All BMPR1A reagents are produced in house and quality controlled, including 5 BMPR1A Antibody, 65 BMPR1A Gene, 4 BMPR1A Lysate, 5 BMPR1A Protein, 3 BMPR1A qPCR. All BMPR1A reagents are ready to use.
Recombinant BMPR1A proteins are expressed by HEK293 Cells with fusion tags as C-human IgG1-Fc, C-human IgG1-Fc & His, C-His.
BMPR1Aantibodies are validated with different applications, which are ELISA, IHC-P.
BMPR1AcDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each BMPR1A of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
Activin receptor-Like Kinase 3 (ALK-3), also known as Bone Morphogenetic Protein Receptor, type IA (BMPR1A), is a type I receptor for bone morphogenetic proteins (BMPs) which belong to the transforming growth factor beta (TGF-β) superfamily. The BMP receptors form a subfamily of transmembrane serine/threonine kinases including the type I receptors BMPR1A and BMPR1B and the type II receptor BMPR2. ALK-3/BMPR1A is expressed in the epithelium during branching morphogenesis. Deletion of BMPR1A in the epithelium with an Sftpc-cre transgene leads to dramatic defects in lung development. ALK-3 and ALK-6 share a high degree of homology, yet possess distinct signaling roles. The transforming growth factor (TGF)-beta type III receptor (TbetaRIII) enhanced both ALK-3 and ALK-6 signaling. TbetaRIII associated with ALK-3 primarily through their extracellular domains, whereas its interaction with ALK-6 required both the extracellular and cytoplasmic domains. ALK-3 plays an essential role in the formation of embryonic ventral abdominal wall, and abrogation of BMP signaling activity due to gene mutations in its signaling components could be one of the underlying causes of omphalocele at birth. The type IA BMP receptor, ALK-3 was specifically required at mid-gestation for normal development of the trabeculae, compact myocardium, interventricular septum, and endocardial cushion. Cardiac muscle lacking ALK-3 was specifically deficient in expressing TGFbeta2, an established paracrine mediator of cushion morphogenesis. Hence, ALK-3 is essential, beyond just the egg cylinder stage, for myocyte-dependent functions and signals in cardiac organogenesis.