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Human sVCAM-1 ELISA
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PRODUCT FAMILY INFORMATION
Acute Injury and Chronic Neurodegeneration Antibodies, Immunoassays, & Histological Stains
Millipore offers a range of products for neurodegeneration research: detection & staining of dying neurons. See below for products for products based on the expertise of Upstate & Chemicon.
A general feature of many neurological diseases, disorders, or injuries is the degeneration of proximal and/or distal neural processes. Key to understanding the degenerative progression is detecting and staining these dying neurons. EMD-Millipore has developed several methods for detecting neurodegeneration in blood/CSF samples and tissue sections. Several ELISA based assays are now available for neurodegenerative biomarkers, including phosphoNF-H, GFAP, and alpha synuculein. In addtion, Millipore’s non-antibody based tissue section stains for various stages of degenerating neurons are very robust regardless of specific insult or mechanism of cell death.
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Description:
Human sVCAM-1 ELISA
Trade Name:
Chemicon (Millipore)
Qty/Pk:
1 kit
Product Overview:
Vascular cell adhesion molecule-1 (VCAM-1, CD106) is a member of the immunoglobulin gene superfamily. Two forms of VCAM-1 with six or seven extracellular Ig-like domains arise due to alternative splicing from a seven-domain VCAM-1 (7D VCAM-1). 7D VCAM-1 is the dominant form expressed by cultured human endothelial cells [Cybulsky et al., 1991; Hession et al., 1991]. Homology of domains 1 through 3 with domains 4 through 6 suggests a gene duplication event [Cybulsky et al., 1991; Hession et al., 1991]. The cDNA of 7D VCAM-1 predicts a core protein of approximately 81 kDa with seven sites for N-linked glycosylation. Upon complete glycosylation the mature protein has a molecular weight of approximately 102 kDa. This observation is in general agreement with the 110 kDa protein immunoprecipitated from cytokine-activated endothelium [Carlos et al., 1990; Rice et al., 1990].
VCAM-1 appears to have been highly conserved through evolution. Both rat and mouse VCAM-1 are highly homologous at the protein level to the human VCAM-1 (77% and 76%, respectively) [Hession et al., 1992].
VCAM-1 supports the adhesion of lymphocytes, monocytes, natural killer cells, eosinophils and basophils, through its interaction with integrin a4b1 (VLA-4). VCAM-1/VLA-4 interaction mediates firm adherence of circulating non-neutrophilic leukocytes to endothelium [Sharar et al., 1995]. VCAM-1 also participates in leukocyte adhesion outside of the vasculature, mediating precursor lymphocyte adhesion to bone marrow stromal cells [Ryan et al. 1991] and B cell binding to lymph node follicular dendritic cells [Feedman et al., 1992]. VCAM-1 is not constitutively expressed on endothelium, but can be up-regulated in vitro in response to LPS, TNF-a, and IL-1 [Carlos & Harlan, 1990; Osborn et al., 1989], as well as to interferon-g and IL-4 [Masinovsky et al. 1990]. VCAM-1 is also present on tissue macrophages, dendrite cells, bone marrow fibroblasts, myoblasts and myotubes.
A soluble form of VCAM-1 has been described [De Maeyer & De Maeyer-Buignard, 1995; Lobb et al., 1991], and soluble VCAM-1 has been found in serum [Gearing et al., 1995]. Increased levels of soluble VCAM-1 can be detected in several disease states, including cancer [Banks et al., 1993; Fortis et al., 1995; Gearing & Newman, 1993; Lai et al., 1995], autoimmune disorders [Gearing & Newman, 1993; Doreduffy et al., 1995; Gruschwitz et al., 1995; Mason et al., 1993; Mrowka & Sieberth, 1995; Spronk et al., 1994; Wellicome et al., 1993], infections [Jakobsen et al., 1994] and inflammations [Gearing & Newman, 1993; Mrowka & Sieberth, 1995; Adams et al., 1995; Lim et al., 1995].
Test Principle:
An anti-VCAM-1 monoclonal antibody is ads |