WordNet

any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
the 1st letter of the Roman alphabet (同)a
the blood group whose red cells carry the A antigen (同)type_A, group A
(pathology) a waxy translucent complex protein resembling starch that results from degeneration of tissue
a non-nitrogenous food substance consisting chiefly of starch; any substance resembling starch
an amber, watery fluid, rich in proteins, that separates out when blood coagulates (同)blood_serum

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蛋白(たんばく)質
answer / ampere
リンパ液 / 血清
arsenicの化学記号

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/09/09 09:41:49」(JST)

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Human Serum amyloid A4
Identifiers
Symbol	SAA4
Alt. symbols	C-SAA
Entrez	6291
HUGO	10516
OMIM	104752
RefSeq	NM_006512
UniProt	P35542
Other data
Locus	Chr. 11 p15.1-p14

Serum amyloid A (SAA) proteins are a family of apolipoproteins associated with high-density lipoprotein (HDL) in plasma. Different isoforms of SAA are expressed constitutively (constitutive SAAs) at different levels or in response to inflammatory stimuli (acute phase SAAs). These proteins are produced predominantly by the liver.^[1] The conservation of these proteins throughout invertebrates and vertebrates suggests that SAAs play a highly essential role in all animals.^[2]

Acute-phase serum amyloid A proteins

Acute-phase serum amyloid A proteins (A-SAAs) are secreted during the acute phase of inflammation. These proteins have several roles, including the transport of cholesterol to the liver for secretion into the bile, the recruitment of immune cells to inflammatory sites, and the induction of enzymes that degrade extracellular matrix. A-SAAs are implicated in several chronic inflammatory diseases, such as amyloidosis, atherosclerosis, and rheumatoid arthritis.^[3] Three acute-phase SAA isoforms have been reported in mice, called SAA1, SAA2, and SAA3. During inflammation, SAA1 and SAA2 are expressed and induced principally in the liver, whereas SAA3 is induced in many distinct tissues. SAA1 and SAA2 genes are regulated in liver cells by the proinflammatory cytokines IL-1, IL-6, and TNF-α. Both SAA1 and SAA2 are induced up to a 1000-fold in mice under acute inflammatory conditions following exposure to bacterial lipopolysaccharide (LPS).^[3] Three A-SAA genes have also been identified in humans,^[4] although the third gene, SAA3, is believed to represent a pseudogene that does not generate messenger RNA or protein.^[5] Molecular weights of the human proteins are estimated at 11.7 kDa for SAA1^[6] and 12.8 kDa for SAA4.^[7]

Serum amyloid A (SAA) is also an acute phase marker that responds rapidly. Similar to CRP, levels of acute-phase SAA increase within hours after inflammatory stimulus, and the magnitude of increase may be greater than that of CRP. Relatively trivial inflammatory stimuli can lead to SAA responses. It has been suggested that SAA levels correlate better with disease activity in early inflammatory joint disease than do ESR and CRP. Although largely produced by hepatocytes, more recent studies show that SAA is produced by adipocytes as well, and its serum concentration is associated with body mass index.^[8]

Constitutive serum amyloid A proteins

A fourth SAA (SAA4) was identified in humans and is expressed constitutively in the liver and, thus, is defined as a constitutive SAA (C-SAA).^[9] A similar protein that is now also called SAA4 has since been identified in the mouse; it had originally been designated SAA5.^[10]^[11]

References

^ Uhlar CM, Whitehead AS (1999). "Serum amyloid A, the major vertebrate acute-phase reactant". Eur. J. Biochem. 265 (2): 501–23. doi:10.1046/j.1432-1327.1999.00657.x. PMID 10504381.
^ Manley PN, Ancsin JB, Kisilevsky R (2006). "Rapid recycling of cholesterol: the joint biologic role of C-reactive protein and serum amyloid A". Med. Hypotheses 66 (4): 784–92. doi:10.1016/j.mehy.2005.10.018. PMID 16337748.
^ ^a ^b Zhang N, Ahsan MH, Purchio AF, West DB (2005). "Serum amyloid A-luciferase transgenic mice: response to sepsis, acute arthritis, and contact hypersensitivity and the effects of proteasome inhibition". J. Immunol. 174 (12): 8125–34. doi:10.4049/jimmunol.174.12.8125. PMID 15944321.
^ Betts JC, Edbrooke MR, Thakker RV, Woo P (1991). "The human acute-phase serum amyloid A gene family: structure, evolution and expression in hepatoma cells". Scand. J. Immunol. 34 (4): 471–82. doi:10.1111/j.1365-3083.1991.tb01570.x. PMID 1656519.
^ Kluve-Beckerman B, Drumm ML, Benson MD (1991). "Nonexpression of the human serum amyloid A three (SAA3) gene". DNA Cell Biol. 10 (9): 651–61. doi:10.1089/dna.1991.10.651. PMID 1755958.
^ http://www.uniprot.org/uniprot/P0DJI8
^ http://www.uniprot.org/blast/?about=P35542[19-130]&key=Chain&id=PRO_0000031583
^ Pincus MR, McPherson RA, Henry JB (2007). Henry's Clinical Diagnosis and Management by Laboratory Methods. Saunders Elsevier. ISBN 1-4160-0287-1.
^ Steel DM, Sellar GC, Uhlar CM, Simon S, DeBeer FC, Whitehead AS (1993). "A constitutively expressed serum amyloid A protein gene (SAA4) is closely linked to, and shares structural similarities with, an acute-phase serum amyloid A protein gene (SAA2)". Genomics 16 (2): 447–54. doi:10.1006/geno.1993.1209. PMID 7686132.
^ de Beer MC, Kindy MS, Lane WS, de Beer FC (1994). "Mouse serum amyloid A protein (SAA5) structure and expression". J. Biol. Chem. 269 (6): 4661–7. PMID 8308037.
^ de Beer MC, de Beer FC, Gerardot CJ et al. (1996). "Structure of the mouse Saa4 gene and its linkage to the serum amyloid A gene family". Genomics 34 (1): 139–42. doi:10.1006/geno.1996.0253. PMID 8661036.

UpToDate Contents

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1. 続発性（AA）アミロイドーシスの病因 pathogenesis of secondary aa amyloidosis
2. 急性期反応物質 acute phase reactants
3. 家族性地中海熱の臨床症状および診断 clinical manifestations and diagnosis of familial mediterranean fever
4. アミロイド疾患の遺伝的要因 genetic factors in the amyloid diseases
5. 心血管疾患におけるＣ－反応性蛋白 c reactive protein in cardiovascular disease

English Journal

Serum Amyloid - A protein and serum Rheumatoid Factor as serological surrogate markers for smoking risk factor in Saudi population.

Al-Sieni AI, Al-Alawy AI, Al-Shehri ZS, Al-Abbasi FA.SourceDepartment of biochemistry, Faculty of science, King Abdul-Aziz University, Jeddah, Saudi Arabia.
Pakistan journal of pharmaceutical sciences.Pak J Pharm Sci.2013 Mar;26(2):239-43.
Tobacco smoking represents major national and international health hazard that interferes with wide range of physiological functions and biomarkers. In the current study we have investigated the influence of tobacco smoking on some biological markers such as serum amyloid protein-A, rheumatoid facto
PMID 23455190

Efficient Amyloid A Clearance in the Absence of Immunoglobulins and Complement Factors.

Sponarova J, Nuvolone M, Whicher C, Frei N, Kana V, Schwarz P, Westermark GT, Aguzzi A.SourceInstitute of Neuropathology, University Hospital of Zurich, Zurich, Switzerland.
The American journal of pathology.Am J Pathol.2013 Feb 20. pii: S0002-9440(13)00051-5. doi: 10.1016/j.ajpath.2012.12.035. [Epub ahead of print]
Amyloid A amyloidosis is a protein misfolding disease characterized by deposition of extracellular aggregates derived from the acute-phase reactant serum amyloid A protein. If untreated, amyloid A amyloidosis leads to irreversible damage of various organs, including the kidneys, liver, and heart. Am
PMID 23454183