Mouse Anti-BMPR2 Recombinant Antibody (CBT226) (V2LY-0625-LY3688)

Bone Morphogenetic Protein Receptor Type 2

On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Binds to BMP7, BMP2 and, less efficiently, BMP4. Binding is weak but enhanced by the presence of type I receptors for BMPs. Mediates induction of adipogenesis by GDF6.

Anterior/posterior pattern specification Source: BHF-UCL
Aortic valve development Source: BHF-UCL
Artery development Source: BHF-UCL
Atrial septum morphogenesis Source: BHF-UCL
Blood vessel development Source: GO_Central
Blood vessel remodeling Source: BHF-UCL
BMP signaling pathway Source: BHF-UCL
Brain development Source: Ensembl
Cellular response to BMP stimulus Source: BHF-UCL
Cellular response to growth factor stimulus Source: GO_Central
Cellular response to starvation Source: BHF-UCL
Chondrocyte development Source: AgBase
Endocardial cushion development Source: BHF-UCL
Endochondral bone morphogenesis Source: AgBase
Endothelial cell apoptotic process Source: UniProtKB
Endothelial cell proliferation Source: UniProtKB
Limb development Source: Ensembl
Lung alveolus development Source: BHF-UCL
Lymphangiogenesis Source: BHF-UCL
Lymphatic endothelial cell differentiation Source: BHF-UCL
Maternal placenta development Source: Ensembl
Mesoderm formation Source: BHF-UCL
Mitral valve morphogenesis Source: BHF-UCL
Negative regulation of BMP signaling pathway Source: Reactome
Negative regulation of cell growth Source: UniProtKB
Negative regulation of cell proliferation involved in heart valve morphogenesis Source: BHF-UCL
Negative regulation of chondrocyte proliferation Source: AgBase
Negative regulation of DNA biosynthetic process Source: BHF-UCL
Negative regulation of muscle cell differentiation Source: Ensembl
Negative regulation of systemic arterial blood pressure Source: BHF-UCL
Negative regulation of vasoconstriction Source: BHF-UCL
Osteoblast differentiation Source: Ensembl
Outflow tract morphogenesis Source: BHF-UCL
Outflow tract septum morphogenesis Source: BHF-UCL
Pharyngeal arch artery morphogenesis Source: BHF-UCL
Positive regulation of axon extension involved in axon guidance Source: Ensembl
Positive regulation of BMP signaling pathway Source: UniProtKB
Positive regulation of bone mineralization Source: BHF-UCL
Positive regulation of cartilage development Source: AgBase
Positive regulation of endothelial cell migration Source: UniProtKB
Positive regulation of endothelial cell proliferation Source: UniProtKB
Positive regulation of epithelial cell migration Source: UniProtKB
Positive regulation of ossification Source: BHF-UCL
Positive regulation of osteoblast differentiation Source: BHF-UCL
Positive regulation of pathway-restricted SMAD protein phosphorylation Source: UniProtKB
Positive regulation of transcription by RNA polymerase II Source: BHF-UCL
Protein phosphorylation Source: GO_Central
Proteoglycan biosynthetic process Source: AgBase
Pulmonary valve development Source: BHF-UCL
Regulation of cell population proliferation Source: HGNC-UCL
Regulation of lung blood pressure Source: BHF-UCL
Retina vasculature development in camera-type eye Source: BHF-UCL
Semi-lunar valve development Source: BHF-UCL
Transmembrane receptor protein serine/threonine kinase signaling pathway Source: BHF-UCL
Tricuspid valve morphogenesis Source: BHF-UCL
Venous blood vessel development Source: BHF-UCL
Ventricular septum morphogenesis Source: BHF-UCL

Cell membrane

Pulmonary hypertension, primary, 1 (PPH1): A rare disorder characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure, and death. The disease can occur from infancy throughout life and it has a mean age at onset of 36 years. Penetrance is reduced. Although familial pulmonary hypertension is rare, cases secondary to known etiologies are more common and include those associated with the appetite-suppressant drugs.
Pulmonary venoocclusive disease 1, autosomal dominant (PVOD1): A disease characterized by widespread fibrous obstruction and intimal thickening of septal veins and preseptal venules, a low diffusing capacity for carbon monoxide, occult alveolar hemorrhage, and nodular ground-glass opacities, septal lines and lymph node enlargement showed by high-resolution computed tomography of the chest. It is frequently associated with pulmonary capillary dilatation and proliferation, and is a rare and devastating cause of pulmonary hypertension.

Extracellular: 27-150 aa
Helical: 151-171 aa
Cytoplasmic: 172-1038 aa