8cmd - Revision history

OCA at 07:07, 21 November 2024

2024-11-21T07:07:12Z

@@ Line 10: / Line 10: @@
 == Function ==
 [https://www.uniprot.org/uniprot/DRA_HUMAN DRA_HUMAN] Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molecules is regulated by HLA-DO. Primary dendritic cells (DCs) also to express HLA-DO. Lysosomal miroenvironment has been implicated in the regulation of antigen loading into MHC II molecules, increased acidification produces increased proteolysis and efficient peptide loading.
 __TOC__
 </StructureSection>

OCA at 12:36, 26 July 2023

2023-07-26T12:36:23Z

← Older revision		Revision as of 12:36, 26 July 2023
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	~~'''Unreleased structure'''~~

	The entry ~~8cmd~~ is ~~ON HOLD~~ until ~~Paper Publication~~		==Human Leukocyte Antigen class II allotype DR1 presenting SARS-CoV-2 Spike peptide S761-775==
			<StructureSection load='8cmd' size='340' side='right'caption='[[8cmd]], [[Resolution\|resolution]] 2.54Å' scene=''>
	~~Authors~~:		== Structural highlights ==
			<table><tr><td colspan='2'>[[8cmd]] is a 9 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndrome_coronavirus_2 Severe acute respiratory syndrome coronavirus 2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8CMD OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8CMD FirstGlance]. <br>
	~~Description~~:		</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 2.54Å</td></tr>
	[[Category: ~~Unreleased Structures~~]]		<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></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=8cmd FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8cmd OCA], [https://pdbe.org/8cmd PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8cmd RCSB], [https://www.ebi.ac.uk/pdbsum/8cmd PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8cmd ProSAT]</span></td></tr>
			</table>
			== Function ==
			[https://www.uniprot.org/uniprot/DRA_HUMAN DRA_HUMAN] Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molecules is regulated by HLA-DO. Primary dendritic cells (DCs) also to express HLA-DO. Lysosomal miroenvironment has been implicated in the regulation of antigen loading into MHC II molecules, increased acidification produces increased proteolysis and efficient peptide loading.
			__TOC__
			</StructureSection>
			[[Category: Homo sapiens]]
			[[Category: Large Structures]]
			[[Category: Severe acute respiratory syndrome coronavirus 2]]
			[[Category: Godkin AJ]]
			[[Category: MacLachlan BJ]]
			[[Category: Mason GH]]
			[[Category: Rizkallah PJ]]
			[[Category: Sourfield DO]]

OCA at 05:35, 22 March 2023

2023-03-22T05:35:59Z

← Older revision		Revision as of 05:35, 22 March 2023
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	'''Unreleased structure'''		'''Unreleased structure'''

	The entry 8cmd is ON HOLD		The entry 8cmd is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "8cmd" [edit=sysop:move=sysop]

2023-03-02T04:20:58Z

Protected "8cmd" [edit=sysop:move=sysop]

← Older revision	Revision as of 04:20, 2 March 2023
(No difference)

OCA: New page: '''Unreleased structure''' The entry 8cmd is ON HOLD Authors: Description: Category: Unreleased Structures

2023-03-02T04:20:57Z

New page: '''Unreleased structure''' The entry 8cmd is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 8cmd is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]