Fibroblast Growth Factor Basic (also known as bFGF) is a pleotropic cytokine that that is a potent mitogenic factor. On binding to its cognate receptor tyrosine kinase, FGFR, bFGF is capable of activation of pathways such as MAPK and PI3K and produce cellular effects in varied cell types. Fibroblast Growth Factor-basic is repoted to induce proliferation of fibroblasts, differentiation, wound healing and regeneration, limb formation, tissue remodelling and angiogenesis. The role of bFGF in chondrocyte proliferation and repair has established the role of bFGF in maintaining cartilage and intervertebral disc homeostasis. Along with VEGF, bFGF is important in angiogenesis and tumorigenesis in response to inflammatory cytokines Monoclonal Anti-Fibroblast Growth Factor Basic recognizes human Fibroblast Growth Factor Basic. It also recognizes bovine bFGF. It shows 0.2% cross-reactivity with bovine FGF acidic. It does not react with human FGF acidic, FGF-4, -6 or -7.
Immunogen
purified, E. coli-derived recombinant human fibroblast growth factor basic.
Application
Monoclonal Anti-Fibroblast Growth Factor Basic may be used as capture antibody in ELISA at a recommended concentration range of 2-8 μg/ml.
Physical form
Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline with 5% trehalose.
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Two members of the fibroblast growth factor (FGF) family, basic FGF (bFGF) and FGF-18, have been implicated in the regulation of articular and intervertebral disc (IVD) cartilage homeostasis. Studies on bFGF from a variety of species have yielded contradictory results
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The possible functional role of basic fibroblast growth factor (bFGF) in regulating the mitotic and metabolic activity of primary human articular chondrocytes was investigated. [EF1]Chondrocytes were enzymatically isolated from femoral head cartilage, and were cultured in vitro in monolayer. bFGF-dependent
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Intervertebral disc (IVD) degeneration is frequently characterized by increased cell proliferation, probably as a tissue regenerative response. Although many growth factors and their receptors have been shown to be expressed normally in the disc, and generally to be over-expressed during
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The Crouzon syndrome, which is associated with fibroblast growth factor receptor (FGFR2) mutations, is characterized by premature fusion of cranial sutures. We used an in vitro model of cultured periosteal fibroblasts from normal subjects and from Crouzon patients with FGFR2
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