Complement component 2: Difference between revisions

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{{For the|the aircraft|Grumman C-2 Greyhound}}{{Short description|Protein-coding genefound in the species Homo sapienshumans}}

{{More footnotes needed|date=April 2023}}

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{{Infobox_gene}}

'''Complement C2''' is a [[protein]] that in humans is encoded by the ''C2'' [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: C2 complement component 2| url = https://www.ncbi.nlm.nih.gov/sites/entrezgene?Db=gene&Cmd=ShowDetailView&TermToSearch=717}}</ref> The protein encoded by this gene is part of the [[classical complement pathway|classical pathway]] of the [[complement system]], acting as a multi-___domain serine protease. Deficiency of C2 has been associated with certain autoimmune diseases.<ref name="entrez"/>

The '''Complement system''' is generated to regulate self protection from infection. The overall Complement system is composed of protein groups that collaborate in destroying foreign invaders, which ultimately remove debris from cells and tissues. When the body detects a foreign invader, the body signals the Complement system and the Complement component 2 protein attaches to Complement system 4 resulting in an [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923430/ immune response.] Complement component 2 protein is critical for regulating the body's immune response. The C2 nerves carry messages to muscles involved in neck flexion.

== Function ==

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Photosensitive patients with C2 type I deficiency have poor prognosis. C2 type I deficiency is caused by a 28-base pair gene deletion, resulting in premature termination codon and lack of C2 protein. Patients with LE associated with complement C4 or C2 deficiencies have a better prognosis than those without inherited deficiencies. Complement component 2 deficiency increases risk of autoimmune disorders which may be managed by receiving the adequate care. Clinically, this is significant since Complement component 2 deficiency increases the risk of recurrent bacterial infections, which may be life-threatening.

== Other Namesnames ==

This gene is also known as:

There are numerous forms of naming this gene. For example:

* ARMD14

* C3/C5 convertase

* {{proper name|CO2}}

* complementComplement component 2

* complementComplement component C2

== References ==

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=== Bibliography ===

{{refbegin}}

* Jonsson G, Truedsson L, Sturfelt G, Oxelius VA, Braconier JH, Sjoholm AG. Hereditary C2 deficiency in Sweden: frequent occurrence of invasive infection, atherosclerosis, and rheumatic disease. Medicine (Baltimore). 2005Jan;84(1):23-34. doi: 10.1097/01.md.0000152371.22747.1e. Citation on PubMed (https://pubmed.ncb{{Dead link|date=December 2023 |bot=InternetArchiveBot |fix-attempted=yes }} i.nlm.nih.gov/15643297)

* Complement+2 at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Sjöholm AG, Jönsson G, Braconier JH, Sturfelt G, Truedsson L. Complement deficiency and disease: an update. Mol Immunol. 2006 Jan;43(1-2):78-85. doi: 10.1016/j.molimm.2005.06.025. PMID 16026838.

* Wen L, Atkinson JP, Giclas PC. Clinical and laboratory evaluation of complement deficiency. J Allergy Clin Immunol. 2004 Apr;113(4):585-93; quiz 594. doi: 10.1016/j.jaci.2004.02.003. PMID 15100659.

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* {{cite journal | vauthors = Kerr MA, Gagnon J | title = The purification and properties of the second component of guinea-pig complement | journal = The Biochemical Journal | volume = 205 | issue = 1 | pages = 59–67 | date = Jul 1982 | pmid = 6922702 | pmc = 1158446 | doi = 10.1042/bj2050059}}

* Liu C-C, Ahearn JM. Complement and systemic lupus erythematosus. 7th ed. In: Wallace DJ, Hahn BH, editors. Dubois’ Lupus Erythematosus. (Chap. 13), Philadelphia: Lippincott Williams & Wilkins (2007). p.&nbsp;214–35.

* Grammatikos AP, Tsokos GC. Immunodeficiency and autoimmunity: lessons from systemic lupus erythematosus. Trends Mol Med (2012) 18:101–8. [[doi: [http://10.1016/j.molmed.2011.10.005 10.1016/j.molmed.2011.10.005]]

* Ippolito A, Wallace DJ, Gladman D, Fortin PR, Urowitz M, Werth V, et al. Auto-antibodies in systemic lupus erythematosus: comparison of historical and current assessment of seropositivity. Lupus (2011) 20:250–5. [[doi:10.1177/0961203310385738]]

* Outer surface lipoproteins from the Lyme disease spirochete exploit the molecular switch mechanism of the complement protease C1s. arrigues et al.Journal of Biological ChemistrySeptember 29, 2022