Mouse FGL2 Alexa Fluor® 532-conjugated Antibody
R&D Systems, part of Bio-Techne | Catalog # FAB5257X
Key Product Details
Species Reactivity
Applications
Label
Antibody Source
Product Specifications
Immunogen
Val20-Pro432
Accession # P12804
Specificity
Clonality
Host
Isotype
Applications for Mouse FGL2 Alexa Fluor® 532-conjugated Antibody
Western Blot
Formulation, Preparation, and Storage
Purification
Formulation
Shipping
Stability & Storage
Background: FGL2
FGL2 (fibrinogen-like protein 2), also called fibroleukin, is a 64-70 kDa secreted glycoprotein of the Fibrinogen-like superfamily. It has prothrombinase activity and also promotes T regulatory (Treg) activity (1-6). The mouse FGL2 gene encodes a 432 amino acid (aa) protein that contains a 19 aa signal sequence and a 413 aa mature sequence with a coiled-coil region and a fibronectin C-terminal homology domain or FRED (1, 2). A 260-280 aa FGL2 complex is thought to be a tetramer formed by covalent disulfide linkage of dimers that are asoociated via coiled-coil interactions (2, 3). Mature mouse FGL2 shares 91% aa identity with rat FGL2, and 77-80% aa identity with human, equine, porcine, bovine and canine FGL2. FGL2 appears to have two modes of action. One mode involves its prothrombinase activity, which requires calcium and acidic phospholipids (4). This mode is thought to be active during hepatitis viral infections when FGL2, produced by macrophages in response to IFN-gamma, induces hepatic apoptosis and fibrin deposition (7). In addition, FGL2 produced by endothelial cells in response to TNF-alpha within cardiac xenografts or allografts promotes coagulation during acute vascular rejection (7-9). A second mode of action involves soluble (not phospholipid-associated) FGL2 and is independent of prothrombinase activity (2). Soluble FGL2 is required for Treg function, and directly suppresses DC, T, and B cell immune reactivity; consequently, some FGL2-deficent mice develop autoimmune glomerulonephritis (5, 6). In vitro, soluble FGL2 can skew T cell polarization toward Th2 and inhibit proliferation of stimulated T cells and maturation of DC (6). In pregnancy, fetal trophoblast cells secrete FGL2. The immune suppressive mode of FGL2 may prevent early fetal loss; however, the procoagulant mode is thought to mediate infection-triggered abortion (10).
Long Name
Alternate Names
Gene Symbol
UniProt
Additional FGL2 Products
Product Documents for Mouse FGL2 Alexa Fluor® 532-conjugated Antibody
Product Specific Notices for Mouse FGL2 Alexa Fluor® 532-conjugated Antibody
This product is provided under an agreement between Life Technologies Corporation and R&D Systems, Inc, and the manufacture, use, sale or import of this product is subject to one or more US patents and corresponding non-US equivalents, owned by Life Technologies Corporation and its affiliates. The purchase of this product conveys to the buyer the non-transferable right to use the purchased amount of the product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components (1) in manufacturing; (2) to provide a service, information, or data to an unaffiliated third party for payment; (3) for therapeutic, diagnostic or prophylactic purposes; (4) to resell, sell, or otherwise transfer this product or its components to any third party, or for any other commercial purpose. Life Technologies Corporation will not assert a claim against the buyer of the infringement of the above patents based on the manufacture, use or sale of a commercial product developed in research by the buyer in which this product or its components was employed, provided that neither this product nor any of its components was used in the manufacture of such product. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, Cell Analysis Business Unit, Business Development, 29851 Willow Creek Road, Eugene, OR 97402, Tel: (541) 465-8300. Fax: (541) 335-0354.
For research use only