Rabbit Monoclonal Antibody
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|AJ1703a||100µl||2-3 days||$ 295.00||Add to cart|
- Citations : 0
SAA4 Antibody - Product Information
|Application ||WB, IHC|
|Calculated MW||14747 Da Da|
|Gene ID 6291|
Serum amyloid A-4 protein, Constitutively expressed serum amyloid A protein, C-SAA, SAA4, CSAA
A synthetic peptide corresponding to residues in human SAA4 was used as an immunogen.
50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.
Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
SAA4 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
SAA4 Antibody - Protein Information
Major acute phase reactant. Apolipoprotein of the HDL complex.
Expressed by the liver; secreted in plasma.
SAA4 Antibody - Related Products
SAA4 Antibody - Research Areas
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Provided below are standard protocols that you may find useful for product applications.
Serum amyloid A (SAA) proteins are family of apolipoproteins of high density lipoprotein (HDL). They can be separated into two distinct groups. First group (SAA1, SAA2, and SAA3) consists of acute phase reactant whose expression level increase in the blood in a response to trauma, infection, inflammation, and neoplasia. These acute phase SAAs associates with HDL during inflammation and remodel the HDL particle by displacing Apo-A1. The second distinct group consists of SAA4 and SAA5 which exist as the minor apolipoproteins on HDL, but this group of SAA constitutes more than 90% of all the SAA during homeostasis, and it is thought to play a role in the normal functioning of the HDL particle (1, 2). The distribution of SAA4 is restricted to two lipoprotein subclasses; therefore, SAA4 has been suggested be a factor in lipid transfer between lipoprotein classes. SAA4 mRNA and protein expression in macrophage-derived foam cells of coronary and carotid arteries suggested a specific role of SAA4 during inflammation including atherosclerosis (3).
1. O Gutfeld et al., JHC 54 (1): 63-73, 2006. 2. MC de Beer et al., J Lipid Res. 36:526-534, 1995. 3. A Hrzenjak et al., Protein Engineering 14(12):949-952, 2001.