2ky5: Difference between revisions

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 ==Solution structure of the PECAM-1 cytoplasmic tail with DPC==
-<StructureSection load='2ky5' size='340' side='right'caption='[[2ky5]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
+<StructureSection load='2ky5' size='340' side='right'caption='[[2ky5]]' scene=''>
 == Structural highlights ==
-<table><tr><td colspan='2'>[[2ky5]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2KY5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2KY5 FirstGlance]. <br>
+<table><tr><td colspan='2'>[[2ky5]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2KY5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2KY5 FirstGlance]. <br>
-</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PECAM-1, PECAM1 ([https://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">Solution NMR</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=2ky5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2ky5 OCA], [https://pdbe.org/2ky5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2ky5 RCSB], [https://www.ebi.ac.uk/pdbsum/2ky5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2ky5 ProSAT]</span></td></tr>
 </table>
 == Function ==
-[[https://www.uniprot.org/uniprot/PECA1_HUMAN PECA1_HUMAN]] Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-690 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).<ref>PMID:12110892</ref> <ref>PMID:18388311</ref> <ref>PMID:19342684</ref>
+[https://www.uniprot.org/uniprot/PECA1_HUMAN PECA1_HUMAN] Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-690 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).<ref>PMID:12110892</ref> <ref>PMID:18388311</ref> <ref>PMID:19342684</ref>
 <div style="background-color:#fffaf0;">
 == Publication Abstract from PubMed ==
@@ Line 22: / Line 22: @@
 __TOC__
 </StructureSection>
-[[Category: Human]]
+[[Category: Homo sapiens]]
 [[Category: Large Structures]]
-[[Category: Structural genomic]]
+[[Category: Lytle BL]]
-[[Category: Lytle, B L]]
+[[Category: Newman DK]]
-[[Category: Newman, D K]]
+[[Category: Paddock C]]
-[[Category: Paddock, C]]
+[[Category: Peterson FC]]
-[[Category: Peterson, F C]]
+[[Category: Volkman BF]]
-[[Category: Volkman, B F]]
-[[Category: Cell adhesion]]
-[[Category: Cesg]]
-[[Category: Itim]]
-[[Category: Membrane association]]
-[[Category: Pecam-1]]
-[[Category: PSI, Protein structure initiative]]
-[[Category: Signal transduction]]