Human Biglycan Alexa Fluor® 750-conjugated Antibody Summary
Asp38-Lys368
Accession # P21810
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
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Preparation and Storage
Background: Biglycan
Biglycan, also known as PG I, is a secreted chondroitin/dermatan sulfate proteoglycan in the small leucine-rich proteoglycan (SLRP) family. SLRP family members are characterized by N-terminal and C-terminal cysteine-rich regions that flank a central region containing 10 - 12 tandem leucine-rich repeats (LRRs). Biglycan function is important in the development and maintenance of many tissues (1, 2). The human Biglycan cDNA encodes a 368 amino acid (aa) precursor with a 19 aa signal sequence and a 18 aa propeptide that is cleaved by BMP-1 (3). Mature Biglycan contains N-linked glycosylation in addition to two glycosaminoglycan (GAG) chains (4). The 45 kDa core protein is approximately one third the molecular weight of the fully glycanated form and can assemble into noncovalently-associated dimers (5). Human Biglycan shares 97% aa sequence identity with bovine, mouse, and rat Biglycan and 57% aa sequence identity with human Decorin. Biglycan binds several matrix proteins, including fibrillar collagens, Matrilin-1, and beta IG-H3 (6 - 8). Its multiple LRRs, N-linked glycosylation, and GAG chains mediate distinct interactions that enable extensive crosslinking and stabilization of the collagen matrix (6 - 8). Mature Biglycan can be further cleaved by proteases, resulting in non-glycanated fragments (9). In osteoarthritis, MMP-13-induced breakdown of Biglycan likely interferes with collagen crosslinking and contributes to cartilage degradation (10). Biglycan also binds and modulates the activity of a variety of non-matrix proteins, including BMP-4, C1q, collectins, TGF-beta, TNF-alpha, and WISP-1 (11, 12). Biglycan functions as a proinflammatory mediator by binding TLR2 and TLR4 on macrophages and inducing TNF-alpha and MIP-2 production (13). Biglycan knockout mice have compromised inflammatory responses and are resistant to LPS-induced septic shock (13). Biglycan binds HDL/Apolipoprotein E complexes in atherosclerotic plaques and also binds SR-A, blocking the uptake and degradation of LDL (14, 15).
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