defects and other congenital anomalies, and a late-onset vascular phenotype characterized by arterial aneurysms with connective tissue abnormalities.

4. Smad proteins SMAD2 and SMAD3 are core transcription factors involved in TGF-beta signaling, and they interact with cofactors to control the expression of TGF-beta-dependent genes.

5. analysis of the structural basis for R-SMAD recognition by MAN1 using SMAD2-MAN1 and SMAD1-MAN1 complex structures

6. SMAD2 single nucleotide polymorphism rs11082639 is associated with metabolic syndrome in a Taiwanese population.

7. TGIF1 homeodomain interacts with Smad2/Smad4 MH1 domains and represses TGF-beta signaling.

8. the crucial role played by Smad2 in promoting Mst1-mediated cell apoptosis and mitochondrial stress, is reported.

9. High Smad2 expression is associated with endometrial carcinoma.

10. Study determined that SMAD2 was a direct target of miR-455, and the restoration of SMAD2 rescued cell growth and invasion that were reduced by DLEU2 knockdown or miR-455 overexpression. In addition, low miR-455 expression and high SMAD2 expression was correlated with poor patient survival.

11. Occupational nickel exposure could increase the expression of Nkx2.1 and pSmad2, which correlated with the nickel-induced oxidative damage and DNA repair change.

12. TFAP2A-AS1 was revealed to act as a miRNA sponge for miR-933 and then regulated the expression of Smad2. CONCLUSIONS Results from the present study suggest that TFAP2A-AS1 acts as a tumor suppressor in BC via the miR-933/SMAD2 axis.

13. ACVR1C/SMAD2 pathway in promoting invasion and growth of retinoblastoma

14. recruitment of the forkhead protein FOXH1 on open chromatin regions integrates the signals of Activin/Smad2 and Wnt/beta-catenin to activate the expression of the ME genes including HAS2 and ALDH3A2 Consistently, H3K27me3 decrease is enriched on open chromatin around regulatory regions

15. PSPC1 increases transforming growth factor-beta1 (TGF-beta1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-beta1 autocrine signaling, promoting epithelial mesenchymal transformation, stemness and metastasis.

16. Results show that SMAD2 expression is regulated by miR361 which directly binds to its 3'UTR, decreasing protein expression.

17. Curcumin can suppress TGF-beta1-induced CTGF expression in human gingival fibroblasts through the interruption of Smad2 signaling.

18. The important role of GP73 in regulating EMT and metastasis in HCC partly by targeting TGF-beta1/Smad2 signaling.

19. Results demonstrated that SMAD2 and SMAD3 are directly targeted by miR505 inhibiting the activity of TGFbeta signaling in prostate cancer (PCa) cells.

20. Findings suggest that TGFbeta is implicated in the pathogenesis of hereditary cerebral hemorrhage with amyloidosis-Dutch type. We found an upregulation in gene expression of several components of the TGFbeta pathway and its direct downstream signaling targets as well as a strong correlation of pSMAD2/3 deposits with cerebral amyloid angiopathy load.

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

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 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.

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

1. 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.

Zebrafish SMAD, Mothers Against DPP Homolog 2 (SMAD2) interaction partners

1. 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.

2. The results of this study found that Bptf and TGF-beta/Smad2 mediate nucleosome remodeling to regulate wnt8a expression and hence neural posteriorization.

3. 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.

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) interaction partners

1. 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.

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

3. GDF11 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) interaction partners

1. Depletion of Dicer and microRNAs may upregulate Smad2/3-related signaling pathway to enhance the progression of chronic kidney disease.

2. High Smad2 expression is associated with pulmonary fibrosis.

3. These data reveal a novel function of CD105 in beige adipocytes: maintaining their thermogenic program by regulating Smad2 signaling.

4. Our findings generate a mouse model to study the roles of SMAD2/3 in the uterus and serve to provide insight into the mechanism by which the endometrium can escape the plethora of growth regulatory proteins

5. Here the authors have demonstrated that TGF-beta/Smad signaling plays an important role in Laser-induced choroidal neovascularization formation through down-regulation of VEGF and TNF-alpha expressions.

6. SnoN plays an important in vivo role in adipocyte differentiation and white adipose tissue development in vivo by decreasing activity in the activin/Smad2 signaling pathway.

7. 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.

8. 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.

9. 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.

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

11. 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.

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

13. NODAL/Activin signaling induces dramatic chromatin landscape changes, and a dynamic transcriptional network regulated by SMAD2, acting via multiple mechanisms.

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

15. cells expressing mutant huntingtin have a dysregulated transcriptional response to epidermal growth factor stimulation

16. Smad2- and Smad3-deficient bone marrow (BM) cells display reduced sensitivity to transforming growth factor-beta (TGFbeta) inhibition.

17. 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)

18. 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.

19. 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.

20. P311 is a novel TGFbeta1/Smad signaling-mediated regulator of transdifferentiation in epidermal stem cells during cutaneous wound healing.