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Human BMPR2 Protein expressed in Wheat germ - ABIN1346791
Miyagi, Mikawa, Hasegawa, Kobayashi, Sho, Matsuyama, Sato: Bone morphogenetic protein receptor expressions in the adult rat brain. in Neuroscience 2011
bmpr2b mediates BMP signaling and is required to establish left-right asymmetry.
Fasudil inhibited leukocyte-endothelial cell interactions and vascular hyperpermeability through modulation of GRP78 and BMPR2 expression.
Heterozygous germline mutations in the gene coding bone morphogenetic receptor type 2 (BMPR2) are detectable in the majority of cases of heritable pulmonary arterial hypertension, and in approximately 20% of cases of idiopathic pulmonary arterial hypertension. [review]
Tumour necrosis factor-alpha selectively reduces BMPR-II transcription and mediates post-translational BMPR-II cleavage via the sheddases, ADAM10 and ADAM17 in pulmonary artery smooth muscle cells.
miR-23a facilitated cell proliferation and migration by targeting BMPR2/Smad1 signaling in hypoxia-induced human pulmonary artery smooth muscle cells.
we employed an shRNA-encoding lentivirus system to inhibit SPG6 expression in AML cells including NB4 and MV4-11cells. Knockdown expression of SPG6 resulted in decreased cell growth and elevated apoptosis of these leukemia cells. Notably, SPG6 deficiency resulted in higher BMPR2 expression indicating that BMPR2 signaling contributes to AML pathogenesis.
Sequencing of BMPR2, CAV1, and KCNK3 coding regions did not identify any pathogenic variants in these genes in infants with pulmonary hypoplasia and pulmonary hypertension.
The present study showed that deletion-duplication mutations in the BMPR2 or ACVRL1 genes may not be associated with non-regression of Pulmonary arterial hypertension.
BMPR2 mutation carriers are more prone to hemoptysis and that hemoptysis is closely correlated to bronchial arterial remodelling and angiogenesis; in turn, pronounced changes in the systemic vasculature correlate with increased pulmonary venous remodelling, creating a distinctive profile in pulmonary arterial hypertension patients harbouring a BMPR2 mutation.
Studying the methylation pattern of the BMPR2 promoter region in pulmonary arterial hypertension patients and controls revealed a a CpG island, suitable for methylation, in the BMPR2 promoter region, in addition to NIT-2, sex-determining region Y, and heat shock factor transcription factor binding sites.No evidence of methylation was detected in this region in patients and controls.
Mutations in the bone morphogenetic protein receptor type-2 gene (BMPR2) have been identified in patients with pulmonary arterial hypertension.
Affected mutation carriers with heritable pulmonary hypertension have hypermethylation of the BMPR2 promotor compared with their unaffected relatives.
increased BMPR2 signal transduction is linked to fragile X syndrome (FXS) and that the BMPR2-LIMK1 pathway is a putative therapeutic target in patients with FXS and possibly other forms of autism
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, 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.
Disrupting BMPR2 impairs TGFbeta1- and BMP4-mediated elastic fiber assembly and is of pathophysiologic significance in pulmonary arterial hypertension.
Cav-1 depletion, oxidative stress-mediated reduction in BMPRII expression, and enhanced TGF-beta-driven SMAD-2/3 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.
High BMPR2 expression is associated with aberrant synaptic development in mouse and Drosophila models of Fragile X syndrome.
BMPR2 deletion extended survival relative to Pten deletion alone, establishing its promoting role in BMP6-driven prostate cancer progression
Dual luciferase report assay verified that miR-3065-5p could bind to the 3'UTR of bone morphogenetic protein receptor type II (BMPR2), which dramatically increased in the beginning of odontoblastic differentiation but decreased in the terminal differentiation stage.
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 effects on Smad2, Smad1/5/8 and Erk1/2 phosphorylation in human pulmonary arterial smooth muscle cells
loss in hippocampus and forebrain impacts exploratory and anxiety-related behaviors
Deleting Bmpr2 in mouse skeletal progenitor cells impaired activin signaling resulting in an increased bone formation rate and high bone mass.
The findings suggest that the mutant ALK2 related to Fibrodysplasia ossificans progressiva is enhanced by bone morphogenetic protein type II receptors via the T203-regulated phosphorylation of ALK2.
BMPR2 has tumor suppressive functions in the stroma by regulating inflammation.
Serotonin can increase ERalpha 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, Bmp7 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 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.
These data suggest that heterozygous null BMPR2 mutations promote SRC-dependent caveolar trafficking defects in PECs and that this may contribute to pulmonary endothelial barrier dysfunction in Hereditary pulmonary arterial hypertension patients
BMPR2 expression potentiated activin A responses whereas depletion of endogenous BMPR2 with short interfering RNAs attenuated activin A-stimulated follicle-stimulating hormone beta transcription in gonadotrope-like cells.
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, AT2, ET-1, ETB, and angiopoietin-1 and with a return to normal of the BMPR-2 expression.
Inhibition of BMPR2 resulted in increased expression of ALK4 and decreased expression of PTX3, HAS2 and PTGS2.
These findings are important because Wnt, BMPR2, and Akt3 promote neurogenesis and cell survival, processes crucial for lifelong viral latency.
the miR-17-92 cluster is involved in granulosa cell proliferation and differentiation by coordinately targeting the PTEN and BMPR2 genes.
Genetic variability is an important component of the number of antral follicles in the bovine ovary.
Stimulation of BMPRII promotes normal pulmonary artery endothelial cell function by activating eNOS.
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