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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 (Montrer IRF6 Kits ELISA) through an increase in TLR4 (Montrer TLR4 Kits ELISA), E-selectin (Montrer SELE Kits ELISA), and VCAM-1 (Montrer VCAM1 Kits ELISA) and ultimately through enhanced leukocyte recruitment.
Data suggest BMP9/GDF2 and BMP10 (Montrer BMP10 Kits ELISA) synergize with TNFA (Montrer TNF Kits ELISA) to increase monocyte recruitment to vascular endothelial cells; process appears to be mediated mainly via ALK2/ACVR1 (Montrer ACRV1 Kits ELISA) (which exhibits protein kinase (Montrer CDK7 Kits ELISA) activity). These studies used in vitro flow monocyte adhesion assay. (BMP9 = growth differentiation factor 2; BMP10 (Montrer BMP10 Kits ELISA) = bone morphogenetic protein 10 (Montrer BMP10 Kits ELISA); TNFA (Montrer TNF Kits ELISA) = tumor necrosis factor alpha (Montrer TNF Kits ELISA); ALK2/ACVR1 (Montrer ACRV1 Kits ELISA) = activin A receptor type 1 (Montrer ACRV1 Kits ELISA))
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.
circulating levels significantly decreased in type 2 diabetes mellitus patients and associated with glucose homoeostasis and insulin (Montrer INS Kits ELISA) sensitivity
the data identify MxA (Montrer MX1 Kits ELISA) as a novel stimulator of BMP4 (Montrer BMP4 Kits ELISA) and BMP9 transcriptional signaling, and suggest it to be a candidate IFN-alpha (Montrer IFNA Kits ELISA)-inducible mechanism that might have a protective role against development of pulmonary arterial hypertension and other vascular diseases.
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 (Montrer IGF1 Kits ELISA) 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 (Montrer PPARG Kits ELISA).
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.
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.
Notch (Montrer NOTCH1 Kits ELISA) signaling may play an important role in BMP9-induced osteogenesis and angiogenesis. It's conceivable that simultaneous activation of the BMP9 and Notch (Montrer NOTCH1 Kits ELISA) pathways should efficiently couple osteogenesis and angiogenesis of MSCs for successful bone tissue engineering.
Western blot analysis demonstrated that following BMP2 (Montrer BMP2 Kits ELISA) and BMP7 (Montrer BMP7 Kits ELISA) cotransfection of MC3T3E1 cells, the protein expression levels of BMP2 (Montrer BMP2 Kits ELISA), BMP4 (Montrer BMP4 Kits ELISA), BMP6 (Montrer BMP6 Kits ELISA), BMP7 (Montrer BMP7 Kits ELISA), BMP9 and Wnt3a (Montrer WNT3A Kits ELISA) were increased compared with control cells
he results of the present study demonstrated that BMP9 promoted the osteoclast differentiation of osteoclast precursors via binding to the ALK1 (Montrer ACVRL1 Kits ELISA) receptor on the cell surface, and inhibiting the ERK1/2 (Montrer MAPK1/3 Kits ELISA) signaling pathways in the cell
that Dkk1 (Montrer DKK1 Kits ELISA) negatively regulates BMP9-induced osteogenic differentiation.
Data show athat beta-catenin (Montrer CTNNB1 Kits ELISA) can be activated by bone morphogenetic protein 9 (BMP9) and the activation of beta-catenin (Montrer CTNNB1 Kits ELISA) 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 (Montrer RUNX2 Kits ELISA) 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 (Montrer MLXIP Kits ELISA)-21 was significantly upregulated by bone morphogenetic protein 9 (BMP9) during the osteogenesis the multilineage cells (MMCs) by suppressing Smad7 (Montrer SMAD7 Kits ELISA) protein.
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