Integrin alpha M

Integrin alpha M

Integrin alpha M (ITGAM) is one protein subunit that forms the heterodimeric integrin alpha-M beta-2 (αMβ2) molecule, also known as "macrophage-1 antigen" (Mac-1) or "complement receptor 3" (CR3).cite journal |author=Solovjov D, Pluskota E, Plow E |title=Distinct roles for the alpha and beta subunits in the functions of integrin alphaMbeta2 |journal=J Biol Chem |volume=280 |issue=2 |pages=1336–45 |year=2005 |pmid=15485828 |doi=10.1074/jbc.M406968200] ITGAM is also known as CR3A, and cluster of differentiation molecule 11B (CD11B). The second chain of αMβ2 is the common integrin β2 subunit known as CD18, and integrin αMβ2 thus belongs to the β2 subfamily (or leukocyte) integrins. [cite journal |author=Larson R, Springer T |title=Structure and function of leukocyte integrins |journal=Immunol Rev |volume=114 |issue= |pages=181–217 |year= |pmid=2196220 |doi=10.1111/j.1600-065X.1990.tb00565.x]

αMβ2 is expressed on the surface of many leukocytes involved in the innate immune system, including monocytes, granulocytes, macrophages, and natural killer cells. It mediates inflammation by regulating leukocyte adhesion and migration and has been implicated in several immune processes such as phagocytosis, cell-mediated cytotoxicity, chemotaxis and cellular activation. It is involved in the complement system due to its capacity to bind inactivated complement component 3b (iC3b). [cite journal |author=Arnaout M, Todd R, Dana N, Melamed J, Schlossman S, Colten H |title=Inhibition of phagocytosis of complement C3- or immunoglobulin G-coated particles and of C3bi binding by monoclonal antibodies to a monocyte-granulocyte membrane glycoprotein (Mol) |journal=J Clin Invest |volume=72 |issue=1 |pages=171–9 |year=1983 |pmid=6874946 |doi=10.1172/JCI110955] The ITGAM (alpha) subunit of integrin αMβ2 is directly involved in causing the adhesion and spreading of cells but cannot mediate cellular migration without the presence of the β2 (CD18) subunit.

In genomewide association studies, single nucleotide polymorphisms in ITGAM had the strongest association with systemic lupus erythematosus, with an odds ratio of 1.65 for the T allele of rs9888739 and lupus. [cite journal |author=Mary K. Crow
title=Collaboration, Genetic Associations, and Lupus Erythematosus
journal=N Engl J Med
volume=358
issue=9
pages=956–961
year=2008
date=February 28, 2008
pmid=18204099
url=http://content.nejm.org/cgi/content/full/358/9/956
doi=10.1056/NEJMe0800096
] [cite journal |author=Geoffrey Hom, Robert R. Graham, Barmak Modrek, et al.
title=Association of Systemic Lupus Erythematosus with C8orf13–BLK and ITGAM–ITGAX
journal=N Engl J Med
volume=358
issue=9
pages=900–909
year=2008
date=February 28, 2008
pmid=18204098
url=http://content.nejm.org/cgi/content/full/358/9/900
doi=10.1056/NEJMoa0707865
]

ee also

* integrin

References

Further reading

PBB_Further_reading
citations =
*cite journal | author=Stewart M, Thiel M, Hogg N |title=Leukocyte integrins. |journal=Curr. Opin. Cell Biol. |volume=7 |issue= 5 |pages= 690–6 |year= 1996 |pmid= 8573344 |doi=
*cite journal | author=Todd RF, Petty HR |title=Beta 2 (CD11/CD18) integrins can serve as signaling partners for other leukocyte receptors. |journal=J. Lab. Clin. Med. |volume=129 |issue= 5 |pages= 492–8 |year= 1997 |pmid= 9142045 |doi=
*cite journal | author=Schymeinsky J, Mócsai A, Walzog B |title=Neutrophil activation via beta2 integrins (CD11/CD18): molecular mechanisms and clinical implications. |journal=Thromb. Haemost. |volume=98 |issue= 2 |pages= 262–73 |year= 2007 |pmid= 17721605 |doi=

External links

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