Browse our anti-GDF2 (GDF2) Antibodies

Human Growth Differentiation Factor 2 (GDF2) interaction partners

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

2. 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 (show LEP Antibodies) signaling pathway.

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

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

5. the combination of BMP-9 and MC-GAG stimulates chondrocytic and osteogenic differentiation of hMSCs.

6. The results demonstrate that although BMP9 alone does not influence leukocyte recruitment, it primes the vascular endothelium to mount a more intense response when challenged with LPS (show IRF6 Antibodies) through an increase in TLR4 (show TLR4 Antibodies), E-selectin (show SELE Antibodies), and VCAM-1 (show VCAM1 Antibodies) and ultimately through enhanced leukocyte recruitment.

7. Data suggest BMP9/GDF2 and BMP10 (show BMP10 Antibodies) synergize with TNFA (show TNF Antibodies) to increase monocyte recruitment to vascular endothelial cells; process appears to be mediated mainly via ALK2/ACVR1 (show ACRV1 Antibodies) (which exhibits protein kinase (show CDK7 Antibodies) activity). These studies used in vitro flow monocyte adhesion assay. (BMP9 = growth differentiation factor 2; BMP10 (show BMP10 Antibodies) = bone morphogenetic protein 10 (show BMP10 Antibodies); TNFA (show TNF Antibodies) = tumor necrosis factor alpha (show TNF Antibodies); ALK2/ACVR1 (show ACRV1 Antibodies) = activin A receptor type 1 (show ACRV1 Antibodies))

8. These results suggest that BMP9-transduced calvarial mesenchymal progenitor cells seeded in a PPCN-g thermoresponsive scaffold is capable of inducing bone formation in vivo and is an effective means of creating tissue engineered bone for critical sized defects.

9. circulating levels significantly decreased in type 2 diabetes mellitus patients and associated with glucose homoeostasis and insulin (show INS Antibodies) sensitivity

10. the data identify MxA (show MX1 Antibodies) as a novel stimulator of BMP4 (show BMP4 Antibodies) and BMP9 transcriptional signaling, and suggest it to be a candidate IFN-alpha (show IFNA Antibodies)-inducible mechanism that might have a protective role against development of pulmonary arterial hypertension and other vascular diseases.

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

1. These results suggest that RUNX1 (show RUNX1 Antibodies) may be an essential modulator in BMP9- induced osteogenic differentiation of mesenchymal stem cells.

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

3. 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.

4. 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.

5. Notch (show NOTCH1 Antibodies) signaling may play an important role in BMP9-induced osteogenesis and angiogenesis. It's conceivable that simultaneous activation of the BMP9 and Notch (show NOTCH1 Antibodies) pathways should efficiently couple osteogenesis and angiogenesis of MSCs for successful bone tissue engineering.

6. Western blot analysis demonstrated that following BMP2 (show BMP2 Antibodies) and BMP7 (show BMP7 Antibodies) cotransfection of MC3T3E1 cells, the protein expression levels of BMP2 (show BMP2 Antibodies), BMP4 (show BMP4 Antibodies), BMP6 (show BMP6 Antibodies), BMP7 (show BMP7 Antibodies), BMP9 and Wnt3a (show WNT3A Antibodies) were increased compared with control cells

7. 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

8. that Dkk1 (show DKK1 Antibodies) negatively regulates BMP9-induced osteogenic differentiation.

9. Data show athat beta-catenin (show CTNNB1 Antibodies) can be activated by bone morphogenetic protein 9 (BMP9) and the activation of beta-catenin (show CTNNB1 Antibodies) plays an important role in the differentiation of C3H10T1/2 cells into cardiomyocyte-like cells induced by BMP9.

10. miR23b inhibits BMP9induced C2C12 myoblast osteogenesis via targeting of the Runx2 (show RUNX2 Antibodies) gene, acting as a suppressor.