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3qzw
From Proteopedia
(Difference between revisions)
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| - | + | ==Plasticity of human CD8 binding to peptide-HLA-A*2402== | |
| - | + | <StructureSection load='3qzw' size='340' side='right' caption='[[3qzw]], [[Resolution|resolution]] 2.80Å' scene=''> | |
| - | + | == Structural highlights == | |
| - | + | <table><tr><td colspan='2'>[[3qzw]] is a 10 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=3QZW OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QZW FirstGlance]. <br> | |
| - | ==Disease== | + | </td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3nfj|3nfj]]</td></tr> |
| + | <tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">HLA-A, HLAA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), B2M, CDABP0092, HDCMA22P ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), CD8A, MAL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr> | ||
| + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3qzw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qzw OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3qzw RCSB], [http://www.ebi.ac.uk/pdbsum/3qzw PDBsum]</span></td></tr> | ||
| + | </table> | ||
| + | == Disease == | ||
[[http://www.uniprot.org/uniprot/CD8A_HUMAN CD8A_HUMAN]] Defects in CD8A are a cause of familial CD8 deficiency (CD8 deficiency) [MIM:[http://omim.org/entry/608957 608957]]. Familial CD8 deficiency is a novel autosomal recessive immunologic defect characterized by absence of CD8+ cells, leading to recurrent bacterial infections. [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref> | [[http://www.uniprot.org/uniprot/CD8A_HUMAN CD8A_HUMAN]] Defects in CD8A are a cause of familial CD8 deficiency (CD8 deficiency) [MIM:[http://omim.org/entry/608957 608957]]. Familial CD8 deficiency is a novel autosomal recessive immunologic defect characterized by absence of CD8+ cells, leading to recurrent bacterial infections. [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref> | ||
| - | + | == Function == | |
| - | ==Function== | + | |
[[http://www.uniprot.org/uniprot/CD8A_HUMAN CD8A_HUMAN]] Identifies cytotoxic/suppressor T-cells that interact with MHC class I bearing targets. CD8 is thought to play a role in the process of T-cell mediated killing. CD8 alpha chains binds to class I MHC molecules alpha-3 domains. [[http://www.uniprot.org/uniprot/1A24_HUMAN 1A24_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. | [[http://www.uniprot.org/uniprot/CD8A_HUMAN CD8A_HUMAN]] Identifies cytotoxic/suppressor T-cells that interact with MHC class I bearing targets. CD8 is thought to play a role in the process of T-cell mediated killing. CD8 alpha chains binds to class I MHC molecules alpha-3 domains. [[http://www.uniprot.org/uniprot/1A24_HUMAN 1A24_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. | ||
| + | <div style="background-color:#fffaf0;"> | ||
| + | == Publication Abstract from PubMed == | ||
| + | The human CD8 functions as a co-receptor for specific T cell recognition, and only one complex structure of human CD8alphaalpha binding to HLA-A*0201 has been solved, revealing the molecular basis of CD8 interacting with its ligand pHLA. Here, we present the complex structures of human CD8alphaalpha bound to HLA-A*2402, which demonstrate two opposite alpha3 domain CD loop shifts (either pull or push) in the HLA heavy chain upon CD8 engagement. Taking the previously reported mouse CD8-pMHC complex structures into account, from the structural view, all of the data indicate the plasticity of CD8 binding to pMHC/HLA, which facilitates its co-receptor function for T cells. The plasticity of CD8 binding appears not to affect the specificity of TCR recognition, as no peptide conformation change extends to the pMHC interface for TCR contacting. | ||
| - | + | Plasticity of human CD8alphaalpha binding to peptide-HLA-A*2402.,Shi Y, Qi J, Iwamoto A, Gao GF Mol Immunol. 2011 Jun 4. PMID:21645925<ref>PMID:21645925</ref> | |
| - | + | ||
| + | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | ||
| + | </div> | ||
==See Also== | ==See Also== | ||
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*[[Major histocompatibility complex|Major histocompatibility complex]] | *[[Major histocompatibility complex|Major histocompatibility complex]] | ||
*[[Multiple sclerosis|Multiple sclerosis]] | *[[Multiple sclerosis|Multiple sclerosis]] | ||
| - | + | == References == | |
| - | == | + | <references/> |
| - | + | __TOC__ | |
| + | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: Gao, G F | + | [[Category: Gao, G F]] |
| - | [[Category: Qi, J | + | [[Category: Qi, J]] |
| - | [[Category: Shi, Y | + | [[Category: Shi, Y]] |
[[Category: Coreceptor]] | [[Category: Coreceptor]] | ||
[[Category: Immune system]] | [[Category: Immune system]] | ||
[[Category: Immunoglobulin family]] | [[Category: Immunoglobulin family]] | ||
Revision as of 11:08, 19 December 2014
Plasticity of human CD8 binding to peptide-HLA-A*2402
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