6ov7 - Revision history

OCA at 07:17, 11 October 2023

2023-10-11T07:17:42Z

←Older revision		Revision as of 07:17, 11 October 2023
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	<StructureSection load='6ov7' size='340' side='right'caption='[[6ov7]], [[Resolution\|resolution]] 1.71Å' scene=''>		<StructureSection load='6ov7' size='340' side='right'caption='[[6ov7]], [[Resolution\|resolution]] 1.71Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6ov7]] is a 4 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=6OV7 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6OV7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6ov7]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6OV7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6OV7 FirstGlance]. <br>
-	</td></tr><tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat">~~GOPC~~, ~~CAL, FIG (~~[~~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]] 1.71Å</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=6ov7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ov7 OCA], [~~http~~://pdbe.org/6ov7 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6ov7 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6ov7 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6ov7 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=6ov7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ov7 OCA], [https://pdbe.org/6ov7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6ov7 RCSB], [https://www.ebi.ac.uk/pdbsum/6ov7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6ov7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN]] Note=A chromosomal aberration involving GOPC is found in a glioblastoma multiforme sample. An intra-chromosomal deletion del(6)(q21q21) is responsible for the formation of GOPC-ROS1 chimeric protein which has a constitutive receptor tyrosine kinase activity.<ref>PMID:12661006</ref>	+	[https://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN] Note=A chromosomal aberration involving GOPC is found in a glioblastoma multiforme sample. An intra-chromosomal deletion del(6)(q21q21) is responsible for the formation of GOPC-ROS1 chimeric protein which has a constitutive receptor tyrosine kinase activity.<ref>PMID:12661006</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN]] Plays a role in intracellular protein trafficking and degradation. May regulate CFTR chloride currents and acid-induced ASIC3 currents by modulating cell surface expression of both channels. May also regulate the intracellular trafficking of the ADR1B receptor. May play a role in autophagy. Overexpression results in CFTR intracellular retention and degradation in the lysosomes.<ref>PMID:11707463</ref> <ref>PMID:14570915</ref> <ref>PMID:15358775</ref>	+	[https://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN] Plays a role in intracellular protein trafficking and degradation. May regulate CFTR chloride currents and acid-induced ASIC3 currents by modulating cell surface expression of both channels. May also regulate the intracellular trafficking of the ADR1B receptor. May play a role in autophagy. Overexpression results in CFTR intracellular retention and degradation in the lysosomes.<ref>PMID:11707463</ref> <ref>PMID:14570915</ref> <ref>PMID:15358775</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: ~~Gill, N P~~]]	+	[[Category: Synthetic construct]]
-	[[Category: ~~Madden, D R~~]]	+	[[Category: Gill NP]]
-	[[Category: ~~Complex]]~~	+	[[Category: Madden DR]]
-	~~[[Category: Inhibitor]]~~	+
-	~~[[Category: Pdz domain]]~~	+
-	~~[[Category: Peptide binding protein~~]]	+

OCA at 09:10, 27 November 2019

2019-11-27T09:10:09Z

←Older revision		Revision as of 09:10, 27 November 2019
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	<StructureSection load='6ov7' size='340' side='right'caption='[[6ov7]], [[Resolution\|resolution]] 1.71Å' scene=''>		<StructureSection load='6ov7' size='340' side='right'caption='[[6ov7]], [[Resolution\|resolution]] 1.71Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6ov7]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6OV7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6OV7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6ov7]] is a 4 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=6OV7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6OV7 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=6ov7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ov7 OCA], [http://pdbe.org/6ov7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6ov7 RCSB], [http://www.ebi.ac.uk/pdbsum/6ov7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6ov7 ProSAT]</span></td></tr>	+	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GOPC, CAL, FIG ([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=6ov7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ov7 OCA], [http://pdbe.org/6ov7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6ov7 RCSB], [http://www.ebi.ac.uk/pdbsum/6ov7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6ov7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 10:		Line 11:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN]] Plays a role in intracellular protein trafficking and degradation. May regulate CFTR chloride currents and acid-induced ASIC3 currents by modulating cell surface expression of both channels. May also regulate the intracellular trafficking of the ADR1B receptor. May play a role in autophagy. Overexpression results in CFTR intracellular retention and degradation in the lysosomes.<ref>PMID:11707463</ref> <ref>PMID:14570915</ref> <ref>PMID:15358775</ref>		[[http://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN]] Plays a role in intracellular protein trafficking and degradation. May regulate CFTR chloride currents and acid-induced ASIC3 currents by modulating cell surface expression of both channels. May also regulate the intracellular trafficking of the ADR1B receptor. May play a role in autophagy. Overexpression results in CFTR intracellular retention and degradation in the lysosomes.<ref>PMID:11707463</ref> <ref>PMID:14570915</ref> <ref>PMID:15358775</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	The CFTR-associated ligand PDZ domain (CALP) binds to the cystic fibrosis transmembrane conductance regulator (CFTR) and mediates lysosomal degradation of mature CFTR. Inhibition of this interaction has been explored as a therapeutic avenue for cystic fibrosis. Previously, we reported the ensemble-based computational design of a novel peptide inhibitor of CALP, which resulted in the most binding-efficient inhibitor to date. This inhibitor, kCAL01, was designed using OSPREY and evinced significant biological activity in in vitro cell-based assays. Here, we report a crystal structure of kCAL01 bound to CALP and compare structural features against iCAL36, a previously developed inhibitor of CALP. We compute side-chain energy landscapes for each structure to not only enable approximation of binding thermodynamics, but also reveal ensemble features that contribute to the comparatively efficient binding of kCAL01. Finally, we compare the previously reported design ensemble for kCAL01 vs. the new crystal structure and show that, despite small differences between the design model and crystal structure, significant biophysical features that enhance inhibitor binding are captured in the design ensemble. This suggests not only that ensemble-based design captured thermodynamically significant features observed in vitro, but also that a design eschewing ensembles would miss the kCAL01 sequence entirely.
		+
		+	Computational Analysis of Energy Landscapes Reveals Dynamic Features that Contribute to Binding of Inhibitors to CFTR-Associated Ligand.,Holt GT, Jou JD, Gill NP, Lowegard AU, Martin JW, Madden DR, Donald BR J Phys Chem B. 2019 Nov 7. doi: 10.1021/acs.jpcb.9b07278. PMID:31697075<ref>PMID:31697075</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 6ov7" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Gill, N P]]		[[Category: Gill, N P]]

OCA at 15:28, 20 November 2019

2019-11-20T15:28:53Z

←Older revision		Revision as of 15:28, 20 November 2019
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-	'''Unreleased structure'''

-	~~The entry~~ 6ov7 is ~~ON HOLD until Paper Publication~~	+	==CFTR Associated Ligand (CAL) PDZ domain bound to peptide kCAL01==
-		+	<StructureSection load='6ov7' size='340' side='right'caption='[[6ov7]], [[Resolution\|resolution]] 1.71Å' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[6ov7]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6OV7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6OV7 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=6ov7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ov7 OCA], [http://pdbe.org/6ov7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6ov7 RCSB], [http://www.ebi.ac.uk/pdbsum/6ov7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6ov7 ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN]] Note=A chromosomal aberration involving GOPC is found in a glioblastoma multiforme sample. An intra-chromosomal deletion del(6)(q21q21) is responsible for the formation of GOPC-ROS1 chimeric protein which has a constitutive receptor tyrosine kinase activity.<ref>PMID:12661006</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN]] Plays a role in intracellular protein trafficking and degradation. May regulate CFTR chloride currents and acid-induced ASIC3 currents by modulating cell surface expression of both channels. May also regulate the intracellular trafficking of the ADR1B receptor. May play a role in autophagy. Overexpression results in CFTR intracellular retention and degradation in the lysosomes.<ref>PMID:11707463</ref> <ref>PMID:14570915</ref> <ref>PMID:15358775</ref>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Gill, N P]]
		+	[[Category: Madden, D R]]
		+	[[Category: Complex]]
		+	[[Category: Inhibitor]]
		+	[[Category: Pdz domain]]
		+	[[Category: Peptide binding protein]]

OCA: Protected "6ov7" [edit=sysop:move=sysop]

2019-05-21T05:51:35Z

Protected "6ov7" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:51, 21 May 2019

OCA: New page: '''Unreleased structure''' The entry 6ov7 is ON HOLD until Paper Publication Authors: Description: Category: Unreleased Structures

2019-05-21T05:51:34Z

New page: '''Unreleased structure''' The entry 6ov7 is ON HOLD until Paper Publication Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 6ov7 is ON HOLD until Paper Publication

Authors:

Description:
[[Category: Unreleased Structures]]