3mrr

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{{STRUCTURE_3mrr| PDB=3mrr | SCENE= }}
 
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===Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide===
 
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==Disease==
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==Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide==
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[[http://www.uniprot.org/uniprot/SO2A1_HUMAN SO2A1_HUMAN]] Defects in SLCO2A1 are the cause of hypertrophic osteoarthropathy, primary, autosomal recessive, type 2 (PHOAR2) [MIM:[http://omim.org/entry/614441 614441]]. PHOAR2 is a disease characterized by digital clubbing, periostosis, acroosteolysis, painful joint enlargement, and variable features of pachydermia that include thickened facial skin and a thickened scalp. Other developmental anomalies include delayed closure of the cranial sutures and congenital heart disease.<ref>PMID:22331663</ref><ref>PMID:22197487</ref><ref>PMID:22553128</ref><ref>PMID:22696055</ref> [[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>
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<StructureSection load='3mrr' size='340' side='right'caption='[[3mrr]], [[Resolution|resolution]] 1.60&Aring;' scene=''>
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== Structural highlights ==
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<table><tr><td colspan='2'>[[3mrr]] is a 3 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3MRR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3MRR FirstGlance]. <br>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.6&#8491;</td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3mrr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3mrr OCA], [https://pdbe.org/3mrr PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3mrr RCSB], [https://www.ebi.ac.uk/pdbsum/3mrr PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3mrr ProSAT]</span></td></tr>
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</table>
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== Disease ==
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[https://www.uniprot.org/uniprot/SO2A1_HUMAN SO2A1_HUMAN] Defects in SLCO2A1 are the cause of hypertrophic osteoarthropathy, primary, autosomal recessive, type 2 (PHOAR2) [MIM:[https://omim.org/entry/614441 614441]. PHOAR2 is a disease characterized by digital clubbing, periostosis, acroosteolysis, painful joint enlargement, and variable features of pachydermia that include thickened facial skin and a thickened scalp. Other developmental anomalies include delayed closure of the cranial sutures and congenital heart disease.<ref>PMID:22331663</ref> <ref>PMID:22197487</ref> <ref>PMID:22553128</ref> <ref>PMID:22696055</ref>
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== Function ==
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[https://www.uniprot.org/uniprot/SO2A1_HUMAN SO2A1_HUMAN] May mediate the release of newly synthesized prostaglandins from cells, the transepithelial transport of prostaglandins, and the clearance of prostaglandins from the circulation. Transports PGD2, as well as PGE1, PGE2 and PGF2A.
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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The structural rules governing peptide/MHC (pMHC) recognition by T cells remain unclear. To address this question, we performed a structural characterization of several HLA-A2/peptide complexes and assessed in parallel their antigenicity, by analyzing the frequency of the corresponding Ag-specific naive T cells in A2(+) and A2(-) individuals, as well as within CD4(+) and CD8(+) subsets. We were able to find a correlation between specific naive T cell frequency and peptide solvent accessibility and/or mobility for a subset of moderately prominent peptides. However, one single structural parameter of the pMHC complexes could not be identified to explain each peptide antigenicity. Enhanced pMHC antigenicity was associated with both highly biased TRAV usage, possibly reflecting favored interaction between particular pMHC complexes and germline TRAV loops, and peptide structural features allowing interactions with a broad range of permissive CDR3 loops. In this context of constrained TCR docking mode, an optimal peptide solvent exposed surface leading to an optimal complementarity with TCR interface may constitute one of the key features leading to high frequency of specific T cells. Altogether our results suggest that frequency of specific T cells depends on the fine-tuning of several parameters, the structural determinants governing TCR-pMHC interaction being just one of them.
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==Function==
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Analysis of relationships between peptide/MHC structural features and naive T cell frequency in humans.,Reiser JB, Legoux F, Gras S, Trudel E, Chouquet A, Leger A, Le Gorrec M, Machillot P, Bonneville M, Saulquin X, Housset D J Immunol. 2014 Dec 15;193(12):5816-26. doi: 10.4049/jimmunol.1303084. Epub 2014 , Nov 12. PMID:25392532<ref>PMID:25392532</ref>
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[[http://www.uniprot.org/uniprot/1A02_HUMAN 1A02_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/SO2A1_HUMAN SO2A1_HUMAN]] May mediate the release of newly synthesized prostaglandins from cells, the transepithelial transport of prostaglandins, and the clearance of prostaglandins from the circulation. Transports PGD2, as well as PGE1, PGE2 and PGF2A. [[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.
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==About this Structure==
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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[[3mrr]] is a 3 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=3MRR OCA].
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</div>
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<div class="pdbe-citations 3mrr" style="background-color:#fffaf0;"></div>
==See Also==
==See Also==
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*[[Beta-2 microglobulin|Beta-2 microglobulin]]
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*[[Beta-2 microglobulin 3D structures|Beta-2 microglobulin 3D structures]]
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*[[Major histocompatibility complex|Major histocompatibility complex]]
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== References ==
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<references/>
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==Reference==
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__TOC__
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<references group="xtra"/><references/>
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</StructureSection>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
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[[Category: Bonneville, M.]]
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[[Category: Large Structures]]
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[[Category: Chouquet, A.]]
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[[Category: Bonneville M]]
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[[Category: Debeaupuis, E.]]
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[[Category: Chouquet A]]
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[[Category: Echasserieau, K.]]
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[[Category: Debeaupuis E]]
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[[Category: Housset, D.]]
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[[Category: Echasserieau K]]
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[[Category: Legoux, F.]]
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[[Category: Housset D]]
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[[Category: Machillot, P.]]
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[[Category: Legoux F]]
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[[Category: Reiser, J B.]]
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[[Category: Machillot P]]
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[[Category: Saulquin, X.]]
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[[Category: Reiser J-B]]
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[[Category: Decapeptide]]
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[[Category: Saulquin X]]
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[[Category: Hla]]
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[[Category: Immune response]]
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[[Category: Immune system]]
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[[Category: Mart1 analogue]]
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[[Category: Melan-a analogue]]
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[[Category: Mhc class i]]
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[[Category: Prostaglandin transporter]]
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[[Category: Self peptide]]
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[[Category: Tumoral peptide]]
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Current revision

Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide

PDB ID 3mrr

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