3mrr - Revision history

OCA at 02:08, 21 November 2024

2024-11-21T02:08:40Z

← Older revision		Revision as of 02:08, 21 November 2024
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	</table>		</table>
	== Disease ==		== Disease ==
	[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>		[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>
	== Function ==		== Function ==
	[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>~~		[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.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==

OCA at 16:38, 1 November 2023

2023-11-01T16:38:35Z

Show changes

OCA at 13:50, 4 May 2022

2022-05-04T13:50:26Z

← Older revision		Revision as of 13:50, 4 May 2022
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	==Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide==		==Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide==
	<StructureSection load='3mrr' size='340' side='right' caption='[[3mrr]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='3mrr' size='340' side='right'caption='[[3mrr]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[3mrr]] is a 3 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=3MRR OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3MRR FirstGlance]. <br>		<table><tr><td colspan='2'>[[3mrr]] is a 3 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=3MRR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3MRR FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3mr9\|3mr9]], [[3mrb\|3mrb]], [[3mrc\|3mrc]], [[3mrd\|3mrd]], [[3mre\|3mre]], [[3mrf\|3mrf]], [[3mrg\|3mrg]], [[3mrh\|3mrh]], [[3mri\|3mri]], [[3mrj\|3mrj]], [[3mrk\|3mrk]], [[3mrl\|3mrl]], [[3mrm\|3mrm]], [[3mrn\|3mrn]], [[3mro\|3mro]], [[3mrp\|3mrp]], [[3mrq\|3mrq]], [[3gsn\|3gsn]], [[3gso\|3gso]], [[3gsq\|3gsq]], [[3gsr\|3gsr]], [[3gsu\|3gsu]], [[3gsv\|3gsv]], [[3gsw\|3gsw]], [[3gsx\|3gsx]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[3mr9\|3mr9]], [[3mrb\|3mrb]], [[3mrc\|3mrc]], [[3mrd\|3mrd]], [[3mre\|3mre]], [[3mrf\|3mrf]], [[3mrg\|3mrg]], [[3mrh\|3mrh]], [[3mri\|3mri]], [[3mrj\|3mrj]], [[3mrk\|3mrk]], [[3mrl\|3mrl]], [[3mrm\|3mrm]], [[3mrn\|3mrn]], [[3mro\|3mro]], [[3mrp\|3mrp]], [[3mrq\|3mrq]], [[3gsn\|3gsn]], [[3gso\|3gso]], [[3gsq\|3gsq]], [[3gsr\|3gsr]], [[3gsu\|3gsu]], [[3gsv\|3gsv]], [[3gsw\|3gsw]], [[3gsx\|3gsx]]</div></td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA, HLA-A, HLAA ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M, BETA-2 MICROGLUBULIN, CDABP0092, HDCMA22P ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA, HLA-A, HLAA ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M, BETA-2 MICROGLUBULIN, 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'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3mrr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3mrr OCA], [~~http~~://pdbe.org/3mrr PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3mrr RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3mrr PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3mrr ProSAT]</span></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=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>
	</table>		</table>
	== Disease ==		== Disease ==
	[[~~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>		[[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> [[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 ==		== 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/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.		[[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/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. [[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.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	==See Also==		==See Also==
	*[[Beta-2 microglobulin\|Beta-2 microglobulin]]		*[[Beta-2 microglobulin 3D structures\|Beta-2 microglobulin 3D structures]]
	*[[~~Major histocompatibility complex~~\|~~Major histocompatibility complex~~]]		*[[MHC 3D structures\|MHC 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
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	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
			[[Category: Large Structures]]
	[[Category: Bonneville, M]]		[[Category: Bonneville, M]]
	[[Category: Chouquet, A]]		[[Category: Chouquet, A]]

OCA at 13:53, 11 August 2016

2016-08-11T13:53:58Z

← Older revision		Revision as of 13:53, 11 August 2016
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	==Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide==		==Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide==
	<StructureSection load='3mrr' size='340' side='right' caption='[[3mrr]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='3mrr' size='340' side='right' caption='[[3mrr]], [[Resolution\|resolution]] 1.60Å' scene=''>
Line 5:		Line 6:
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3mr9\|3mr9]], [[3mrb\|3mrb]], [[3mrc\|3mrc]], [[3mrd\|3mrd]], [[3mre\|3mre]], [[3mrf\|3mrf]], [[3mrg\|3mrg]], [[3mrh\|3mrh]], [[3mri\|3mri]], [[3mrj\|3mrj]], [[3mrk\|3mrk]], [[3mrl\|3mrl]], [[3mrm\|3mrm]], [[3mrn\|3mrn]], [[3mro\|3mro]], [[3mrp\|3mrp]], [[3mrq\|3mrq]], [[3gsn\|3gsn]], [[3gso\|3gso]], [[3gsq\|3gsq]], [[3gsr\|3gsr]], [[3gsu\|3gsu]], [[3gsv\|3gsv]], [[3gsw\|3gsw]], [[3gsx\|3gsx]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3mr9\|3mr9]], [[3mrb\|3mrb]], [[3mrc\|3mrc]], [[3mrd\|3mrd]], [[3mre\|3mre]], [[3mrf\|3mrf]], [[3mrg\|3mrg]], [[3mrh\|3mrh]], [[3mri\|3mri]], [[3mrj\|3mrj]], [[3mrk\|3mrk]], [[3mrl\|3mrl]], [[3mrm\|3mrm]], [[3mrn\|3mrn]], [[3mro\|3mro]], [[3mrp\|3mrp]], [[3mrq\|3mrq]], [[3gsn\|3gsn]], [[3gso\|3gso]], [[3gsq\|3gsq]], [[3gsr\|3gsr]], [[3gsu\|3gsu]], [[3gsv\|3gsv]], [[3gsw\|3gsw]], [[3gsx\|3gsx]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA, HLA-A, HLAA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M, BETA-2 MICROGLUBULIN, CDABP0092, HDCMA22P ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA, HLA-A, HLAA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M, BETA-2 MICROGLUBULIN, CDABP0092, 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://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3mrr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3mrr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3mrr RCSB], [http://www.ebi.ac.uk/pdbsum/3mrr PDBsum]</span></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=3mrr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3mrr OCA], [http://pdbe.org/3mrr PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3mrr RCSB], [http://www.ebi.ac.uk/pdbsum/3mrr PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3mrr ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 20:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
			<div class="pdbe-citations 3mrr" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==

OCA at 10:44, 28 January 2015

2015-01-28T10:44:18Z

← Older revision		Revision as of 10:44, 28 January 2015
Line 2:		Line 2:
	<StructureSection load='3mrr' size='340' side='right' caption='[[3mrr]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='3mrr' size='340' side='right' caption='[[3mrr]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[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]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3MRR FirstGlance]. <br>		<table><tr><td colspan='2'>[[3mrr]] is a 3 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=3MRR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3MRR FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3mr9\|3mr9]], [[3mrb\|3mrb]], [[3mrc\|3mrc]], [[3mrd\|3mrd]], [[3mre\|3mre]], [[3mrf\|3mrf]], [[3mrg\|3mrg]], [[3mrh\|3mrh]], [[3mri\|3mri]], [[3mrj\|3mrj]], [[3mrk\|3mrk]], [[3mrl\|3mrl]], [[3mrm\|3mrm]], [[3mrn\|3mrn]], [[3mro\|3mro]], [[3mrp\|3mrp]], [[3mrq\|3mrq]], [[3gsn\|3gsn]], [[3gso\|3gso]], [[3gsq\|3gsq]], [[3gsr\|3gsr]], [[3gsu\|3gsu]], [[3gsv\|3gsv]], [[3gsw\|3gsw]], [[3gsx\|3gsx]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3mr9\|3mr9]], [[3mrb\|3mrb]], [[3mrc\|3mrc]], [[3mrd\|3mrd]], [[3mre\|3mre]], [[3mrf\|3mrf]], [[3mrg\|3mrg]], [[3mrh\|3mrh]], [[3mri\|3mri]], [[3mrj\|3mrj]], [[3mrk\|3mrk]], [[3mrl\|3mrl]], [[3mrm\|3mrm]], [[3mrn\|3mrn]], [[3mro\|3mro]], [[3mrp\|3mrp]], [[3mrq\|3mrq]], [[3gsn\|3gsn]], [[3gso\|3gso]], [[3gsq\|3gsq]], [[3gsr\|3gsr]], [[3gsu\|3gsu]], [[3gsv\|3gsv]], [[3gsw\|3gsw]], [[3gsx\|3gsx]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA, HLA-A, HLAA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~]), B2M, BETA-2 MICROGLUBULIN, CDABP0092, HDCMA22P ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA, HLA-A, HLAA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M, BETA-2 MICROGLUBULIN, CDABP0092, 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://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3mrr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3mrr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3mrr RCSB], [http://www.ebi.ac.uk/pdbsum/3mrr PDBsum]</span></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=3mrr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3mrr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3mrr RCSB], [http://www.ebi.ac.uk/pdbsum/3mrr PDBsum]</span></td></tr>
	</table>		</table>
Line 11:		Line 11:
	== 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/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.		[[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.
			<div style="background-color:#fffaf0;">
			== Publication Abstract from PubMed ==
			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.

			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>

			From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
			</div>

	==See Also==		==See Also==
Line 19:		Line 27:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Homo sapiens~~]]		[[Category: Human]]
	[[Category: Bonneville, M]]		[[Category: Bonneville, M]]
	[[Category: Chouquet, A]]		[[Category: Chouquet, A]]

OCA at 17:52, 18 December 2014

2014-12-18T17:52:18Z

← Older revision		Revision as of 17:52, 18 December 2014
Line 1:		Line 1:
	~~{{STRUCTURE_3mrr\| PDB=3mrr \| SCENE= }}~~		==Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide==
	===Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide===		<StructureSection load='3mrr' size='340' side='right' caption='[[3mrr]], [[Resolution\|resolution]] 1.60Å' scene=''>
			== Structural highlights ==
	==Disease==		<table><tr><td colspan='2'>[[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]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3MRR FirstGlance]. <br>
	[[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>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3mr9\|3mr9]], [[3mrb\|3mrb]], [[3mrc\|3mrc]], [[3mrd\|3mrd]], [[3mre\|3mre]], [[3mrf\|3mrf]], [[3mrg\|3mrg]], [[3mrh\|3mrh]], [[3mri\|3mri]], [[3mrj\|3mrj]], [[3mrk\|3mrk]], [[3mrl\|3mrl]], [[3mrm\|3mrm]], [[3mrn\|3mrn]], [[3mro\|3mro]], [[3mrp\|3mrp]], [[3mrq\|3mrq]], [[3gsn\|3gsn]], [[3gso\|3gso]], [[3gsq\|3gsq]], [[3gsr\|3gsr]], [[3gsu\|3gsu]], [[3gsv\|3gsv]], [[3gsw\|3gsw]], [[3gsx\|3gsx]]</td></tr>
			<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA, HLA-A, HLAA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), B2M, BETA-2 MICROGLUBULIN, CDABP0092, HDCMA22P ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
	==Function==		<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=3mrr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3mrr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3mrr RCSB], [http://www.ebi.ac.uk/pdbsum/3mrr PDBsum]</span></td></tr>
			</table>
			== Disease ==
			[[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>
			== 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/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.		[[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.

	~~==About this Structure==~~
	[[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].

	==See Also==		==See Also==
	*[[Beta-2 microglobulin\|Beta-2 microglobulin]]		*[[Beta-2 microglobulin\|Beta-2 microglobulin]]
	*[[Major histocompatibility complex\|Major histocompatibility complex]]		*[[Major histocompatibility complex\|Major histocompatibility complex]]
			== References ==
	==~~Reference~~==		<references/>
	<references ~~group="xtra"~~/><~~references~~/>		__TOC__
			</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Bonneville, M.]]		[[Category: Bonneville, M]]
	[[Category: Chouquet, A.]]		[[Category: Chouquet, A]]
	[[Category: Debeaupuis, E.]]		[[Category: Debeaupuis, E]]
	[[Category: Echasserieau, K.]]		[[Category: Echasserieau, K]]
	[[Category: Housset, D.]]		[[Category: Housset, D]]
	[[Category: Legoux, F.]]		[[Category: Legoux, F]]
	[[Category: Machillot, P.]]		[[Category: Machillot, P]]
	[[Category: Reiser, J B.]]		[[Category: Reiser, J B]]
	[[Category: Saulquin, X.]]		[[Category: Saulquin, X]]
	[[Category: Decapeptide]]		[[Category: Decapeptide]]
	[[Category: Hla]]		[[Category: Hla]]

OCA at 22:25, 24 March 2013

2013-03-24T22:25:25Z

← Older revision		Revision as of 22:25, 24 March 2013
Line 1:		Line 1:
	~~[[Image:3mrr.png\|left\|200px]]~~

	{{STRUCTURE_3mrr\| PDB=3mrr \| SCENE= }}		{{STRUCTURE_3mrr\| PDB=3mrr \| SCENE= }}
			===Crystal Structure of MHC class I HLA-A2 molecule complexed with Human Prostaglandin Transporter decapeptide===

	===~~Crystal Structure~~ of ~~MHC class I HLA~~-~~A2 molecule complexed with Human Prostaglandin Transporter decapeptide===~~		==Disease==
			[[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>

			==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/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.

	==About this Structure==		==About this Structure==
Line 12:		Line 14:
	*[[Beta-2 microglobulin\|Beta-2 microglobulin]]		*[[Beta-2 microglobulin\|Beta-2 microglobulin]]
	*[[Major histocompatibility complex\|Major histocompatibility complex]]		*[[Major histocompatibility complex\|Major histocompatibility complex]]

			==Reference==
			<references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Bonneville, M.]]		[[Category: Bonneville, M.]]

OCA at 11:39, 20 October 2012

2012-10-20T11:39:59Z

← Older revision		Revision as of 11:39, 20 October 2012
Line 7:		Line 7:

	==About this Structure==		==About this Structure==
	[[3mrr]] is a 3 chain structure ~~of [[Beta-2 microglobulin]] and [[Major histocompatibility complex]]~~ 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].		[[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].

	==See Also==		==See Also==

OCA at 06:11, 26 July 2012

2012-07-26T06:11:04Z

@@ Line 1: / Line 1: @@
-[[Image:3mrr.jpg|left|200px]]
+[[Image:3mrr.png|left|200px]]
 {{STRUCTURE_3mrr|  PDB=3mrr  |  SCENE=  }}
@@ Line 13: / Line 7: @@
 ==About this Structure==
-[[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].
+[[3mrr]] is a 3 chain structure of [[Beta-2 microglobulin]] and [[Major histocompatibility complex]] 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].
 [[Category: Homo sapiens]]
 [[Category: Bonneville, M.]]
@@ Line 24: / Line 22: @@
 [[Category: Reiser, J B.]]
 [[Category: Saulquin, X.]]

OCA: Protected "3mrr" [edit=sysop:move=sysop]

2011-05-25T05:46:22Z

Protected "3mrr" [edit=sysop:move=sysop]

← Older revision	Revision as of 05:46, 25 May 2011
(No difference)