6u26 - Revision history

OCA at 14:33, 6 March 2024

2024-03-06T14:33:33Z

←Older revision		Revision as of 14:33, 6 March 2024
Line 3:		Line 3:
	<StructureSection load='6u26' size='340' side='right'caption='[[6u26]], [[Resolution\|resolution]] 1.53Å' scene=''>		<StructureSection load='6u26' size='340' side='right'caption='[[6u26]], [[Resolution\|resolution]] 1.53Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6u26]] is a 2 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=6U26 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6U26 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6u26]] is a 2 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=6U26 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6U26 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=063:4-{[(1R)-6-{2-[2-({N~5~-[N,N-bis(tert-butoxycarbonyl)carbamimidoyl]-N~2~-(tert-butoxycarbonyl)-L-ornithyl}amino)ethoxy]ethoxy}-1-methyl-1-{2-oxo-2-[(1,3-thiazol-2-yl)amino]ethyl}-1,2,3,4-tetrahydroisoquinolin-7-yl]oxy}-2-fluoro[1,1-biphenyl]-4-carboxylic+acid'>063</scene>~~</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='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PCSK9, NARC1, PSEC0052 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=063:4-{[(1R)-6-{2-[2-({N~5~-[N,N-bis(tert-butoxycarbonyl)carbamimidoyl]-N~2~-(tert-butoxycarbonyl)-L-ornithyl}amino)ethoxy]ethoxy}-1-methyl-1-{2-oxo-2-[(1,3-thiazol-2-yl)amino]ethyl}-1,2,3,4-tetrahydroisoquinolin-7-yl]oxy}-2-fluoro[1,1-biphenyl]-4-carboxylic+acid'>063</scene></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=6u26 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6u26 OCA], [~~http~~://pdbe.org/6u26 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6u26 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6u26 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6u26 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=6u26 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6u26 OCA], [https://pdbe.org/6u26 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6u26 RCSB], [https://www.ebi.ac.uk/pdbsum/6u26 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6u26 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN]] Defects in PCSK9 are the cause of hypercholesterolemia autosomal dominant type 3 (HCHOLA3) [MIM:[~~http~~://omim.org/entry/603776 603776]]. A familial condition characterized by elevated circulating cholesterol contained in either low-density lipoproteins alone or also in very-low-density lipoproteins.<ref>PMID:12730697</ref>	+	[https://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN] Defects in PCSK9 are the cause of hypercholesterolemia autosomal dominant type 3 (HCHOLA3) [MIM:[https://omim.org/entry/603776 603776]. A familial condition characterized by elevated circulating cholesterol contained in either low-density lipoproteins alone or also in very-low-density lipoproteins.<ref>PMID:12730697</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN]] Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.<ref>PMID:17461796</ref> <ref>PMID:18197702</ref> <ref>PMID:18660751</ref> <ref>PMID:18039658</ref> <ref>PMID:22074827</ref> <ref>PMID:22580899</ref> <ref>PMID:22493497</ref>	+	[https://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN] Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.<ref>PMID:17461796</ref> <ref>PMID:18197702</ref> <ref>PMID:18660751</ref> <ref>PMID:18039658</ref> <ref>PMID:22074827</ref> <ref>PMID:22580899</ref> <ref>PMID:22493497</ref>
-	~~<div style="background-color:#fffaf0;">~~	+
-	~~== Publication Abstract from PubMed ==~~	+
-	Proprotein convertase substilisin-like/kexin type 9 (PCSK9) is a serine protease involved in a protein-protein interaction with the low-density lipoprotein (LDL) receptor that has both human genetic and clinical validation. Blocking this protein-protein interaction prevents LDL receptor degradation and thereby decreases LDL cholesterol levels. Our pursuit of small-molecule direct binders for this difficult to drug PPI target utilized affinity selection/mass spectrometry, which identified one confirmed hit compound. An X-ray crystal structure revealed that this compound was binding in an unprecedented allosteric pocket located between the catalytic and C-terminal domain. Optimization of this initial hit, using two distinct strategies, led to compounds with high binding affinity to PCSK9. Direct target engagement was demonstrated in the cell lysate with a cellular thermal shift assay. Finally, ligand-induced protein degradation was shown with a proteasome recruiting tag attached to the high-affinity allosteric ligand for PCSK9.	+

-	From Screening to Targeted Degradation: Strategies for the Discovery and Optimization of Small Molecule Ligands for PCSK9.,Petrilli WL, Adam GC, Erdmann RS, Abeywickrema P, Agnani V, Ai X, Baysarowich J, Byrne N, Caldwell JP, Chang W, DiNunzio E, Feng Z, Ford R, Ha S, Huang Y, Hubbard B, Johnston JM, Kavana M, Lisnock JM, Liang R, Lu J, Lu Z, Meng J, Orth P, Palyha O, Parthasarathy G, Salowe SP, Sharma S, Shipman J, Soisson SM, Strack AM, Youm H, Zhao K, Zink DL, Zokian H, Addona GH, Akinsanya K, Tata JR, Xiong Y, Imbriglio JE Cell Chem Biol. 2019 Oct 22. pii: S2451-9456(19)30322-8. doi:, 10.1016/j.chembiol.2019.10.002. PMID:31653597<ref>PMID:31653597</ref>	+	==See Also==
-		+	*[[PCSK9\|PCSK9]]
-	~~From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>~~	+
-	~~</div>~~	+
-	~~<div class~~=~~"pdbe-citations 6u26" style~~=~~"background-color:#fffaf0;"></div>~~	+
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Orth, P]]	+	[[Category: Orth P]]
-	~~[[Category: Autocatalytic cleavage]]~~	+
-	~~[[Category: Cholesterol clearance]]~~	+
-	~~[[Category: Cholesterol metabolism]]~~	+
-	~~[[Category: Disulfide bond]]~~	+
-	~~[[Category: Glycoprotein]]~~	+
-	~~[[Category: Hydrolase]]~~	+
-	~~[[Category: Hydrolase-hydrolase inhibitor complex]]~~	+
-	~~[[Category: Inhibitor]]~~	+
-	~~[[Category: Ldlr]]~~	+
-	~~[[Category: Lipid metabolism]]~~	+
-	~~[[Category: Pcsk9]]~~	+
-	~~[[Category: Phosphoprotein]]~~	+
-	~~[[Category: Protease]]~~	+
-	~~[[Category: Secreted]]~~	+
-	~~[[Category: Serine protease~~]]	+

OCA at 16:25, 29 January 2020

2020-01-29T16:25:20Z

←Older revision		Revision as of 16:25, 29 January 2020
Line 3:		Line 3:
	<StructureSection load='6u26' size='340' side='right'caption='[[6u26]], [[Resolution\|resolution]] 1.53Å' scene=''>		<StructureSection load='6u26' size='340' side='right'caption='[[6u26]], [[Resolution\|resolution]] 1.53Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6u26]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6U26 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6U26 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6u26]] is a 2 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=6U26 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6U26 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=063:4-{[(1R)-6-{2-[2-({N~5~-[N,N-bis(tert-butoxycarbonyl)carbamimidoyl]-N~2~-(tert-butoxycarbonyl)-L-ornithyl}amino)ethoxy]ethoxy}-1-methyl-1-{2-oxo-2-[(1,3-thiazol-2-yl)amino]ethyl}-1,2,3,4-tetrahydroisoquinolin-7-yl]oxy}-2-fluoro[1,1-biphenyl]-4-carboxylic+acid'>063</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=063:4-{[(1R)-6-{2-[2-({N~5~-[N,N-bis(tert-butoxycarbonyl)carbamimidoyl]-N~2~-(tert-butoxycarbonyl)-L-ornithyl}amino)ethoxy]ethoxy}-1-methyl-1-{2-oxo-2-[(1,3-thiazol-2-yl)amino]ethyl}-1,2,3,4-tetrahydroisoquinolin-7-yl]oxy}-2-fluoro[1,1-biphenyl]-4-carboxylic+acid'>063</scene></td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PCSK9, NARC1, PSEC0052 ([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=6u26 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6u26 OCA], [http://pdbe.org/6u26 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6u26 RCSB], [http://www.ebi.ac.uk/pdbsum/6u26 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6u26 ProSAT]</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=6u26 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6u26 OCA], [http://pdbe.org/6u26 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6u26 RCSB], [http://www.ebi.ac.uk/pdbsum/6u26 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6u26 ProSAT]</span></td></tr>
	</table>		</table>
Line 24:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Orth, P]]		[[Category: Orth, P]]

OCA at 06:55, 6 November 2019

2019-11-06T06:55:42Z

←Older revision		Revision as of 06:55, 6 November 2019
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 6u26 is ~~ON HOLD~~ ~~until Paper~~ Publication	+	==PCSK9 in complex with compound 16==
		+	<StructureSection load='6u26' size='340' side='right'caption='[[6u26]], [[Resolution\|resolution]] 1.53Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[6u26]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6U26 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6U26 FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=063:4-{[(1R)-6-{2-[2-({N~5~-[N,N-bis(tert-butoxycarbonyl)carbamimidoyl]-N~2~-(tert-butoxycarbonyl)-L-ornithyl}amino)ethoxy]ethoxy}-1-methyl-1-{2-oxo-2-[(1,3-thiazol-2-yl)amino]ethyl}-1,2,3,4-tetrahydroisoquinolin-7-yl]oxy}-2-fluoro[1,1-biphenyl]-4-carboxylic+acid'>063</scene></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=6u26 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6u26 OCA], [http://pdbe.org/6u26 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6u26 RCSB], [http://www.ebi.ac.uk/pdbsum/6u26 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6u26 ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN]] Defects in PCSK9 are the cause of hypercholesterolemia autosomal dominant type 3 (HCHOLA3) [MIM:[http://omim.org/entry/603776 603776]]. A familial condition characterized by elevated circulating cholesterol contained in either low-density lipoproteins alone or also in very-low-density lipoproteins.<ref>PMID:12730697</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN]] Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.<ref>PMID:17461796</ref> <ref>PMID:18197702</ref> <ref>PMID:18660751</ref> <ref>PMID:18039658</ref> <ref>PMID:22074827</ref> <ref>PMID:22580899</ref> <ref>PMID:22493497</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Proprotein convertase substilisin-like/kexin type 9 (PCSK9) is a serine protease involved in a protein-protein interaction with the low-density lipoprotein (LDL) receptor that has both human genetic and clinical validation. Blocking this protein-protein interaction prevents LDL receptor degradation and thereby decreases LDL cholesterol levels. Our pursuit of small-molecule direct binders for this difficult to drug PPI target utilized affinity selection/mass spectrometry, which identified one confirmed hit compound. An X-ray crystal structure revealed that this compound was binding in an unprecedented allosteric pocket located between the catalytic and C-terminal domain. Optimization of this initial hit, using two distinct strategies, led to compounds with high binding affinity to PCSK9. Direct target engagement was demonstrated in the cell lysate with a cellular thermal shift assay. Finally, ligand-induced protein degradation was shown with a proteasome recruiting tag attached to the high-affinity allosteric ligand for PCSK9.

-	~~Authors~~:	+	From Screening to Targeted Degradation: Strategies for the Discovery and Optimization of Small Molecule Ligands for PCSK9.,Petrilli WL, Adam GC, Erdmann RS, Abeywickrema P, Agnani V, Ai X, Baysarowich J, Byrne N, Caldwell JP, Chang W, DiNunzio E, Feng Z, Ford R, Ha S, Huang Y, Hubbard B, Johnston JM, Kavana M, Lisnock JM, Liang R, Lu J, Lu Z, Meng J, Orth P, Palyha O, Parthasarathy G, Salowe SP, Sharma S, Shipman J, Soisson SM, Strack AM, Youm H, Zhao K, Zink DL, Zokian H, Addona GH, Akinsanya K, Tata JR, Xiong Y, Imbriglio JE Cell Chem Biol. 2019 Oct 22. pii: S2451-9456(19)30322-8. doi:, 10.1016/j.chembiol.2019.10.002. PMID:31653597<ref>PMID:31653597</ref>

-	~~Description~~:	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	[[Category: ~~Unreleased~~ Structures]]	+	</div>
		+	<div class="pdbe-citations 6u26" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Orth, P]]
		+	[[Category: Autocatalytic cleavage]]
		+	[[Category: Cholesterol clearance]]
		+	[[Category: Cholesterol metabolism]]
		+	[[Category: Disulfide bond]]
		+	[[Category: Glycoprotein]]
		+	[[Category: Hydrolase]]
		+	[[Category: Hydrolase-hydrolase inhibitor complex]]
		+	[[Category: Inhibitor]]
		+	[[Category: Ldlr]]
		+	[[Category: Lipid metabolism]]
		+	[[Category: Pcsk9]]
		+	[[Category: Phosphoprotein]]
		+	[[Category: Protease]]
		+	[[Category: Secreted]]
		+	[[Category: Serine protease]]

OCA at 03:51, 10 October 2019

2019-10-10T03:51:32Z

←Older revision		Revision as of 03:51, 10 October 2019
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6u26 is ON HOLD	+	The entry 6u26 is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "6u26" [edit=sysop:move=sysop]

2019-08-28T14:02:42Z

Protected "6u26" [edit=sysop:move=sysop]

←Older revision

Revision as of 14:02, 28 August 2019

OCA: New page: '''Unreleased structure''' The entry 6u26 is ON HOLD Authors: Description: Category: Unreleased Structures

2019-08-28T14:02:41Z

New page: '''Unreleased structure''' The entry 6u26 is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 6u26 is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]