5men - Revision history

OCA at 18:41, 1 November 2023

OCA — Wed, 01 Nov 2023 18:41:09 GMT

←Older revision		Revision as of 18:41, 1 November 2023
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	<StructureSection load='5men' size='340' side='right'caption='[[5men]], [[Resolution\|resolution]] 2.81Å' scene=''>		<StructureSection load='5men' size='340' side='right'caption='[[5men]], [[Resolution\|resolution]] 2.81Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5men]] is a 5 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5MEN OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=5MEN FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5men]] is a 5 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=5MEN OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5MEN FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=EDO:1~~,2~~-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>~~</td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 2.81Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat">~~[[5meo\|5meo]]~~, ~~[[5mep\|5mep]], [[5meq\|5meq]], [[5mer\|5mer]], [[4mnq\|4mnq]]</td~~></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></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 HUMAN]), B2M, CDABP0092, HDCMA22P ([http~~:/~~/www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M, HDCMA22P ([http://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=5men FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5men OCA], [https://pdbe.org/5men PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5men RCSB], [https://www.ebi.ac.uk/pdbsum/5men PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5men ProSAT]</span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=5men FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5men OCA], [~~http~~://pdbe.org/5men PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5men RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5men PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5men ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[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>	+	[https://www.uniprot.org/uniprot/HLAA_HUMAN HLAA_HUMAN] Selection of immunotherapy in solid cancer;Birdshot chorioretinopathy;Prediction of phenytoin or carbamazepine toxicity. Alleles A02:01 and A24:02 are associated with increased susceptibility to diabetes mellitus, insulin-dependent (IDDM) (PubMed:22245737, PubMed:18802479, PubMed:16731854, PubMed:22522618). In a glucose-dependent way, allele A02:01 may aberrantly present the signal peptide of preproinsulin (ALWGPDPAAA) on the surface of pancreatic beta cells to autoreactive CD8-positive T cells, potentially driving T-cell mediated cytotoxicity in pancreatic islets (PubMed:22245737, PubMed:18802479). Allele A24:02 may present the signal peptide of preproinsulin (LWMRLLPLL) and contribute to acute pancreatic beta-cell destruction and early onset of IDDM (PubMed:16731854, PubMed:22522618).<ref>PMID:16731854</ref> <ref>PMID:18802479</ref> <ref>PMID:22245737</ref> <ref>PMID:22522618</ref> Allele A03:01 is associated with increased susceptibility to multiple sclerosis (MS), an autoimmune disease of the central nervous system (PubMed:10746785). May contribute to the initiation phase of the disease by presenting myelin PLP1 self-peptide (KLIETYFSK) to autoreactive CD8-positive T cells capable of initiating the first autoimmune attacks (PubMed:18953350).<ref>PMID:10746785</ref> <ref>PMID:18953350</ref> Allele A26:01 is associated with increased susceptibility to Behcet disease (BD) in the Northeast Asian population. Especially in the HLA-B51-negative BD populations, HLA-A26 is significantly associated with the onset of BD.<ref>PMID:30872678</ref> Allele A*29:02 is associated with increased susceptibility to birdshot chorioretinopathy (BSCR). May aberrantly present retinal autoantigens and induce autoimmune uveitis.<ref>PMID:1728143</ref>
	== Function ==		== Function ==
-	[~~[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~~/~~B2MG_HUMAN B2MG_HUMAN]] Component~~ of the ~~class I major histocompatibility complex~~ (~~MHC~~). ~~Involved~~ in the ~~presentation~~ of peptide antigens to the immune ~~system~~.	+	[https://www.uniprot.org/uniprot/HLAA_HUMAN HLAA_HUMAN] Antigen-presenting major histocompatibility complex class I (MHCI) molecule. In complex with B2M/beta 2 microglobulin displays primarily viral and tumor-derived peptides on antigen-presenting cells for recognition by alpha-beta T cell receptor (TCR) on HLA-A-restricted CD8-positive T cells, guiding antigen-specific T cell immune response to eliminate infected or transformed cells (PubMed:2456340, PubMed:2784196, PubMed:1402688, PubMed:7504010, PubMed:9862734, PubMed:10449296, PubMed:12138174, PubMed:12393434, PubMed:15893615, PubMed:17189421, PubMed:19543285, PubMed:21498667, PubMed:24192765, PubMed:7694806, PubMed:24395804, PubMed:28250417). May also present self-peptides derived from the signal sequence of secreted or membrane proteins, although T cells specific for these peptides are usually inactivated to prevent autoreactivity (PubMed:25880248, PubMed:7506728, PubMed:7679507). Both the peptide and the MHC molecule are recognized by TCR, the peptide is responsible for the fine specificity of antigen recognition and MHC residues account for the MHC restriction of T cells (PubMed:12796775, PubMed:18275829, PubMed:19542454, PubMed:28250417). Typically presents intracellular peptide antigens of 8 to 13 amino acids that arise from cytosolic proteolysis via IFNG-induced immunoproteasome or via endopeptidase IDE/insulin-degrading enzyme (PubMed:17189421, PubMed:20364150, PubMed:17079320, PubMed:26929325, PubMed:27049119). Can bind different peptides containing allele-specific binding motifs, which are mainly defined by anchor residues at position 2 and 9 (PubMed:7504010, PubMed:9862734).<ref>PMID:10449296</ref> <ref>PMID:12138174</ref> <ref>PMID:12393434</ref> <ref>PMID:12796775</ref> <ref>PMID:1402688</ref> <ref>PMID:15893615</ref> <ref>PMID:17079320</ref> <ref>PMID:17189421</ref> <ref>PMID:18275829</ref> <ref>PMID:19542454</ref> <ref>PMID:19543285</ref> <ref>PMID:20364150</ref> <ref>PMID:21498667</ref> <ref>PMID:24192765</ref> <ref>PMID:24395804</ref> <ref>PMID:2456340</ref> <ref>PMID:25880248</ref> <ref>PMID:26929325</ref> <ref>PMID:27049119</ref> <ref>PMID:2784196</ref> <ref>PMID:28250417</ref> <ref>PMID:7504010</ref> <ref>PMID:7506728</ref> <ref>PMID:7679507</ref> <ref>PMID:7694806</ref> <ref>PMID:9862734</ref> Allele A01:01: Presents a restricted peptide repertoire including viral epitopes derived from IAV NP/nucleoprotein (CTELKLSDY), IAV PB1/polymerase basic protein 1 (VSDGGPNLY), HAdV-11 capsid L3/hexon protein (LTDLGQNLLY), SARS-CoV-2 3a/ORF3a (FTSDYYQLY) as well as tumor peptide antigens including MAGE1 (EADPTGHSY), MAGEA3 (EVDPIGHLY) and WT1 (TSEKRPFMCAY), all having in common a canonical motif with a negatively charged Asp or Glu residue at position 3 and a Tyr anchor residue at the C-terminus (PubMed:1402688, PubMed:7504010, PubMed:17189421, PubMed:20364150, PubMed:25880248, PubMed:30530481, PubMed:19177349, PubMed:24395804, PubMed:26758806, PubMed:32887977). A number of HLA-A01:01-restricted peptides carry a post-translational modification with oxidation and N-terminal acetylation being the most frequent (PubMed:25880248). Fails to present highly immunogenic peptides from the EBV latent antigens (PubMed:18779413).<ref>PMID:1402688</ref> <ref>PMID:17189421</ref> <ref>PMID:18779413</ref> <ref>PMID:19177349</ref> <ref>PMID:20364150</ref> <ref>PMID:24395804</ref> <ref>PMID:25880248</ref> <ref>PMID:26758806</ref> <ref>PMID:30530481</ref> <ref>PMID:7504010</ref> Allele A02:01: A major allele in human populations, presents immunodominant viral epitopes derived from IAV M/matrix protein 1 (GILGFVFTL), HIV-1 env (TLTSCNTSV), HIV-1 gag-pol (ILKEPVHGV), HTLV-1 Tax (LLFGYPVYV), HBV C/core antigen (FLPSDFFPS), HCMV UL83/pp65 (NLVPMVATV) as well as tumor peptide antigens including MAGEA4 (GVYDGREHTV), WT1 (RMFPNAPYL) and CTAG1A/NY-ESO-1 (SLLMWITQC), all having in common hydrophobic amino acids at position 2 and at the C-terminal anchors.<ref>PMID:11502003</ref> <ref>PMID:12138174</ref> <ref>PMID:12796775</ref> <ref>PMID:17079320</ref> <ref>PMID:18275829</ref> <ref>PMID:19542454</ref> <ref>PMID:20619457</ref> <ref>PMID:22245737</ref> <ref>PMID:26929325</ref> <ref>PMID:2784196</ref> <ref>PMID:28250417</ref> <ref>PMID:7694806</ref> <ref>PMID:7935798</ref> <ref>PMID:8630735</ref> <ref>PMID:8805302</ref> <ref>PMID:8906788</ref> <ref>PMID:9177355</ref> Allele A03:01: Presents viral epitopes derived from IAV NP (ILRGSVAHK), HIV-1 nef (QVPLRPMTYK), HIV-1 gag-pol (AIFQSSMTK), SARS-CoV-2 N/nucleoprotein (KTFPPTEPK) as well as tumor peptide antigens including PMEL (LIYRRRLMK), NODAL (HAYIQSLLK), TRP-2 (RMYNMVPFF), all having in common hydrophobic amino acids at position 2 and Lys or Arg anchor residues at the C-terminus (PubMed:7504010, PubMed:7679507, PubMed:9862734, PubMed:19543285, PubMed:21943705, PubMed:2456340, PubMed:32887977). May also display spliced peptides resulting from the ligation of two separate proteasomal cleavage products that are not contiguous in the parental protein (PubMed:27049119).<ref>PMID:19543285</ref> <ref>PMID:21943705</ref> <ref>PMID:2456340</ref> <ref>PMID:27049119</ref> <ref>PMID:7504010</ref> <ref>PMID:7679507</ref> <ref>PMID:9862734</ref> Allele A11:01: Presents several immunodominant epitopes derived from HIV-1 gag-pol and HHV-4 EBNA4, containing the peptide motif with Val, Ile, Thr, Leu, Tyr or Phe at position 2 and Lys anchor residue at the C-terminus. Important in the control of HIV-1, EBV and HBV infections (PubMed:10449296). Presents an immunodominant epitope derived from SARS-CoV-2 N/nucleoprotein (KTFPPTEPK) (PubMed:32887977).<ref>PMID:10449296</ref> <ref>PMID:32887977</ref> Allele A23:01: Interacts with natural killer (NK) cell receptor KIR3DL1 and may contribute to functional maturation of NK cells and self-nonself discrimination during innate immune response.<ref>PMID:17182537</ref> Allele A24:02: Presents viral epitopes derived from HIV-1 nef (RYPLTFGWCF), EBV lytic- and latent-cycle antigens BRLF1 (TYPVLEEMF), BMLF1 (DYNFVKQLF) and LMP2 (IYVLVMLVL), SARS-CoV nucleocapsid/N (QFKDNVILL), as well as tumor peptide antigens including PRAME (LYVDSLFFL), all sharing a common signature motif, namely an aromatic residue Tyr or Phe at position 2 and a nonhydrophobic anchor residue Phe, Leu or Iso at the C-terminus (PubMed:9047241, PubMed:12393434, PubMed:24192765, PubMed:20844028). Interacts with natural killer (NK) cell receptor KIR3DL1 and may contribute to functional maturation of NK cells and self-nonself discrimination during innate immune response (PubMed:17182537, PubMed:18502829).<ref>PMID:12393434</ref> <ref>PMID:17182537</ref> <ref>PMID:18502829</ref> <ref>PMID:20844028</ref> <ref>PMID:24192765</ref> <ref>PMID:9047241</ref> Allele A26:01: Presents several epitopes derived from HIV-1 gag-pol (EVIPMFSAL, ETKLGKAGY) and env (LVSDGGPNLY), carrying as anchor residues preferentially Glu at position 1, Val or Thr at position 2 and Tyr at the C-terminus.<ref>PMID:15893615</ref> Allele A29:02: Presents peptides having a common motif, namely a Glu residue at position 2 and Tyr or Leu anchor residues at the C-terminus.<ref>PMID:8622959</ref> Allele A32:01: Interacts with natural killer (NK) cell receptor KIR3DL1 and may contribute to functional maturation of NK cells and self-nonself discrimination during innate immune response.<ref>PMID:17182537</ref> Allele A68:01: Presents viral epitopes derived from IAV NP (KTGGPIYKR) and HIV-1 tat (ITKGLGISYGR), having a common signature motif namely, Val or Thr at position 2 and positively charged residues Arg or Lys at the C-terminal anchor.<ref>PMID:1448153</ref> <ref>PMID:1448154</ref> <ref>PMID:2784196</ref> Allele A74:01: Presents immunodominant HIV-1 epitopes derived from gag-pol (GQMVHQAISPR, QIYPGIKVR) and rev (RQIHSISER), carrying an aliphatic residue at position 2 and Arg anchor residue at the C-terminus. May contribute to viral load control in chronic HIV-1 infection.<ref>PMID:21498667</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Cole~~, D K~~]]	+	[[Category: Cole DK]]
-	[[Category: Crowther, M]]	+	[[Category: Crowther M]]
-	[[Category: Lloyd, A]]	+	[[Category: Lloyd A]]
-	[[Category: Rizkallah~~, P J~~]]	+	[[Category: Rizkallah PJ]]
-	[[Category: Sewell~~, A K]]~~	+	[[Category: Sewell AK]]
-	~~[[Category: 1e6-tcr]]~~	+
-	~~[[Category: Cross-reactivity]]~~	+
-	~~[[Category: Hla-a02]]~~	+
-	~~[[Category: Immune system]]~~	+
-	~~[[Category: Immuno~~]]	+

OCA at 07:17, 19 August 2020

OCA — Wed, 19 Aug 2020 07:17:14 GMT

←Older revision		Revision as of 07:17, 19 August 2020
Line 1:		Line 1:

	==Human Leukocyte Antigen A02 presenting ILAKFLHWL, in complex with cognate T-Cell Receptor==		==Human Leukocyte Antigen A02 presenting ILAKFLHWL, in complex with cognate T-Cell Receptor==
-	<StructureSection load='5men' size='340' side='right' caption='[[5men]], [[Resolution\|resolution]] 2.81Å' scene=''>	+	<StructureSection load='5men' size='340' side='right'caption='[[5men]], [[Resolution\|resolution]] 2.81Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5men]] is a 5 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5MEN OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5MEN FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5men]] is a 5 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5MEN OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=5MEN FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5meo\|5meo]], [[5mep\|5mep]], [[5meq\|5meq]], [[5mer\|5mer]], [[4mnq\|4mnq]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5meo\|5meo]], [[5mep\|5mep]], [[5meq\|5meq]], [[5mer\|5mer]], [[4mnq\|4mnq]]</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=5men FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5men OCA], [http://pdbe.org/5men PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5men RCSB], [http://www.ebi.ac.uk/pdbsum/5men PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5men ProSAT]</span></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 HUMAN]), B2M, CDABP0092, HDCMA22P ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M, HDCMA22P ([http://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'>[http://proteopedia.org/fgij/fg.htm?mol=5men FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5men OCA], [http://pdbe.org/5men PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5men RCSB], [http://www.ebi.ac.uk/pdbsum/5men PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5men ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 23:		Line 24:

	==See Also==		==See Also==
-	*[[Beta-2 microglobulin\|Beta-2 microglobulin]]	+	*[[Beta-2 microglobulin 3D structures\|Beta-2 microglobulin 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Cole, D K]]		[[Category: Cole, D K]]
	[[Category: Crowther, M]]		[[Category: Crowther, M]]

OCA at 09:42, 22 March 2017

OCA — Wed, 22 Mar 2017 09:42:03 GMT

←Older revision		Revision as of 09:42, 22 March 2017
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	</div>		</div>
	<div class="pdbe-citations 5men" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5men" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Beta-2 microglobulin\|Beta-2 microglobulin]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:32, 15 December 2016

OCA — Thu, 15 Dec 2016 11:32:27 GMT

←Older revision		Revision as of 11:32, 15 December 2016
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	== Function ==		== Function ==
	[[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/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/1A02_HUMAN 1A02_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 ==
		+	T-cell cross-reactivity is essential for effective immune surveillance, but has also been implicated as a pathway to autoimmunity. Previous studies have demonstrated that T-cell receptors (TCRs) that focus on a minimal motif within the peptide are able to facilitate a high level of T-cell cross-reactivity. However, the structural database shows that most TCRs exhibit less focussed antigen binding involving contact with more peptide residues. To further explore the structural features that allow the clonally expressed TCR to functionally engage with multiple peptide-major histocompatibility complexes (pMHCs), we examined the ILA1 CD8+ T-cell clone that responds to a peptide sequence derived from human telomerase reverse transcriptase (hTERT). The ILA1 TCR contacted its pMHC with a broad peptide-binding footprint encompassing spatially distant peptide residues. Despite the lack of focused TCR-peptide binding , the ILA1 T-cell clone was still cross-reactive. Overall, the TCR-peptide contacts apparent in the structure correlated well with the level of degeneracy at different peptide positions. Thus, the ILA1 TCR was less tolerant of changes at peptide residues that were at, or adjacent to, key contact sites. This study provides new insights into the molecular mechanisms that control T-cell cross-reactivity, with important implications for pathogen surveillance, autoimmunity and transplant rejection.
		+
		+	Structural mechanism underpinning cross-reactivity of a CD8+ T-cell clone that recognises a peptide derived from human telomerase reverse transcriptase.,Cole DK, van den Berg HA, Lloyd A, Crowther MD, Beck K, Ekeruche-Makinde J, Miles JJ, Bulek AM, Dolton G, Schauenburg AJ, Wall A, Fuller A, Clement M, Laugel B, Rizkallah PJ, Wooldridge L, Sewell AK J Biol Chem. 2016 Nov 30. pii: jbc.M116.741603. PMID:27903649<ref>PMID:27903649</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 5men" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA: Protected "5men" [edit=sysop:move=sysop]

OCA — Sun, 11 Dec 2016 02:18:41 GMT

Protected "5men" [edit=sysop:move=sysop]

←Older revision

Revision as of 02:18, 11 December 2016

OCA: New page: ==Human Leukocyte Antigen A02 presenting ILAKFLHWL, in complex with cognate T-Cell Receptor== == Structural highlights ==
<table><tr><td colspan='2'>[[5men]] is a 5 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5MEN OCA]. For a guided tour on the structure components use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5MEN FirstGlance]. 
</td></tr><tr id='ligand'><td class="sblockLbl">[[Ligand|Ligands:]]</td><td class="sblockDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
<tr id='related'><td class="sblockLbl">[[Related_structure|Related:]]</td><td class="sblockDat">[[5meo|5meo]], [[5mep|5mep]], [[5meq|5meq]], [[5mer|5mer]], [[4mnq|4mnq]]</td></tr>
<tr id='resources'><td class="sblockLbl">Resources:</td><td class="sblockDat">[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5men FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5men OCA], [http://pdbe.org/5men PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5men RCSB], [http://www.ebi.ac.uk/pdbsum/5men PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5men ProSAT]</td></tr>
</table>
== Disease ==
[[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 ==
[[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/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.
== References ==
<references/>
TOC
</StructureSection>
[[Category: Cole, D K]]
[[Category: Crowther, M]]
[[Category: Lloyd, A]]
[[Category: Rizkallah, P J]]
[[Category: Sewell, A K]]
[[Category: 1e6-tcr]]
[[Category: Cross-reactivity]]
[[Category: Hla-a02]]
[[Category: Immune system]]
[[Category: Immuno]]