Browse our anti-GDF2 (GDF2) Antibodies

Human Growth Differentiation Factor 2 (GDF2) interaction partners

1. INHA inhibits BMP9-induced osteogenic differentiation through blocking BMP/Smad signal and activating NF-kappaB signal in mesenchymal stem cells.

2. BMP9 acts as an endogenous inhibitor of cardiac fibrosis and improves ventricular function in heart failure.

3. BMP-9 has an effect on endothelial cells and a role in atherosclerosis [review]

4. BMP9-induced osteogenic signaling in mesenchymal stem cells requires intact Notch signaling.

5. During human periodontal ligament stem cell (hPDLSC) differentiation, BMP9 can induce osteogenesis, and MKK3/6-p38-MAPK pathway was involved in the osteogenesis and had positive regulation for osteogenesis of hPDLSCs.

6. BMP9pretreated ovarian cancer cells had downregulated expression of the epithelial marker Ecadherin, which was accompanied by an upregulation of the mesenchymal markers Ncadherin, Snail, Slug, and Twist. Taken together, the findings of the present study indicated that BMP9 conferred resistance to Cisplatin in ovarian cancer cells by inducing epithelialmesenchymal transition

7. BMP9 promoted the expression of ECM in NPCs via inhibition of Notch1 and DLL1

8. Case-control analyses reveal significant overrepresentation of rare variants in ATP13A3, AQP1 and SOX17, and provide independent validation of a critical role for GDF2 in heritable pulmonary arterial hypertension.

9. Low BMP9 expression is associated with breast cancer.

10. BMP-9 was found the most effective to induce osteogenic transdifferentiation of fat tissue in vitro

11. Epigenetic Regulation of GDF2 Suppresses Anoikis in Ovarian and Breast Epithelia.

12. levels of the angiogenesis mediators endoglin, HB-EGF, BMP-9 and FGF-2 in patients with severe sepsis and septic shock

13. BMP9 is highly expressed in bladder cancer cells. BMP9 promotes bladder cancer cell proliferation and migration through up-regulation of lncRNA UCA1.

14. Bone morphogenetic protein 9 (BMP9) was identified as a target of miR-149 in MG63 cells, and BMP9 expression was negatively correlated with miR149 level in osteosarcoma clinical samples. miR-149 promotes osteosarcoma progression via targeting BMP9.

15. The binding free energies indicate that ALK-3 preferably binds to BMP-2 instead of BMP-9. The structural analysis shows that ALK-3 binding with BMP-2 occurs in a perfectly symmetry pathway, whereas this symmetry is lost for possible ALK-3 interactions with BMP-9

16. The BMP9-induced phosphorylation of Smad1/5/8 was increased with the overexpression of RUNX3, and yet was decreased with the knockdown of RUNX3. Collectively, our findings suggest that RUNX3 is an essential modulator of the BMP9-induced osteoblast lineage differentiation of mesenchymal stem cells (MSCs).

17. BMP9 is overexpressed in hepatic stellate cells in a cohort of liver fibrosis patients.

18. our study indicates that BMP9 can inhibit the growth and metastasis of breast cancer cells, which may be related to interaction between pre-adipocytes/adipocytes and MDA-MB-231 cells via leptin signaling pathway.

19. BMP9 interacts with a hydrophobic surface of the N-terminal orphan domain of ENG, which adopts a new duplicated fold generated by circular permutation.

20. this is the first study that accurately identifies BMP9 as a profibrotic factor in fibroblasts.

Mouse (Murine) Growth Differentiation Factor 2 (GDF2) interaction partners

1. BMP9 acts as an endogenous inhibitor of cardiac fibrosis and improves ventricular function in heart failure.

2. BMP9 is a negative regulator of oval cell expansion in cholestatic injury, its deletion enhancing liver regeneration

3. BMP9 stimulates regeneration of a synovial joint that forms an articulation with the stump bone.

4. suggests that Hmox1 is likely to potentiate osteogenic differentiation and yet decrease adipogenic differentiation induced by BMP9 possibly through regulation of multiple signaling pathways

5. Low BMP9 expression is associated with breast cancer.

6. our data show that in a tumor environment BMP9 and BMP10 play different roles and thus blocking their shared receptor ALK1 is maybe not appropriate. Indeed, BMP9, but not BMP10, acts as a quiescence factor on tumor growth, lung metastasis and vessel normalization.

7. These results suggest that RUNX1 may be an essential modulator in BMP9- induced osteogenic differentiation of mesenchymal stem cells.

8. results provide a better understanding into how BMP-9 induces osteoblast differentiation and its synergy with IGF-2 at the signaling level.

9. Our findings provide a clearer understanding of the cellular pathways utilized by BMP-9 for chondrogenesis that may help improve current therapies for regenerative cartilage repair.

10. Constitutive expression of low levels of BMP-9 stabilises hepatocyte function in the healthy liver. High levels of BMP-9 cause enhanced damage upon acute or chronic injury.

11. Notch signaling may play an important role in BMP9-induced osteogenesis and angiogenesis. It's conceivable that simultaneous activation of the BMP9 and Notch pathways should efficiently couple osteogenesis and angiogenesis of MSCs for successful bone tissue engineering.

12. Western blot analysis demonstrated that following BMP2 and BMP7 cotransfection of MC3T3E1 cells, the protein expression levels of BMP2, BMP4, BMP6, BMP7, BMP9 and Wnt3a were increased compared with control cells

13. he results of the present study demonstrated that BMP9 promoted the osteoclast differentiation of osteoclast precursors via binding to the ALK1 receptor on the cell surface, and inhibiting the ERK1/2 signaling pathways in the cell

14. that Dkk1 negatively regulates BMP9-induced osteogenic differentiation.

15. Data show athat beta-catenin can be activated by bone morphogenetic protein 9 (BMP9) and the activation of beta-catenin plays an important role in the differentiation of C3H10T1/2 cells into cardiomyocyte-like cells induced by BMP9.

16. miR23b inhibits BMP9induced C2C12 myoblast osteogenesis via targeting of the Runx2 gene, acting as a suppressor.

17. We have established a producer line that stably expresses a high level of active BMP9 protein. Such producer line should be a valuable resource for generating biologically active BMP9 protein for studying BMP9 signaling

18. Data show that microRNA miR-21 was significantly upregulated by bone morphogenetic protein 9 (BMP9) during the osteogenesis the multilineage cells (MMCs) by suppressing Smad7 protein.

19. Hh signaling is involved and plays a regulatory role in the osteogenic differentiation of MSCs induced by BMP9.

20. data indicate that BMP9 and BMP13 (BMP9 might be more effective) promoted the differentiation of C3H10T1/2 cells into cardiomyocyte-like cells