Amyloidosis - Mechanisms and Prospects for Therapy by S. Sarantseva

By S. Sarantseva

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Journal of American Society of Nephrology, Vol. 20, No. 3, (March 2009), pp. , Sletten, K. & Westermark, P. (2009). Fibril protein fragmentation pattern in systemic AL-amyloidosis. Journal of Pathology, Vol. 219, No. 4, (December 2009), pp. B. N. (2001). Amyloid load and clinical outcome in AA amyloidosis in relation to circulating concentration of serum amyloid A protein. Lancet, Vol. 358, No. 9275, (July 2001), pp. D. & Muñoz-Gómez, J. (2001). The clinical significance of amyloid fat deposits in rheumatoid arthritis: A systematic long-term followup study using abdominal fat aspiration.

4. SAA SAA is produced primarily in the liver under proinflammatory cytokines stimulation; it is also a central acute-phase protein, like C-reactive protein (CRP). SAA complexes with a carrier protein, being transported into serum by high-density lipoprotein (HDL) in combination with apolipoprotein E, and plays an important role in enterohepatic cholesterol circulation. In obese individuals, the frequency of SAA mRNA expression and blood SAA level are both significantly high. Thus, the biologically versatile SAA has a significant relationship with lipid metabolism.

Evidence for an off- pathway oligomer at acidic pH. J Biol Chem 277,15: 12666-79. Stevens, F. J. (2000). Four structural risk factors identify most fibril-forming kappa light chains. Amyloid 7,3: 200-211. Stevens, P. , Hanson, D. , Westholm, F. , Schiffer, M. and Stevens, F. J. (1995). Recombinant immunoglobulin variable domains generated from synthetic genes provide a system for in vitro characterization of light-chain amyloid proteins. Protein Sci 4: 421-32. Vrana, J. , Gamez, J. , Madden, B.

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