2aty: Difference between revisions

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{{STRUCTURE_2aty|  PDB=2aty  |  SCENE=  }}
===Complement receptor chimaeric conjugate CR2-Ig===
{{ABSTRACT_PUBMED_16375923}}


==About this Structure==
==Complement receptor chimaeric conjugate CR2-Ig==
[[2aty]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2ATY OCA].  
<StructureSection load='2aty' size='340' side='right'caption='[[2aty]]' scene=''>
 
== Structural highlights ==
==Reference==
<table><tr><td colspan='2'>[[2aty]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2ATY OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2ATY FirstGlance]. <br>
<ref group="xtra">PMID:016375923</ref><references group="xtra"/><references/>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray solution scattering</td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2aty FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2aty OCA], [https://pdbe.org/2aty PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2aty RCSB], [https://www.ebi.ac.uk/pdbsum/2aty PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2aty ProSAT]</span></td></tr>
</table>
== Disease ==
[https://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[https://omim.org/entry/610927 610927]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref>  Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[https://omim.org/entry/614699 614699]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>
== Function ==
[https://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN] Receptor for complement C3Dd, for the Epstein-Barr virus on human B-cells and T-cells and for HNRPU. Participates in B lymphocytes activation.<ref>PMID:7753047</ref> [https://www.uniprot.org/uniprot/IGHG1_MOUSE IGHG1_MOUSE]
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
  <jmolCheckbox>
    <scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/at/2aty_consurf.spt"</scriptWhenChecked>
    <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
    <text>to colour the structure by Evolutionary Conservation</text>
  </jmolCheckbox>
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=2aty ConSurf].
<div style="clear:both"></div>
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Aslam, M.]]
[[Category: Large Structures]]
[[Category: Gilbert, H E.]]
[[Category: Mus musculus]]
[[Category: Guthridge, J M.]]
[[Category: Aslam M]]
[[Category: Holers, V M.]]
[[Category: Gilbert HE]]
[[Category: Perkins, S J.]]
[[Category: Guthridge JM]]
[[Category: Antibody]]
[[Category: Holers VM]]
[[Category: Complement]]
[[Category: Perkins SJ]]
[[Category: Immune system]]
[[Category: Immunoglobulin fold]]

Latest revision as of 12:14, 14 February 2024

Complement receptor chimaeric conjugate CR2-IgComplement receptor chimaeric conjugate CR2-Ig

Structural highlights

2aty is a 2 chain structure with sequence from Homo sapiens and Mus musculus. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:X-ray solution scattering
Resources:FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT

Disease

CR2_HUMAN Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:610927. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.[1] Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:614699. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.[2]

Function

CR2_HUMAN Receptor for complement C3Dd, for the Epstein-Barr virus on human B-cells and T-cells and for HNRPU. Participates in B lymphocytes activation.[3] IGHG1_MOUSE

Evolutionary Conservation

Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf.

References

  1. ↑ Wu H, Boackle SA, Hanvivadhanakul P, Ulgiati D, Grossman JM, Lee Y, Shen N, Abraham LJ, Mercer TR, Park E, Hebert LA, Rovin BH, Birmingham DJ, Chang DM, Chen CJ, McCurdy D, Badsha HM, Thong BY, Chng HH, Arnett FC, Wallace DJ, Yu CY, Hahn BH, Cantor RM, Tsao BP. Association of a common complement receptor 2 haplotype with increased risk of systemic lupus erythematosus. Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):3961-6. Epub 2007 Feb 22. PMID:17360460 doi:0609101104
  2. ↑ Thiel J, Kimmig L, Salzer U, Grudzien M, Lebrecht D, Hagena T, Draeger R, Volxen N, Bergbreiter A, Jennings S, Gutenberger S, Aichem A, Illges H, Hannan JP, Kienzler AK, Rizzi M, Eibel H, Peter HH, Warnatz K, Grimbacher B, Rump JA, Schlesier M. Genetic CD21 deficiency is associated with hypogammaglobulinemia. J Allergy Clin Immunol. 2012 Mar;129(3):801-810.e6. doi:, 10.1016/j.jaci.2011.09.027. Epub 2011 Oct 27. PMID:22035880 doi:10.1016/j.jaci.2011.09.027
  3. ↑ Barel M, Balbo M, Gauffre A, Frade R. Binding sites of the Epstein-Barr virus and C3d receptor (CR2, CD21) for its three intracellular ligands, the p53 anti-oncoprotein, the p68 calcium binding protein and the nuclear p120 ribonucleoprotein. Mol Immunol. 1995 Apr;32(6):389-97. PMID:7753047
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