|Other Names||Fibulin-5, FIBL-5, Developmental arteries and neural crest EGF-like protein, Dance, Urine p50 protein, UP50, FBLN5, DANCE|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Essential for elastic fiber formation, is involved in the assembly of continuous elastin (ELN) polymer and promotes the interaction of microfibrils and ELN (PubMed:18185537). Stabilizes and organizes elastic fibers in the skin, lung and vasculature (By similarity). Promotes adhesion of endothelial cells through interaction of integrins and the RGD motif. Vascular ligand for integrin receptors which may play a role in vascular development and remodeling (PubMed:10428823). May act as an adapter that mediates the interaction between FBN1 and ELN (PubMed:17255108).|
|Cellular Location||Secreted Secreted, extracellular space, extracellular matrix. Note=co-localizes with ELN in elastic fibers.|
|Tissue Location||Expressed in skin fibroblasts (at protein level)(PubMed:17035250). Expressed predominantly in heart, ovary, and colon but also in kidney, pancreas, testis, lung and placenta Not detectable in brain, liver, thymus, prostate, or peripheral blood leukocytes (PubMed:10428823).|
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The protein encoded by this gene is a secreted,extracellular matrix protein containing an Arg-Gly-Asp (RGD) motifand calcium-binding EGF-like domains. It promotes adhesion ofendothelial cells through interaction of integrins and the RGDmotif. It is prominently expressed in developing arteries but lessso in adult vessels. However, its expression is reinduced inballoon-injured vessels and atherosclerotic lesions, notably inintimal vascular smooth muscle cells and endothelial cells.Therefore, the protein encoded by this gene may play a role invascular development and remodeling. Defects in this gene are acause of autosomal dominant cutis laxa, autosomal recessive cutislaxa type I (CL type I), and age-related macular degeneration type3 (ARMD3).
Schneider, R., et al. J. Mol. Biol. 401(4):605-617(2010)Zhou, S., et al. Biochem. Biophys. Res. Commun. 398(2):247-253(2010)Rose, J.E., et al. Mol. Med. 16 (7-8), 247-253 (2010) :Joslyn, G., et al. Alcohol. Clin. Exp. Res. 34(5):800-812(2010)Zhao, J., et al. BMC Med. Genet. 11, 96 (2010) :
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