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bmpr2b mediates BMP signaling and is required to establish left-right asymmetry.
A burden of rare variants in BMPR2 significantly contributed to the risk of pulmonary arterial hypertension. In the remaining one family, the patient carried a pathogenic variant in a member of potassium channels, KCNK3 (show KCNK3 ELISA Kits), which was the first replicative finding of channelopathy in an Asian population.
The SMYD2 may promote BMP signaling by directly methylating BMPR2, which, in turn, stimulates BMPR2 kinase activity and activation of the BMP pathway.
This review focuses on recent advances in rescuing BMPRII expression, function or signaling to prevent and reverse pulmonary vascular remodeling in pulmonary arterial hypertension and its feasibility for clinical translation. Furthermore, it summarizes the role of described miRNAs that directly target the BMPR2 gene in blood vessels. [review]
Endothelial BMPR2 signaling in pulmonary arterial hypertension is impaired by deletion of Vegfr3 (show FLT4 ELISA Kits).
Disrupting BMPR2 impairs TGFbeta1 (show TGFB1 ELISA Kits)- and BMP4 (show BMP4 ELISA Kits)-mediated elastic fiber assembly and is of pathophysiologic significance in pulmonary arterial hypertension.
Cav-1 (show CAV1 ELISA Kits) depletion, oxidative stress-mediated reduction in BMPRII expression, and enhanced TGF-beta (show TGFB1 ELISA Kits)-driven SMAD-2 (show SMAD2 ELISA Kits)/3 signaling promote pulmonary vascular remodeling in inflamed lungs.
This analysis identified features of unaffected mutation carriers iPSC-induced pluripotent stem cell-derived endothelial cells related to modifiers of BMPR2 signaling or to differentially expressed genes.
Decreased expression of bone morphogenetic protein receptor type 2 (BMPR2) is associated with all forms of PAH, and a mutation in this receptor is seen in 70% of patients with the heritable form of PAH (HPAH), and in 20% of sporadic cases of idiopathic PAH.
HPAH-associated BMPRII mutation increases pulmonary microvascular endothelial cells adhesiveness for monocytes in response to inflammatory mediators.
BMPR2 downregulation may have a role in neuroblastoma (show ARHGEF16 ELISA Kits)
These results suggested that endogenous PTH enhanced BMPR2 expression by a cAMP/PKA/CREB pathway in osteoblasts, and increased RUNX2 expression through transduction of the BMP/pSMAD1/5/8 signaling pathway
BMPR2 gene transfer reduced TGF-beta (show TGFB1 ELISA Kits) effects on Smad2 (show SMAD2 ELISA Kits), Smad1 (show SMAD1 ELISA Kits)/5/8 and Erk1/2 (show MAPK1/3 ELISA Kits) phosphorylation in human pulmonary arterial smooth muscle cells
Deleting Bmpr2 in mouse skeletal progenitor cells impaired activin (show Actbeta ELISA Kits) signaling resulting in an increased bone formation rate and high bone mass.
The findings suggest that the mutant ALK2 (show ACRV1 ELISA Kits) related to Fibrodysplasia ossificans progressiva is enhanced by bone morphogenetic protein type II receptors via the T203-regulated phosphorylation of ALK2 (show ACRV1 ELISA Kits).
BMPR2 has tumor suppressive functions in the stroma by regulating inflammation.
Serotonin can increase ERalpha (show ESR1 ELISA Kits) expression in human pulmonary arterial smooth muscle cells and antagonism of oestrogen receptor alpha reverses serotonin-dependent PH in the mouse and increases bone morphogenetic protein receptor type 2 expression
BMPR2 preserves mitochondrial function and DNA during reoxygenation to promote endothelial cell survival and reverse pulmonary hypertension.
Members of the miR-17 family influence gastrulation by suppressing Bmpr2 expression at the primitive streak.
Report temporal regulation of BMPR2 mRNA expression in the oocyte, granulosa and theca cells of developing preovulatory follicles in the pig.
Losartan therapy was associated with persistent overexpressions of ANG II (show AGT ELISA Kits), AT2 (show AGTR2 ELISA Kits), ET-1 (show EDN1 ELISA Kits), ETB (show EDNRB ELISA Kits), and angiopoietin-1 (show ANGPT1 ELISA Kits) and with a return to normal of the BMPR-2 expression.
the miR-17-92 cluster is involved in granulosa cell proliferation and differentiation by coordinately targeting the PTEN and BMPR2 genes.
Stimulation of BMPRII promotes normal pulmonary artery endothelial cell function by activating eNOS (show NOS3 ELISA Kits).
This gene encodes a member of the bone morphogenetic protein (BMP) receptor family of transmembrane serine/threonine kinases. The ligands of this receptor are BMPs, which are members of the TGF-beta superfamily. BMPs are involved in endochondral bone formation and embryogenesis. These proteins transduce their signals through the formation of heteromeric complexes of two different types of serine (threonine) kinase receptors: type I receptors of about 50-55 kD and type II receptors of about 70-80 kD. Type II receptors bind ligands in the absence of type I receptors, but they require their respective type I receptors for signaling, whereas type I receptors require their respective type II receptors for ligand binding. Mutations in this gene have been associated with primary pulmonary hypertension, both familial and fenfluramine-associated, and with pulmonary venoocclusive disease.
bone morphogenetic protein receptor type II
, bone morphogenetic protein receptor type-2
, bone morphogenetic protein receptor type II b
, BMP type II receptor
, BMP type-2 receptor
, type II activin receptor-like kinase
, type II receptor for bone morphogenetic protein-4
, bone morphogenic protein receptor, type II (serine/threonine kinase)
, bone morphogenic protein receptor type 2