Mouse Anti-BMPR1A Recombinant Antibody (CBFYC-0580) (CBMAB-C0634-FY)

bone morphogenetic protein receptor, type IA

The bone morphogenetic protein (BMP) receptors are a family of transmembrane serine/threonine kinases that include the type I receptors BMPR1A and BMPR1B and the type II receptor BMPR2. These receptors are also closely related to the activin receptors, ACVR1 and ACVR2. The ligands of these receptors are members of the TGF-beta superfamily. TGF-betas and activins transduce their signals through the formation of heteromeric complexes with 2 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.

Bone Morphogenetic Protein Receptor Type 1A; Bone Morphogenetic Protein Receptor, Type IA; Serine/Threonine-Protein Kinase Receptor R5; Activin Receptor-Like Kinase 3; BMP Type-1A Receptor; EC 2.7.11.30; ACVRLK3; BMPR-1A; ALK-3

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. Receptor for BMP2, BMP4, GDF5 and GDF6. Positively regulates chondrocyte differentiation through GDF5 interaction. Mediates induction of adipogenesis by GDF6.

Atrioventricular node cell development Source: BHF-UCL
Atrioventricular valve development Source: BHF-UCL
BMP signaling pathway Source: BHF-UCL
BMP signaling pathway involved in heart development Source: BHF-UCL
Cardiac conduction system development Source: BHF-UCL
Cardiac right ventricle morphogenesis Source: BHF-UCL
Cellular response to BMP stimulus Source: BHF-UCL
Cellular response to growth factor stimulus Source: GO_Central
Chondrocyte differentiation Source: Ensembl
Developmental growth Source: Ensembl
Dorsal/ventral axis specification Source: Ensembl
Dorsal/ventral pattern formation Source: GO_Central
Dorsal aorta morphogenesis Source: BHF-UCL
Ectoderm development Source: Ensembl
Embryonic digit morphogenesis Source: Ensembl
Embryonic organ development Source: BHF-UCL
Endocardial cushion formation Source: BHF-UCL
Endocardial cushion morphogenesis Source: BHF-UCL
Fibrous ring of heart morphogenesis Source: BHF-UCL
Heart formation Source: Ensembl
Hindlimb morphogenesis Source: Ensembl
Immune response Source: BHF-UCL
In utero embryonic development Source: Ensembl
Lateral mesoderm development Source: Ensembl
Lung development Source: Ensembl
Mesendoderm development Source: Ensembl
Mesoderm formation Source: Ensembl
Mitral valve morphogenesis Source: BHF-UCL
Mullerian duct regression Source: Ensembl
Negative regulation of BMP signaling pathway Source: Reactome
Negative regulation of gene expression Source: BHF-UCL
Negative regulation of muscle cell differentiation Source: Ensembl
Negative regulation of neurogenesis Source: Ensembl
Negative regulation of smooth muscle cell migration Source: BHF-UCL
Neural crest cell development Source: Ensembl
Neural plate mediolateral regionalization Source: Ensembl
Odontogenesis of dentin-containing tooth Source: Ensembl
Osteoblast differentiation Source: Ensembl
Outflow tract morphogenesis Source: BHF-UCL
Outflow tract septum morphogenesis Source: BHF-UCL
Paraxial mesoderm structural organization Source: Ensembl
Pharyngeal arch artery morphogenesis Source: BHF-UCL
Pituitary gland development Source: Ensembl
Positive regulation of BMP signaling pathway Source: Reactome
Positive regulation of bone mineralization Source: BHF-UCL
Positive regulation of cardiac muscle cell proliferation Source: BHF-UCL
Positive regulation of cardiac ventricle development Source: BHF-UCL
Positive regulation of epithelial cell proliferation Source: Ensembl
Positive regulation of mesenchymal cell proliferation Source: Ensembl
Positive regulation of osteoblast differentiation Source: BHF-UCL
Positive regulation of pathway-restricted SMAD protein phosphorylation Source: BHF-UCL
Positive regulation of pri-miRNA transcription by RNA polymerase II Source: Ensembl
Positive regulation of SMAD protein signal transduction Source: BHF-UCL
Positive regulation of transcription by RNA polymerase II Source: BHF-UCL
Positive regulation of transforming growth factor beta2 production Source: BHF-UCL
Positive regulation of vascular associated smooth muscle cell proliferation Source: BHF-UCL
Protein phosphorylation Source: HGNC-UCL
Regulation of cardiac muscle cell proliferation Source: BHF-UCL
Regulation of cellular senescence Source: Ensembl
Regulation of lateral mesodermal cell fate specification Source: Ensembl
Roof of mouth development Source: Ensembl
Somitogenesis Source: Ensembl
Stem cell population maintenance Source: Ensembl
Transforming growth factor beta receptor signaling pathway Source: ProtInc
Tricuspid valve morphogenesis Source: BHF-UCL
Ventricular compact myocardium morphogenesis Source: BHF-UCL
Ventricular septum morphogenesis Source: BHF-UCL
Ventricular trabecula myocardium morphogenesis Source: BHF-UCL

Cell membrane; Cell surface

Juvenile polyposis syndrome (JPS): Autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers.
Polyposis syndrome, mixed hereditary 2 (HMPS2): A disease is characterized by atypical juvenile polyps, colonic adenomas, and colorectal carcinomas.
A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.

Extracellular: 24-152 aa
Helical: 153-176 aa
Cytoplasmic: 177-532 aa

Glycosylated.