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The protein encoded by GDF2 is a member of the bone morphogenetic protein (BMP) family and the TGF-beta superfamily. Additionally we are shipping GDF2 Kits (59) and GDF2 Proteins (21) and many more products for this protein.
Showing 10 out of 82 products:
Human Polyclonal GDF2 Primary Antibody for IHC (p), WB - ABIN388817
Herrera, van Dinther, Ten Dijke, Inman: Autocrine bone morphogenetic protein-9 signals through activin receptor-like kinase-2/Smad1/Smad4 to promote ovarian cancer cell proliferation. in Cancer research 2009
Show all 5 references for ABIN388817
Human Polyclonal GDF2 Primary Antibody for EIA, IHC (p) - ABIN357458
Majumdar, Wang, Morris: BMP-2 and BMP-9 promotes chondrogenic differentiation of human multipotential mesenchymal cells and overcomes the inhibitory effect of IL-1. in Journal of cellular physiology 2001
Show all 3 references for ABIN357458
Human Polyclonal GDF2 Primary Antibody for ELISA - ABIN449713
Scharpfenecker, van Dinther, Liu, van Bezooijen, Zhao, Pukac, Löwik, ten Dijke: BMP-9 signals via ALK1 and inhibits bFGF-induced endothelial cell proliferation and VEGF-stimulated angiogenesis. in Journal of cell science 2007
Human Polyclonal GDF2 Primary Antibody for WB - ABIN4256550
David, Mallet, Keramidas, Lamandé, Gasc, Dupuis-Girod, Plauchu, Feige, Bailly: Bone morphogenetic protein-9 is a circulating vascular quiescence factor. in Circulation research 2008
BMP9 inhibited the proliferation and migration of the A549 cells.
his study shows that BMP9 inhibition is associated with Osteosarcoma (OS) development and that enhanced expression of BMP9 may be a potential treatment method for OS
IGF1 (show IGF1 Antibodies) can enhance BMP9-induced osteogenic differentiation in mesenchymal stem cells.
In ovarian and breast epithelial cells, epigenetic regulation of GDF2 suppresses anoikis.
BMP9 also influenced the expression of PPARgamma (show PPARG Antibodies).
Data suggest ALK1 (show ACVRL1 Antibodies) and ACVR2A (show ACVR2A Antibodies)/ACVR2B (show ACVR2B Antibodies), acting as BMP9 co-receptors, rearrange pro-domains of BMP9--pro-domain dimer complex leading to displacement of pro-domains after receptor binding, release of mature non-dimer BPM9, and activation of signaling.
DLL4 (show DLL4 Antibodies)/Notch1 (show NOTCH1 Antibodies) and BMP9 interdependent signaling induces endothelial cell quiescence via P27KIP1 (show CDKN1B Antibodies)/thrombospondin pathway.
BMP9 Crosstalk with the Hippo Pathway Regulates Endothelial Cell Matricellular and Chemokine (show CCL1 Antibodies) Responses
BMP-9 induces vascular smooth muscle cell osteogenic differentiation and calcification via ALK1 (show ACVRL1 Antibodies), Smad (show SMAD1 Antibodies) and ALP (show ALP Antibodies) dependent mechanisms.
This review summarizes the indirect connection between BMP9 and liver fibrosis, with a focus on the BMP9 signaling pathway members ALK1 (show ACVRL1 Antibodies), endoglin (show ENG Antibodies), Id1 (show ID1 Antibodies), hepcidin (show HAMP Antibodies) and Snail (show SNAI1 Antibodies). [review]
that Dkk1 (show DKK1 Antibodies) negatively regulates BMP9-induced osteogenic differentiation.
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.
miR23b inhibits BMP9induced C2C12 myoblast osteogenesis via targeting of the Runx2 (show RUNX2 Antibodies) gene, acting as a suppressor.
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
Data show that microRNA miR (show MLXIP Antibodies)-21 was significantly upregulated by bone morphogenetic protein 9 (BMP9) during the osteogenesis the multilineage cells (MMCs) by suppressing Smad7 (show SMAD7 Antibodies) protein.
Hh signaling is involved and plays a regulatory role in the osteogenic differentiation of MSCs induced by BMP9.
data indicate that BMP9 and BMP13 (show GDF6 Antibodies) (BMP9 might be more effective) promoted the differentiation of C3H10T1/2 cells into cardiomyocyte-like cells
BMP9/ALK1 (show ACVRL1 Antibodies) augmented vasculogenesis and angiogenesis, and thereby enhanced neovascularization. Thus, we suggest that BMP9/ALK1 (show ACVRL1 Antibodies) may improve the efficacy of EPC (show TCF21 Antibodies)-based therapies for treating ischemic diseases.
result was supported by the identification of the regulation by BMP9 and BMP10 (show BMP10 Antibodies) of several genes known to be involved in this process
BMP-9 induces vascular smooth muscle cell osteogenic differentiation and calcification via ALK1 (show ACVRL1 Antibodies), Smad (show SMAD1 Antibodies) and ALP (show CCL21A Antibodies) dependent mechanisms.
The protein encoded by this gene is a member of the bone morphogenetic protein (BMP) family and the TGF-beta superfamily. This group of proteins is characterized by a polybasic proteolytic processing site which is cleaved to produce a mature protein containing seven conserved cysteine residues. The members of this family are regulators of cell growth and differentiation in both embryonic and adult tissues. Studies in rodents suggest that this protein plays a role in the adult liver and in differentiation of cholinergic central nervous system neurons.
bone morphogenetic protein 9
, growth/differentiation factor 2