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3kla
From Proteopedia
(Difference between revisions)
(New page: '''Unreleased structure''' The entry 3kla is ON HOLD Authors: Chen, J.L., Morgan, A.J., Stewart-Jones, G., Shepherd, D., Bossi, G., Wooldridge, L. Description: Ca2+ release from the en...) |
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| - | '''Unreleased structure''' | ||
| - | + | ==Ca2+ release from the endoplasmic reticulum of NY-ESO-1 specific T cells is modulated by the affinity of T cell receptor and by the use of the CD8 co-receptor== | |
| + | <StructureSection load='3kla' size='340' side='right'caption='[[3kla]], [[Resolution|resolution]] 1.65Å' scene=''> | ||
| + | == Structural highlights == | ||
| + | <table><tr><td colspan='2'>[[3kla]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KLA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3KLA FirstGlance]. <br> | ||
| + | </td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">HLA-A, HLAA ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M, CDABP0092, HDCMA22P ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=3kla FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kla OCA], [https://pdbe.org/3kla PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3kla RCSB], [https://www.ebi.ac.uk/pdbsum/3kla PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3kla ProSAT]</span></td></tr> | ||
| + | </table> | ||
| + | == Disease == | ||
| + | [[https://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[https://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 == | ||
| + | [[https://www.uniprot.org/uniprot/1A02_HUMAN 1A02_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[https://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. | ||
| + | == 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/kl/3kla_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=3kla ConSurf]. | ||
| + | <div style="clear:both"></div> | ||
| + | <div style="background-color:#fffaf0;"> | ||
| + | == Publication Abstract from PubMed == | ||
| + | Although several cancer immunotherapy strategies are based on the use of analog peptides and on the modulation of the TCR affinity of adoptively transferred T cells, it remains unclear whether tumor-specific T cell activation by strong and weak TCR stimuli evoke different Ca(2+) signatures from the Ca(2+) intracellular stores and whether the amplitude of Ca(2+) release from the endoplasmic reticulum (ER) can be further modulated by coreceptor binding to peptide/MHC. In this study, we combined functional, structural, and kinetic measurements to correlate the intensity of Ca(2+) signals triggered by the stimulation of the 1G4 T cell clone specific to the tumor epitope NY-ESO-1(157-165). Two analogs of the NY-ESO-1(157-165) peptide, having similar affinity to HLA-A2 molecules, but a 6-fold difference in binding affinity for the 1G4 TCR, resulted in different Ca(2+) signals and T cell activation. 1G4 stimulation by the stronger stimulus emptied the ER of stored Ca(2+), even in the absence of CD8 binding, resulting in sustained Ca(2+) influx. In contrast, the weaker stimulus induced only partial emptying of stored Ca(2+), resulting in significantly diminished and oscillatory Ca(2+) signals, which were enhanced by CD8 binding. Our data define the range of TCR/peptide MHC affinities required to induce depletion of Ca(2+) from intracellular stores and provide insights into the ability of T cells to tailor the use of the CD8 coreceptor to enhance Ca(2+) release from the ER. This, in turn, modulates Ca(2+) influx from the extracellular environment, ultimately controlling T cell activation. | ||
| - | + | Ca2+ release from the endoplasmic reticulum of NY-ESO-1-specific T cells is modulated by the affinity of TCR and by the use of the CD8 coreceptor.,Chen JL, Morgan AJ, Stewart-Jones G, Shepherd D, Bossi G, Wooldridge L, Hutchinson SL, Sewell AK, Griffiths GM, van der Merwe PA, Jones EY, Galione A, Cerundolo V J Immunol. 2010 Feb 15;184(4):1829-39. Epub 2010 Jan 6. PMID:20053942<ref>PMID:20053942</ref> | |
| - | + | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |
| + | </div> | ||
| + | <div class="pdbe-citations 3kla" style="background-color:#fffaf0;"></div> | ||
| - | + | ==See Also== | |
| + | *[[Beta-2 microglobulin 3D structures|Beta-2 microglobulin 3D structures]] | ||
| + | == References == | ||
| + | <references/> | ||
| + | __TOC__ | ||
| + | </StructureSection> | ||
| + | [[Category: Human]] | ||
| + | [[Category: Large Structures]] | ||
| + | [[Category: Bossi, G]] | ||
| + | [[Category: Chen, J L]] | ||
| + | [[Category: Morgan, A J]] | ||
| + | [[Category: Shepherd, D]] | ||
| + | [[Category: Stewart-Jones, G]] | ||
| + | [[Category: Wooldridge, L]] | ||
| + | [[Category: Disulfide bond]] | ||
| + | [[Category: Glycoprotein]] | ||
| + | [[Category: Immune response]] | ||
| + | [[Category: Immune system]] | ||
| + | [[Category: Immunoglobulin domain]] | ||
| + | [[Category: Immunology]] | ||
| + | [[Category: Membrane]] | ||
| + | [[Category: Mhc]] | ||
| + | [[Category: Mhc i]] | ||
| + | [[Category: Transmembrane]] | ||
| + | [[Category: Tumour]] | ||
Current revision
Ca2+ release from the endoplasmic reticulum of NY-ESO-1 specific T cells is modulated by the affinity of T cell receptor and by the use of the CD8 co-receptor
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Categories: Human | Large Structures | Bossi, G | Chen, J L | Morgan, A J | Shepherd, D | Stewart-Jones, G | Wooldridge, L | Disulfide bond | Glycoprotein | Immune response | Immune system | Immunoglobulin domain | Immunology | Membrane | Mhc | Mhc i | Transmembrane | Tumour
