FSTL1 Recombinant Rabbit Monoclonal Antibody (026), Invitrogen™

Description

• This product is preservative free
• It is recommended to add sodium azide to avoid contamination (final concentration 0.05%-0.1%)
• Recombinant rabbit monoclonal antibodies are produced using in vitro expression systems
• The expression systems are developed by cloning in the specific antibody DNA sequences from immunoreactive rabbits
• Then, individual clones are screened to select the best candidates for production
• The advantages of using recombinant rabbit monoclonal antibodies include: better specificity and sensitivity, lot-to-lot consistency, animal origin-free formulations, and broader immunoreactivity to diverse targets due to larger rabbit immune repertoire
• This antibody has specificity for Human FSTL1
• Follistatin-like protein 1 (FSTL1) is a widely-expressed, extracellular glycoprotein that is homologously grouped into the osteonectin (BM-40/SPARC) family of secreted proteins based on its possession of both a follistatin-like and extracellular calcium-binding domain
• Initially identified as a TGF-beta-inducible protein in a cloned mouse osteoblast cell line, FSTL1 has since been implicated in an array of cell-type-specific functions, such as the regulation of proliferation, differentiation, apoptosis and migration, as well as a number of biological processes, including embryonic development, inflammatory response, angiogenesis, tumorigenesis, and immune disease pathogenesis
• Highly conserved across mammalian species and widely expressed in human tissues, FSTL1 can be upregulated through signaling mediators of the innate immune system,such as TLR4 agonists and the arthritogenic cytokine IL-1beta via NFkappaB pathways, to stimulate the expression and secretion of pro-inflammatory cytokines, including TNF-alpha, IL-1beta, IL-6 and IL-8
• While cells of mesenchymal lineage are capable of FSTL1 production, FSTL1 expression is notably absent from cells of hematopoietic lineage under normal physiological conditions
• Macrophages and monocytes are, however, capable of taking up FSTL1 at sites of inflammation where FSTL1 stimulation can cause the expression of caspase-1 and its resultant enzymatic cleavage of active IL-1beta from pro-IL-1beta
• Whereas the overexpression of FSTL1 has been noted as a substantial contributor to the progression of immune diseases like rheumatoid arthritis (RA) and osteoarthritis (OA), diminished FSTL1 serum levels have been identified as playing a significant part in both ovarian and endometrial carcinogenesis, where it directly affects cell proliferation, migration and invasion.