Betacellulin

Betacellulin is a protein that in humans is encoded by the BTC gene located on chromosome 4 at locus 4q13-q21.[5] Betacellulin, is a part of an Epidermal Growth Factor (EGF) family that has been spotted in the conditioned cell lines that was taken from mice pancreatic Beta cell tumor. When a sequence of the purified protein and a cloned cDNA was extracted, it supported the claim that in fact betacellulin is a new ligand formed from the epidermal growth factor receptor (EGFR). As the role a EGFR, betacellulin is manifested by different form of muscles and tissues, it also has a great effect of nitrogen that is used for retinal pigment epithelial cells and vascular smooth muscle cells. While many studies attest a role for betacellulin in the differentiation of pancreatic β-cells, the last decade witnessed the association of betacellulin with many additional biological processes, ranging from reproduction to the control of neural stem cells.[6]Betacellulin is a member of the EGF family of growth factors. It is synthesized primarily as a transmembrane precursor, which is then processed to mature molecule by proteolytic events. This protein is a ligand for the EGF receptor.[5]

BTC
Available structures PDB Ortholog search: PDBe RCSB List of PDB id codes 1IOX, 1IP0
Identifiers
Aliases	BTC, entrez:685, betacellulin
External IDs	OMIM: 600345 MGI: 99439 HomoloGene: 1309 GeneCards: BTC
Gene location (Human) Chr. Chromosome 4 (human)[1] Band 4q13.3 Start 74,744,759 bp[1] End 74,794,523 bp[1]
Gene location (Mouse) Chr. Chromosome 5 (mouse)[2] Band 5 E2|5 44.78 cM Start 91,357,261 bp[2] End 91,402,994 bp[2]
Gene ontology Molecular function • GO:0001948 protein binding • Ras guanyl-nucleotide exchange factor activity • phosphatidylinositol-4,5-bisphosphate 3-kinase activity • protein tyrosine kinase activity • epidermal growth factor receptor binding • growth factor activity Cellular component • integral component of membrane • membrane • cell membrane • extracellular region • intracellular • extracellular • clathrin-coated vesicle membrane Biological process • positive regulation of urine volume • positive regulation of fibroblast proliferation • negative regulation of apoptotic process • MAPK cascade • positive regulation of cell differentiation • positive regulation of cell proliferation • positive regulation of mitotic nuclear division • positive regulation of cell division • regulation of cell motility • phosphatidylinositol phosphorylation • epidermal growth factor receptor signaling pathway • ERBB2 signaling pathway • peptidyl-tyrosine phosphorylation • regulation of receptor activity • positive regulation of protein kinase B signaling • signal transduction • negative regulation of epidermal growth factor receptor signaling pathway • membrane organization Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	685	12223
Ensembl	ENSG00000174808	ENSMUSG00000082361
UniProt	P35070	Q05928
RefSeq (mRNA)	NM_001729 NM_001316963	NM_007568
RefSeq (protein)	NP_001303892 NP_001720	NP_031594
Location (UCSC)	Chr 4: 74.74 – 74.79 Mb	Chr 5: 91.36 – 91.4 Mb
PubMed search	[3]	[4]
Wikidata
View/Edit Human View/Edit Mouse

As a typical EGFR ligand, betacellulin is expressed by a variety of cell types and tissues, and the soluble growth factor is proteolytically cleaved from a larger membrane-anchored precursor.[7] Betacellulin stimulated the proliferation of retinal pigment epithelial and vascular smooth muscle cells at a concentration of [difference]30 pM (1 ng/ml) but did not stimulate the growth of several other cell types, such as endothelial cells and fetal lung fibroblasts.[8]Betacellulin chemically bonds and activates tyrosine residues phosphorylation of the epidemic growth factor. Osteoblasts, which are responsible for forming and mineralizing osteoid, express EGF receptors and alter rates of proliferation and differentiation in response to EGF receptor activation. Transgenic mice over-expressing the EGF-like ligand betacellulin (BTC) exhibit increased cortical bone deposition; however, because the transgene is ubiquitously expressed in these mice, the identity of cells affected by BTC and responsible for increased cortical bone thickness remains unknown. We have therefore examined the influence of BTC upon mesenchymal stem cell (MSC) and pre-osteoblast differentiation and proliferation. BTC decreases the expression of osteogenic markers in both MSCs and pre-osteoblasts increases in proliferation require hypoxia-inducible factor-alpha (HIF-alpha), as an HIF antagonist prevents BTC-driven proliferation. Both MSCs and pre-osteoblasts express EGF receptors ErbB1, ErbB2, and ErbB3, with no change in expression under osteogenic differentiation. These are the first data that demonstrate an influence of BTC upon MSCs and the first to implicate HIF-alpha in BTC-mediated proliferation.[9] as you can see the role of Betacellulinis a bit flexible enough to divert its response based on part where it binds.