Serum amyloid A

You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.

Jump to: navigation, search
Human Serum amyloid A1
Identifiers
Symbol SAA1
Entrez 6288
HUGO 10513
OMIM 104750
RefSeq NM_199161
UniProt P02735
Other data
Locus Chr. 11 p15.1
Human Serum amyloid A2
Identifiers
Symbol SAA2
Entrez 6289
HUGO 10514
OMIM 104751
RefSeq NM_030754
UniProt P02735
Other data
Locus Chr. 11 p15.1-p14
Human Serum amyloid A3, pseudogene
Identifiers
Symbol SAA3P
Alt. Symbols SAA3
Entrez 6290
HUGO 10515
UniProt P22614
Other data
Locus Chr. 11 p15.1-p14
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 predominantly produced by the liver.[1] The conservation of these proteins throughout invertebrates and vertebrates suggests SAAs play a highly essential role in all animals.[1]

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.[1] Three acute phase SAA isoforms have been reported in mice, called SAA1, SAA2 and SAA3. During inflammation, SAA1 and SAA2 are principally expressed and induced in the liver, while 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).[1] Three A-SAA genes have also been identified in humans[1], although the third gene, SAA3, is believed to represent a pseudogene that does not generate messenger RNA or protein.[1]

Constitutive serum amyloid A proteins

A fourth SAA (SAA4) was identified in humans and is expressed constitutively in the liver thus is defined as a constitutive SAA (C-SAA).[1] A similar protein has since been identified in the mouse that is now also called SAA4; it had originally been designated SAA5.[1][1]

References


sv:Serum amyloid A
WikiDoc Help Menu

Quick Start..

Editing basics

Advanced editing

Communicating your edits

Help Videos You Can Watch


Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

Personal tools