SMAD Family Member 9 (SMAD9) ELISA Kits

Human SMAD Family Member 9 (SMAD9) Interaktionspartner

1. The SNPs of the rs6435156 and rs1048829 locus in the BMPR2 gene, the rs121909287 loci in the ACVRL1 gene, and the rs397514716 locus in the SMAD9 gene were associated with a risk of essential hypertension (EH) in Han Chinese.

2. Our results exclude a significant role for the SMAD9v90m mutation in juvenile polyposis syndrome

3. Differential expression of TGF-beta superfamily members and role of Smad1/5/9-signalling in chondral versus endochondral chondrocyte differentiation.

4. Mutations in SMAD9 gene encoding for transforming growth factor (TGF)-[beta] superfamily have been identified in Pulmonary Arterial Hypertension.

5. Phosphorylated Smad1/5/8/9 specifically bound to the BREs of Smad8/9 gene. The present study reveals that Smad8/9 is a unique R-Smad regulated through the BMP pathway at the mRNA level.

6. Case Report: hamartomatous olyposis and gastrointestinal ganglioneuromas with SMAD9 germline mutation that reduces PTEN expression.

7. 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.

8. ATP production by NaF promotes hypertrophy-like changes via activation of phospho-Smad8

9. TNF activated NF-kappaB pathway and inhibited the phosphorylation of Smad 1/5/8 and BMP-2-induced osteoblastic differentiation in BMMSCs

10. CREBZF, a novel Smad8-binding protein.

11. Data suggest that Smads 1, 5 and 8 as potential prognostic markers and therapeutic targets for mTOR inhibition therapy of prostate cancer.

12. Endoglin promotes transforming growth factor beta-mediated Smad 1/5/8 signaling and inhibits endothelial cell migration through its association with GIPC

13. Study described the first mutation in SMAD8 in a patient with IPAH, and suggested the involvement of SMAD8 in the pathogenesis of PAH.

14. 5-HT transactivates the serine kinase receptor, BMPR 1A, to activate Smads 1/5/8 via Rho and Rho kinase in in bovine and human pulmonary artery smooth muscle cells

15. increases of p16(INK4a) and p21(WAF1/cip1) expression in response to BMP4 were mediated by the Smad1/5/8 signaling pathway.

Mouse (Murine) SMAD Family Member 9 (SMAD9) Interaktionspartner

1. Sphingosine 1 phosphate also up-regulated runt-related transcription factor 2 (Runx2) expression through S1PR2/RhoA/ROCK/Smad1/5/8 signaling.

2. Phosphorylated Smad1/5/8/9 specifically bound to the BREs of Smad8/9 gene. The present study reveals that Smad8/9 is a unique R-Smad regulated through the BMP pathway at the mRNA level.

3. BetA can enhance in vivo osteogenic potentials of BMP2, possibly via stimulating Smad 1/5/8 and p38 pathways, and combination of both agents can be considered as a therapeutic strategy for bone diseases.

4. findings suggest that Smad9 is a new type of transcriptional regulator in BMP signaling.

5. The findings demonstrate for the first time that KMUP-1 can promote osteoblast maturation and differentiation in vitro via BMP-2/Smad1/5/8 and Wnt/beta-catenin pathways.

6. Data indicate that PDGF-AA promotes mesenchymal stem cel migration via bone morphogenetic protein 2 (BMP2)-smad proteins smad1/5/8 activation requires lysosome-mediated degradation of PDGF alpha Receptor (PDGFRalpha).

7. our data suggest a pivotal role for canonical BMP signaling demonstrating distinguished nonoverlapping function of pSmad8 with pSmad1 and pSmad5 in hfSCs regulation and hair morphogenesis but a redundant role in adult hair progenitors differentiation.

8. Data show that HtrA1 is produced during osteoclastogenesis, and negatively regulates osteoblast differentiation, osteoblast differentiation and BMP2-induced Smad1/5/8, ERK1/2 and p38 phosphorylation in pre-osteoblasts.

9. FGF2 inhibited BMP9-induced osteogenic differentiation by blocking BMP9-induced Smads signaling and subsequently reducing Smads dependent up-regulation of ALK1 and ALK2 in mesenchymal stem cells.

10. 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.

11. BMP4-mediated signaling in adult mouse ovary-derived oogonial stem cells cultured in vitro drives differentiation of these cells into oocytes through Smad1/5/8 activation and transcriptional up-regulation of key meiosis-initiating genes.

12. Endogenous FGF2 is necessary for BMP-2 induced nuclear accumulation and co-localization of Runx-2 and phospho-Smads1/5/8.

13. Smad8/BMP2-engineered mesenchymal stem cells induce accelerated recovery of the biomechanical properties of the Achilles tendon

14. ALK5 phosphorylates endoglin on Ser 646 & 649 in endothelial cells. Losing pSer646 prevents inhibition of TGF-beta-induced Smad1/5/8 signaling & cell migration. Losing both pSer646 & pSer649 prevents inhibition of BMP-9-mediated Smad1/5/8 signaling.

15. Dynamic regulation of Smad expression during mesenchyme to epithelium transition in the metanephric kidney.

16. Smad8 has critical function in the development of the mammalian central nervous system.

17. results suggest that BMP2/BMP4 signalling through SMAD 8 is required for transcriptional activation of the mouse Msx1 gene

18. we demonstrate that BMP-2, -5, and -7 stimulate receptor-activated Smad1, 5, and 8, which in turn causes oligomerization of Smad4 in the nucleus.

19. Initially expressed only in the visceral yolk sac endoderm and shows a highly restricted pattern of expression in the embryo proper at later stages.

20. Data show that Smad8 expression is ubiquitous during testis development but becomes cell-specific in the adult.

Cow (Bovine) SMAD Family Member 9 (SMAD9) Interaktionspartner

1. 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.