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Product Name
Anti-Fetuin-A antibody
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Description
Rabbit monoclonal to Fetuin-A
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Tested applications
IHC-P
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Species reactivity
Mouse Fetuin-A / AHSG
Has cross-reactivity in ELISA with ; Human FetuinA/AHSG -
Alternative names
mCG_3209 antibody; Fgfr-4 antibody; Mpk-11 antibody; Fibroblast growth factor receptor 4 antibody
- Immunogen
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Isotype
Rabbit IgG
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Preparation
This antibody was obtained from a rabbit immunized with purified, recombinant Mouse Fetuin-A / AHSG (rM Fetuin-A / AHSG; NP_032037.2; Met1-Ile345).
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Clonality
Monoclonal
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Formulation
0.2 μm filtered solution in PBS with 5% trehalose
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Storage instructions
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles. -
Applications
IHC-P: 1-10 μg/mL
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Validations
Fetuin-A / AHSG Antibody, Rabbit MAb, Immunohistochemistry
Immunochemical staining of mouse AHSG in mouse liver (from 2 donors) with rabbit monoclonal antibody (5 µg/mL, formalin-fixed paraffin embedded sections).
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Background
Fetuin-A, also known as Alpha-2-HS-Glycoprotein (AHSG), belongs to the Fetuin family, is a plasma binding protein, and is more abundant in fetal than adult blood. It is involved in several functions, such as endocytosis, brain development and the formation of bone tissue. Fetuins are carrier proteins like albumin. Fetuin-A forms soluble complexes with calcium and phosphate and thus is a carrier of otherwise insoluble calcium phosphate. Thus Fetuin-A is a potent inhibitor of pathological calcification. The circulating levels of fetuin-A, a well-described inhibitor of calcification, regulate the cell-dependent process of osteogenesis. The low circulating fetuin-A levels are associated with a greater prevalence and/or severity of Vascular calcification (VC) and increased risk for all-cause and cardiovascular mortality. However, high circulating fetuin-A levels appear to induce insulin resistance and, in non-dialyzed subjects with diabetic nephropathy, are directly related to VC burden. The emerging role of fetuin-A deficiency as a risk factor in dialysis patients was documented in cross-sectional studies demonstrating a significant correlation with all-cause and cardiovascular mortality. Additionally, Human fetuin-A is a negative acute phase protein involved in inflammatory diseases, thus being a potential physiological regulator of meprin activity. Fetuin-A is a broad-range protease inhibitor. Fetuin-A and cystatin C as endogenous proteolytic regulators of meprin activity broadens our understanding of the proteolytic network in plasma.
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References
- Mehrotra R. (2007) Emerging role for fetuin-A as contributor to morbidity and mortality in chronic kidney disease. Kidney Int. 72(2): 137-40.
- Westenfeld R, et al. (2007) Vascular calcification and fetuin-A deficiency in chronic kidney disease. Trends Cardiovasc Med. 17(4): 124-8.
- Heiss A, et al. (2008). Hierarchical role of fetuin-A and acidic serum proteins in the formation and stabilization of calcium phosphate particles. J Biol Chem. 283 (21): 14815-25.
- Jahnen-Dechent W, et al. (2008). Mineral chaperones: a role for fetuin-A and osteopontin in the inhibition and regression of pathologic calcification. J Mol Med. 86 (4): 379-89.
- Hedrich J, et al. (2010) Fetuin-A and cystatin C are endogenous inhibitors of human meprin metalloproteases. Biochemistry. 49(39): 8599-607.
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