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.
Bone Morphogenetic Protein Receptor II (BMPR-II) is a Type II Serine/Threonine Kinase that mediates cellular responses to BMPs. BMPR-II is characterized by lacking of a GS domain, and presence of a C-terminal extension typical of type II receptors. BMPRII binds BMP2, BMP4 and BMP7 weakly in the absence of type I receptor, and the binding can be facilitated by the presence of the type I receptor, including BMPR-IA/Brk1, BMPR-IB, and ActR-I. BMPR-II plays a key role in cell growth. Defects in BMPR-II have been linked to primary pulmonary hypertension. Human and mouse BMPR-II are highly conserved and share 97 % amino acid sequence identity.
Bone Morphogenetic Protein Receptor Type-1A (BMPR1A) belongs to the TKL Ser/Thr protein kinase family and TGFB receptor subfamily, including the type I receptors BMPR1A and BMPR1B and the type II receptor BMPR2. BMPR1A is a single-pass type I membrane protein and highly expressed in skeletal muscle. BMPR1A contains one GS domain and one protein protein kinase domain. BMPR1A is necessary for the extracellular matrix depostition by osteoblasts. BMPR1A can activate SMAD transcriptional regulators, binding with ligands. Defects in BMPR1A are a cause of juvenile polyposis syndrome, Cowden disease and hereditary mixed polyposis syndrome 2 (HMPS2).
The deletion of BNIP3L results in retention of mitochondria during lens fiber cell remodeling, and that deletion of BNIP3L also results in the retention of endoplasmic reticulum and Golgi apparatus. BNIP3L localizes to the endoplasmic reticulum and Golgi apparatus of wild-type newborn mouse lenses and is contained within mitochondria, endoplasmic reticulum and Golgi apparatus isolated from adult mouse liver. As the cells become packed with keratin bundles, Bnip3L expression triggers mitophagy to rid the cells of the last remaining 'living' characteristic, thus completing the march from 'living' to 'dead' within the hair follicle. during retinal development tissue hypoxia triggers HIF1A/HIF-1 stabilization, resulting in increased expression of the mitophagy receptor BNIP3L/NIX. BNIP3L-dependent mitophagy results in a metabolic shift toward glycolysis essential for RGC neurogenesis. BNIP3L could be a potential therapeutic target for ischemic stroke
Brother of CDO is a protein that in humans is encoded by the BOC gene. CDON and BOC are cell surface receptors of the immunoglobulin (Ig)/fibronectin type III repeat family involved in myogenic differentiation. CDON and BOC are coexpressed during development, form complexes with each other in a cis fashion, and are related to each other in their ectodomains, but each has a unique long cytoplasmic tail.
Galactolipase, also known as PNLIPRP2, is a lipase with broad substrate specificity. It can hydrolyze both phospholipids and galactolipids. Galactolipase acts preferentially on monoglycerides, phospholipids and galactolipids. It also hydrolyses milk fat with a lower catalytic efficiency. The expressed galactolipase shows a lipolytic activity that is, however, only marginally dependent on the presence of colipase. The lipolytic activity of pancreatic extracts and human pancreatic juice on Labrasol is mainly due to the combined action of carboxyl ester hydrolase and galactolipase.
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