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bmpr2b mediates BMP signaling and is required to establish left-right asymmetry.
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)
Bone morphogenetic protein 2 (show BMP2 ELISA Kits) expression increases and may contribute to partitioning of energy storage into visceral and subcutaneous AT depots
Depletion of BMPR2 mediated by a collection of miRs induced by IL6 (show IL6 ELISA Kits) and subsequent STAT3 (show STAT3 ELISA Kits) phosphorylation is a novel mechanism participating to fibroproliferative and vascular injuries in idiopathic pulmonary fibrosis.
Pathogenic BMPR2 mutations were identified in 8 of 72 (11.1%) patients with IPAH and 6 of 9 (66.7%) patients with HPAH.
In solid ameloblastoma, positive correlations were observed between the stromal and parenchymal expression of BMP-2 (show BMP2 ELISA Kits) and between the stromal expression of BMP-2 (show BMP2 ELISA Kits) and BMP-4 (show BMP4 ELISA Kits), as well as between the stromal expression of BMPR-II and BMP-4 (show BMP4 ELISA Kits) and the stromal and parenchymal expression of BMPR-II.
In a cohort with idiopathic or hereditary pulmonary arterial hypertension, a possibly associated mutation was found in 11.10% of the idiopathic cases (n = 16) and in 68.18% of the hereditary cases. There were 19 mutations found in BMPR2.
Further investigation on clinical ESCC samples and non-tumorous adjacent tissue found that tumors with triple-positive BMP6 (show BMP6 ELISA Kits), ALK2 (show ACRV1 ELISA Kits) and BMPRII had deeper growth than tumors with only BMP6 (show BMP6 ELISA Kits) expression
Case Report: sarcoid-like reaction due to pulmonary hypertension in the context of the BMPR2 mutation.
The genetic-interactions among BMPR-2, ALK-1 (show ACVRL1 ELISA Kits), and 5-HTT (show SLC6A4 ELISA Kits) polymorphisms, elevated BMP-2 (show BMP2 ELISA Kits) and 5-HT (show DDC ELISA Kits) levels and differential gene expression substantiated the strong genetic contribution in high altitude pulmonary edema pathophysiology.
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.
Bmp4 (show BMP4 ELISA Kits), Bmp7 (show BMP7 ELISA Kits) and bmpr2 signalling regulates the pre-implantation development of extra-embryonic cell lineages in the mouse embryo
Mutations in BMPR2 underlie most heritable cases and a small proportion of sporadic cases of idiopathic pulmonary arterial hypertension.
BMP9 (show GDF2 ELISA Kits) is identified as the preferred ligand for preventing apoptosis and enhancing monolayer integrity in endothelial cells from subjects with pulmonary arterial hypertension who bear mutations in the gene encoding BMPR2.
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