6pz5 - Revision history

OCA at 07:38, 11 October 2023

OCA — Wed, 11 Oct 2023 07:38:35 GMT

←Older revision		Revision as of 07:38, 11 October 2023
Line 3:		Line 3:
	<StructureSection load='6pz5' size='340' side='right'caption='[[6pz5]], [[Resolution\|resolution]] 1.53Å' scene=''>		<StructureSection load='6pz5' size='340' side='right'caption='[[6pz5]], [[Resolution\|resolution]] 1.53Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6pz5]] 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=6PZ5 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6PZ5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6pz5]] 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=6PZ5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6PZ5 FirstGlance]. <br>
-	</td></tr><tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat">~~HLA~~-B, ~~HLAB (~~[~~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])~~</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]] 1.53Å</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=6pz5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6pz5 OCA], [~~http~~://pdbe.org/6pz5 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6pz5 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6pz5 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6pz5 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=6pz5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6pz5 OCA], [https://pdbe.org/6pz5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6pz5 RCSB], [https://www.ebi.ac.uk/pdbsum/6pz5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6pz5 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/~~1B27_HUMAN 1B27_HUMAN~~]~~] Defects in HLA-B are a cause~~ of ~~susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM~~:~~[http://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing~~ spondylitis~~, a subset~~ of ~~psoriatic~~ arthritis~~, reactive arthritis (e.g. Reiter~~ syndrome~~), arthritis~~ associated with ~~inflammatory bowel~~ disease ~~and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions~~ of ~~the same disease~~. ~~Ankylosing spondylitis~~ is ~~the form of rheumatoid arthritis~~ affecting the ~~spine and~~ is ~~considered the prototype of seronegative spondyloarthropathies~~. ~~It produces pain and stiffness as a result of inflammation of~~ the ~~sacroiliac, intervertebral, and costovertebral joints~~. ~~Note=In the Greek Cypriot population, a~~ restricted number of HLA-~~B27~~ subtypes ~~are~~ associated with ankylosing spondylitis and other ~~B27~~-related diseases and an elevated frequency of the B~~2702~~ allele in ankylosing spondylitis patients is identified. The allele B~~2707~~ seems to have a protective role in ~~this population~~ because it was found only in the healthy controls.<ref>PMID:15603872</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/HLAB_HUMAN HLAB_HUMAN] Prediction of allopurinol toxicity;NON RARE IN EUROPE: Ankylosing spondylitis;Prediction of flucloxacilline toxicity;Giant cell arteritis;Takayasu arteritis;Reactive arthritis;Behcet disease;Stevens-Johnson syndrome;Prediction of phenytoin or carbamazepine toxicity;Pulmonary arterial hypertension associated with connective tissue disease;Prediction of abacavir toxicity. Disease susceptibility is associated with variants affecting the gene represented in this entry. Increased susceptibility to Stevens-Johnson syndrome is conferred by allele B15:02.<ref>PMID:15057820</ref> Disease susceptibility is associated with variants affecting the gene represented in this entry. A restricted number of HLA-B27 subtypes can be associated with ankylosing spondylitis and other B27-related diseases, and an elevated frequency of the B27:02 allele in ankylosing spondylitis patients is identified. The allele B27:07 seems to have a protective role in some populations because it was found only in the healthy controls.<ref>PMID:15603872</ref> There is evidence that HLA-B51 is associated with susceptibility to Behcet disease (BD). However, it is not certain whether HLA-B51 itself or a closely linked gene is responsible for susceptibility. The world distribution of HLA-B51 in healthy people corresponds to the global distribution of BD; in Southern hemisphere countries (Africa, South Pacific, etc.) and in some parts of Europe, the prevalence of HLA-B51 in healthy people is low or null, corresponding to a low prevalence of BD. The wide variation that exists in the relative risk of HLA-B51 would support other nongenetic risk factors.<ref>PMID:23291587</ref> The presence of allele B57:01 is associated with increased susceptibility to abacavir hypersensitivity [MIM:[https://omim.org/entry/142830 142830] in HIV-1 patients.<ref>PMID:11888582</ref> Allele group B08 is associated with increased susceptibility to rheumatoid arthritis, where affected individuals have antibodies to cyclic citrullinated peptide (anti-CCP-positive rheumatoid arthritis).<ref>PMID:22286218</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/~~1B27_HUMAN 1B27_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/HLAB_HUMAN HLAB_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-B-restricted CD8-positive T cells, guiding antigen-specific T cell immune response to eliminate infected or transformed cells (PubMed:25808313, PubMed:29531227, PubMed:9620674, PubMed:23209413). 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:7743181, PubMed:18991276). 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:29531227, PubMed:9620674, PubMed:24600035). Typically presents intracellular peptide antigens of 8 to 13 amino acids that arise from cytosolic proteolysis via constitutive proteasome and IFNG-induced immunoproteasome (PubMed:23209413). Can bind different peptides containing allele-specific binding motifs, which are mainly defined by anchor residues at position 2 and 9 (PubMed:25808313, PubMed:29531227).<ref>PMID:18991276</ref> <ref>PMID:23209413</ref> <ref>PMID:24600035</ref> <ref>PMID:25808313</ref> <ref>PMID:29531227</ref> <ref>PMID:7743181</ref> <ref>PMID:9620674</ref> Allele B07:02: Displays peptides sharing a common signature motif, namely a Pro residue at position 2 and mainly a Leu anchor residue at the C-terminus (PubMed:7743181). Presents a long peptide (APRGPHGGAASGL) derived from the cancer-testis antigen CTAG1A/NY-ESO-1, eliciting a polyclonal CD8-positive T cell response against tumor cells (PubMed:29531227). Presents viral epitopes derived from HIV-1 gag-pol (TPQDLNTML) and Nef (RPQVPLRPM) (PubMed:25808313). Presents an immunodominant epitope derived from SARS-CoV-2 N/nucleoprotein (SPRWYFYYL) (PubMed:32887977). Displays self-peptides including a peptide derived from the signal sequence of HLA-DPB1 (APRTVALTA) (PubMed:7743181).<ref>PMID:25808313</ref> <ref>PMID:29531227</ref> <ref>PMID:32887977</ref> <ref>PMID:7743181</ref> Allele B08:01: Presents to CD8-positive T cells viral epitopes derived from EBV/HHV-4 EBNA3 (QAKWRLQTL), eliciting cytotoxic T cell response.<ref>PMID:9620674</ref> Allele B13:02: Presents multiple HIV-1 epitopes derived from gag (RQANFLGKI, GQMREPRGSDI), nef (RQDILDLWI), gag-pol (RQYDQILIE, GQGQWTYQI) and rev (LQLPPLERL), all having in common a Gln residue at position 2 and mainly hydrophobic amino acids Leu, Ile or Val at the C-terminus. Associated with succesful control of HIV-1 infection.<ref>PMID:17251285</ref> Allele B18:01: Preferentially presents octomeric and nonameric peptides sharing a common motif, namely a Glu at position 2 and Phe or Tyr anchor residues at the C-terminus (PubMed:14978097, PubMed:23749632, PubMed:18991276). Presents an EBV/HHV-4 epitope derived from BZLF1 (SELEIKRY) (PubMed:23749632). May present to CD8-positive T cells an antigenic peptide derived from MAGEA3 (MEVDPIGHLY), triggering an anti-tumor immune response (PubMed:12366779). May display a broad repertoire of self-peptides with a preference for peptides derived from RNA-binding proteins (PubMed:14978097).<ref>PMID:12366779</ref> <ref>PMID:14978097</ref> <ref>PMID:18991276</ref> <ref>PMID:23749632</ref> Allele B27:05: Presents to CD8-positive T cells immunodominant viral epitopes derived from HCV POLG (ARMILMTHF), HIV-1 gag (KRWIILGLNK), IAV NP (SRYWAIRTR), SARS-CoV-2 N/nucleoprotein (QRNAPRITF), EBV/HHV-4 EBNA4 (HRCQAIRKK) and EBV/HHV-4 EBNA6 (RRIYDLIEL), confering longterm protection against viral infection (PubMed:19139562, PubMed:18385228, PubMed:15113903, PubMed:9620674, PubMed:32887977). Can present self-peptides derived from cytosolic and nuclear proteins. All peptides carry an Arg at position 2 (PubMed:1922338). The peptide-bound form interacts with NK cell inhibitory receptor KIR3DL1 and inhibits NK cell activation in a peptide-specific way, being particularly sensitive to the nature of the amino acid side chain at position 8 of the antigenic peptide (PubMed:8879234, PubMed:15657948). KIR3DL1 fails to recognize HLA-B27:05 in complex with B2M and EBV/HHV-4 EBNA6 (RRIYDLIEL) peptide, which can lead to increased activation of NK cells during infection (PubMed:15657948). May present an altered repertoire of peptides in the absence of TAP1-TAP2 and TAPBPL (PubMed:9620674).<ref>PMID:15113903</ref> <ref>PMID:15657948</ref> <ref>PMID:18385228</ref> <ref>PMID:19139562</ref> <ref>PMID:1922338</ref> <ref>PMID:8879234</ref> <ref>PMID:9620674</ref> Allele B40:01: Presents immunodominant viral epitopes derived from EBV/HHV-4 LMP2 (IEDPPFNSL) and SARS-CoV-2 N/nucleoprotein (MEVTPSGTWL), triggering memory CD8-positive T cell response (PubMed:18991276, PubMed:32887977). Displays self-peptides sharing a signature motif, namely a Glu at position 2 and a Leu anchor residue at the C-terminus (PubMed:18991276).<ref>PMID:18991276</ref> <ref>PMID:32887977</ref> Allele B41:01: Displays self-peptides sharing a signature motif, namely a Glu at position 2 and Ala or Pro anchor residues at the C-terminus.<ref>PMID:18991276</ref> Allele B44:02: Presents immunodominant viral epitopes derived from EBV/HHV-4 EBNA4 (VEITPYKPTW) and EBNA6 (AEGGVGWRHW, EENLLDFVRF), triggering memory CD8-positive T cell response (PubMed:9620674, PubMed:18991276). Displays self-peptides sharing a signature motif, namely a Glu at position 2 and Phe, Tyr or Trp anchor residues at the C-terminus (PubMed:18991276).<ref>PMID:18991276</ref> <ref>PMID:9620674</ref> Allele B45:01: Displays self-peptides sharing a signature motif, namely a Glu at position 2 and Ala or Pro anchor residues at the C-terminus.<ref>PMID:18991276</ref> Allele B46:01: Preferentially presents nonameric peptides sharing a signature motif, namely Ala and Leu at position 2 and Tyr, Phe, Leu, or Met anchor residues at the C-terminus. The peptide-bound form interacts with KIR2DL3 and inhibits NK cell cytotoxic response in a peptide-specific way.<ref>PMID:28514659</ref> Allele B47:01: Displays self-peptides sharing a signature motif, namely an Asp at position 2 and Leu or Met anchor residues at the C-terminus.<ref>PMID:18991276</ref> Allele B49:01: Displays self-peptides sharing a signature motif, namely a Glu at position 2 and Ile or Val anchor residues at the C-terminus.<ref>PMID:18991276</ref> Allele B50:01: Displays self-peptides sharing a signature motif, namely a Glu at position 2 and Ala or Pro anchor residues at the C-terminus.<ref>PMID:18991276</ref> Allele B51:01: Presents an octomeric HIV-1 epitope derived from gag-pol (TAFTIPSI) to the public TRAV17/TRBV7-3 TCR clonotype, strongly suppressing HIV-1 replication.<ref>PMID:24600035</ref> Allele B54:01: Displays peptides sharing a common signature motif, namely a Pro residue at position 2 and Ala anchor residue at the C-terminus.<ref>PMID:7743181</ref> Allele B55:01: Displays peptides sharing a common signature motif, namely a Pro residue at position 2 and Ala anchor residue at the C-terminus.<ref>PMID:7743181</ref> Allele B56:01: Displays peptides sharing a common signature motif, namely a Pro residue at position 2 and Ala anchor residue at the C-terminus.<ref>PMID:7743181</ref> Allele B57:01: The peptide-bound form recognizes KIR3DL1 and inhibits NK cell cytotoxic response.<ref>PMID:22020283</ref> <ref>PMID:25480565</ref> Allele B67:01: Displays peptides sharing a common signature motif, namely a Pro residue at position 2 and Leu anchor residue at the C-terminus.<ref>PMID:7743181</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	</div>		</div>
	<div class="pdbe-citations 6pz5" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 6pz5" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Beta-2 microglobulin 3D structures\|Beta-2 microglobulin 3D structures]]
		+	*[[MHC 3D structures\|MHC 3D structures]]
		+	*[[MHC I 3D structures\|MHC I 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Gras, S]]	+	[[Category: Gras S]]
-	~~[[Category: Ankylosing spondylitis]]~~	+
-	~~[[Category: Hla]]~~	+
-	~~[[Category: Hla-b*27:03]]~~	+
-	~~[[Category: Hla-b*27:05]]~~	+
-	~~[[Category: Hla-b27]]~~	+
-	~~[[Category: Immune system~~]]	+

OCA at 10:51, 4 December 2019

OCA — Wed, 04 Dec 2019 10:51:13 GMT

←Older revision		Revision as of 10:51, 4 December 2019
Line 3:		Line 3:
	<StructureSection load='6pz5' size='340' side='right'caption='[[6pz5]], [[Resolution\|resolution]] 1.53Å' scene=''>		<StructureSection load='6pz5' size='340' side='right'caption='[[6pz5]], [[Resolution\|resolution]] 1.53Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6pz5]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6PZ5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6PZ5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6pz5]] 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=6PZ5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6PZ5 FirstGlance]. <br>
-	</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=6pz5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6pz5 OCA], [http://pdbe.org/6pz5 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6pz5 RCSB], [http://www.ebi.ac.uk/pdbsum/6pz5 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6pz5 ProSAT]</span></td></tr>	+	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA-B, HLAB ([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])</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=6pz5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6pz5 OCA], [http://pdbe.org/6pz5 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6pz5 RCSB], [http://www.ebi.ac.uk/pdbsum/6pz5 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6pz5 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 10:		Line 11:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_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/1B27_HUMAN 1B27_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 ==
		+	Expression of human leukocyte antigen (HLA)-B27 is strongly associated with predisposition towards ankylosing spondylitis (AS) and other spondyloarthropathies. However, the exact involvement of HLA-B27 in disease initiation and progression remains unclear. The homodimer theory, which proposes that HLA-B27 heavy chains aberrantly form homodimers, is a central hypothesis that attempts to explain the role of HLA-B27 in disease pathogenesis. Here we examined the ability of the 8 most prevalent HLA-B27 allotypes (HLA-B27:02 - HLA-B27:09) to form homodimers. We observed that HLA-B27:03, a disease-associated HLA-B27 subtype, showed a significantly reduced ability to form homodimers in comparison to all other allotypes, including the non-disease-associated/protective allotypes HLA-B27:06 and HLA-B27:09. We used X-ray crystallography and site-directed mutagenesis to unravel the molecular and structural mechanisms in HLA-B27:03 that are responsible for its compromised ability to form homodimers. We show that polymorphism at position-59, which differentiates HLA-B27:03 from all other allotypes, is responsible for its compromised ability to form homodimers. Indeed, histidine-59 in HLA-B27:03 leads to a series of local conformational changes that act in concert to reduce the accessibility of the nearby cysteine-67, an essential amino acid residue for the formation of HLA-B27 homodimers. Considered together, the ability of both protective and disease-associated HLA-B27 allotypes to form homodimers and the failure of HLA-B*27:03 to form homodimers challenge the role of HLA-B27 homodimers in AS pathoetiology. Rather, this work implicates other features such as peptide binding and antigen presentation as pivotal mechanisms for disease pathogenesis.
		+
		+	Allelic association with ankylosing spondylitis fails to correlate with human leukocyte antigen B27 homodimer formation.,Lim Kam Sian TCC, Indumathy S, Halim H, Greule A, Cryle MJ, Bowness P, Rossjohn J, Gras S, Purcell AW, Schittenhelm RB J Biol Chem. 2019 Nov 18. pii: RA119.010257. doi: 10.1074/jbc.RA119.010257. PMID:31740583<ref>PMID:31740583</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 6pz5" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Gras, S]]		[[Category: Gras, S]]

OCA at 06:54, 27 November 2019

OCA — Wed, 27 Nov 2019 06:54:34 GMT

←Older revision		Revision as of 06:54, 27 November 2019
Line 1:		Line 1:
-	'''Unreleased structure'''

-	The entry ~~6pz5~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	==Crystal Structure of HLA-B*2703 in complex with LRN, a self-peptide==
-		+	<StructureSection load='6pz5' size='340' side='right'caption='[[6pz5]], [[Resolution\|resolution]] 1.53Å' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[6pz5]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6PZ5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6PZ5 FirstGlance]. <br>
-	~~Description:~~	+	</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=6pz5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6pz5 OCA], [http://pdbe.org/6pz5 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6pz5 RCSB], [http://www.ebi.ac.uk/pdbsum/6pz5 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6pz5 ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[http://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</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/1B27_HUMAN 1B27_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: Large Structures]]
		+	[[Category: Gras, S]]
		+	[[Category: Ankylosing spondylitis]]
		+	[[Category: Hla]]
		+	[[Category: Hla-b*27:03]]
		+	[[Category: Hla-b*27:05]]
		+	[[Category: Hla-b27]]
		+	[[Category: Immune system]]

OCA at 15:02, 14 August 2019

OCA — Wed, 14 Aug 2019 15:02:35 GMT

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OCA: Protected "6pz5" [edit=sysop:move=sysop]

OCA — Wed, 07 Aug 2019 04:22:07 GMT

Protected "6pz5" [edit=sysop:move=sysop]

←Older revision

Revision as of 04:22, 7 August 2019

OCA: New page: '''Unreleased structure''' The entry 6pz5 is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Wed, 07 Aug 2019 04:22:06 GMT

New page: '''Unreleased structure''' The entry 6pz5 is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 6pz5 is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]