5bo1 - Revision history

OCA at 08:28, 27 September 2023

OCA — Wed, 27 Sep 2023 08:28:02 GMT

←Older revision		Revision as of 08:28, 27 September 2023
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5bo1]] is a 6 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=5BO1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5BO1 FirstGlance]. <br>		<table><tr><td colspan='2'>[[5bo1]] is a 6 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=5BO1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5BO1 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</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]] 2.56Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</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=5bo1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bo1 OCA], [https://pdbe.org/5bo1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5bo1 RCSB], [https://www.ebi.ac.uk/pdbsum/5bo1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5bo1 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=5bo1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bo1 OCA], [https://pdbe.org/5bo1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5bo1 RCSB], [https://www.ebi.ac.uk/pdbsum/5bo1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5bo1 ProSAT]</span></td></tr>
	</table>		</table>

OCA at 06:01, 7 June 2023

OCA — Wed, 07 Jun 2023 06:01:29 GMT

←Older revision		Revision as of 06:01, 7 June 2023
Line 3:		Line 3:
	<StructureSection load='5bo1' size='340' side='right'caption='[[5bo1]], [[Resolution\|resolution]] 2.56Å' scene=''>		<StructureSection load='5bo1' size='340' side='right'caption='[[5bo1]], [[Resolution\|resolution]] 2.56Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5bo1]] is a 6 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=5BO1 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5BO1 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5bo1]] is a 6 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=5BO1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5BO1 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>~~</td></tr>~~	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">JAG1, JAGL1 ([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'>[https://proteopedia.org/fgij/fg.htm?mol=5bo1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bo1 OCA], [https://pdbe.org/5bo1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5bo1 RCSB], [https://www.ebi.ac.uk/pdbsum/5bo1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5bo1 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=5bo1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bo1 OCA], [~~http~~://pdbe.org/5bo1 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5bo1 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5bo1 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5bo1 ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Defects in JAG1 are the cause of Alagille syndrome type 1 (ALGS1) [MIM:[~~http~~://omim.org/entry/118450 118450]]. Alagille syndrome is an autosomal dominant multisystem disorder defined clinically by hepatic bile duct paucity and cholestasis in association with cardiac, skeletal, and ophthalmologic manifestations. There are characteristic facial features and less frequent clinical involvement of the renal and vascular systems.<ref>PMID:9207788</ref> <ref>PMID:9207787</ref> <ref>PMID:9585603</ref> <ref>PMID:10220506</ref> <ref>PMID:10533065</ref> <ref>PMID:11058898</ref> <ref>PMID:11157803</ref> <ref>PMID:11139247</ref> <ref>PMID:11180599</ref> <ref>PMID:12442286</ref> <ref>PMID:12497640</ref> <ref>PMID:15712272</ref> <ref>PMID:16575836</ref> Defects in JAG1 are a cause of tetralogy of Fallot (TOF) [MIM:[~~http~~://omim.org/entry/187500 187500]]. TOF is a congenital heart anomaly which consists of pulmonary stenosis, ventricular septal defect, dextroposition of the aorta (aorta is on the right side instead of the left) and hypertrophy of the right ventricle. This condition results in a blue baby at birth due to inadequate oxygenation. Surgical correction is emergent.<ref>PMID:9207787</ref> <ref>PMID:11152664</ref>	+	[https://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN] Defects in JAG1 are the cause of Alagille syndrome type 1 (ALGS1) [MIM:[https://omim.org/entry/118450 118450]. Alagille syndrome is an autosomal dominant multisystem disorder defined clinically by hepatic bile duct paucity and cholestasis in association with cardiac, skeletal, and ophthalmologic manifestations. There are characteristic facial features and less frequent clinical involvement of the renal and vascular systems.<ref>PMID:9207788</ref> <ref>PMID:9207787</ref> <ref>PMID:9585603</ref> <ref>PMID:10220506</ref> <ref>PMID:10533065</ref> <ref>PMID:11058898</ref> <ref>PMID:11157803</ref> <ref>PMID:11139247</ref> <ref>PMID:11180599</ref> <ref>PMID:12442286</ref> <ref>PMID:12497640</ref> <ref>PMID:15712272</ref> <ref>PMID:16575836</ref> Defects in JAG1 are a cause of tetralogy of Fallot (TOF) [MIM:[https://omim.org/entry/187500 187500]. TOF is a congenital heart anomaly which consists of pulmonary stenosis, ventricular septal defect, dextroposition of the aorta (aorta is on the right side instead of the left) and hypertrophy of the right ventricle. This condition results in a blue baby at birth due to inadequate oxygenation. Surgical correction is emergent.<ref>PMID:9207787</ref> <ref>PMID:11152664</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Ligand for multiple Notch receptors and involved in the mediation of Notch signaling. May be involved in cell-fate decisions during hematopoiesis. Seems to be involved in early and late stages of mammalian cardiovascular development. Inhibits myoblast differentiation (By similarity). Enhances fibroblast growth factor-induced angiogenesis (in vitro).<ref>PMID:9462510</ref> <ref>PMID:18660822</ref>	+	[https://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN] Ligand for multiple Notch receptors and involved in the mediation of Notch signaling. May be involved in cell-fate decisions during hematopoiesis. Seems to be involved in early and late stages of mammalian cardiovascular development. Inhibits myoblast differentiation (By similarity). Enhances fibroblast growth factor-induced angiogenesis (in vitro).<ref>PMID:9462510</ref> <ref>PMID:18660822</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 25:		Line 24:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	~~[[Category: Leon-Boenig, G de]]~~	+	[[Category: Payandeh J]]
-	[[Category: Payandeh, J]]	+	[[Category: De Leon-Boenig G]]
-	[[Category: ~~Antagonist]]~~	+
-	~~[[Category: Jag]]~~	+
-	~~[[Category: Notch]]~~	+
-	~~[[Category: Signaling protein~~-~~immune system complex~~]]	+

OCA at 08:51, 11 March 2020

OCA — Wed, 11 Mar 2020 08:51:38 GMT

←Older revision		Revision as of 08:51, 11 March 2020
Line 1:		Line 1:
		+
	==Crystal structure of a human Jag1 fragment in complex with an anti-Jag1 Fab==		==Crystal structure of a human Jag1 fragment in complex with an anti-Jag1 Fab==
-	<StructureSection load='5bo1' size='340' side='right' caption='[[5bo1]], [[Resolution\|resolution]] 2.56Å' scene=''>	+	<StructureSection load='5bo1' size='340' side='right'caption='[[5bo1]], [[Resolution\|resolution]] 2.56Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5bo1]] is a 6 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5BO1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5BO1 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5bo1]] is a 6 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=5BO1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5BO1 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</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=5bo1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bo1 OCA], [http://pdbe.org/5bo1 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5bo1 RCSB], [http://www.ebi.ac.uk/pdbsum/5bo1 PDBsum]</span></td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">JAG1, JAGL1 ([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=5bo1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bo1 OCA], [http://pdbe.org/5bo1 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5bo1 RCSB], [http://www.ebi.ac.uk/pdbsum/5bo1 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5bo1 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 23:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Leon-Boenig, G de]]		[[Category: Leon-Boenig, G de]]
	[[Category: Payandeh, J]]		[[Category: Payandeh, J]]

OCA at 10:01, 2 December 2015

OCA — Wed, 02 Dec 2015 10:01:25 GMT

←Older revision		Revision as of 10:01, 2 December 2015
Line 10:		Line 10:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Ligand for multiple Notch receptors and involved in the mediation of Notch signaling. May be involved in cell-fate decisions during hematopoiesis. Seems to be involved in early and late stages of mammalian cardiovascular development. Inhibits myoblast differentiation (By similarity). Enhances fibroblast growth factor-induced angiogenesis (in vitro).<ref>PMID:9462510</ref> <ref>PMID:18660822</ref>		[[http://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Ligand for multiple Notch receptors and involved in the mediation of Notch signaling. May be involved in cell-fate decisions during hematopoiesis. Seems to be involved in early and late stages of mammalian cardiovascular development. Inhibits myoblast differentiation (By similarity). Enhances fibroblast growth factor-induced angiogenesis (in vitro).<ref>PMID:9462510</ref> <ref>PMID:18660822</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Prevailing dogma holds that cell-cell communication through Notch ligands and receptors determines binary cell fate decisions during progenitor cell divisions, with differentiated lineages remaining fixed. Mucociliary clearance in mammalian respiratory airways depends on secretory cells (club and goblet) and ciliated cells to produce and transport mucus. During development or repair, the closely related Jagged ligands (JAG1 and JAG2) induce Notch signalling to determine the fate of these lineages as they descend from a common proliferating progenitor. In contrast to such situations in which cell fate decisions are made in rapidly dividing populations, cells of the homeostatic adult airway epithelium are long-lived, and little is known about the role of active Notch signalling under such conditions. To disrupt Jagged signalling acutely in adult mammals, here we generate antibody antagonists that selectively target each Jagged paralogue, and determine a crystal structure that explains selectivity. We show that acute Jagged blockade induces a rapid and near-complete loss of club cells, with a concomitant gain in ciliated cells, under homeostatic conditions without increased cell death or division. Fate analyses demonstrate a direct conversion of club cells to ciliated cells without proliferation, meeting a conservative definition of direct transdifferentiation. Jagged inhibition also reversed goblet cell metaplasia in a preclinical asthma model, providing a therapeutic foundation. Our discovery that Jagged antagonism relieves a blockade of cell-to-cell conversion unveils unexpected plasticity, and establishes a model for Notch regulation of transdifferentiation.
		+
		+	Therapeutic antibodies reveal Notch control of transdifferentiation in the adult lung.,Lafkas D, Shelton A, Chiu C, de Leon Boenig G, Chen Y, Stawicki SS, Siltanen C, Reichelt M, Zhou M, Wu X, Eastham-Anderson J, Moore H, Roose-Girma M, Chinn Y, Hang JQ, Warming S, Egen J, Lee WP, Austin C, Wu Y, Payandeh J, Lowe JB, Siebel CW Nature. 2015 Nov 18. doi: 10.1038/nature15715. PMID:26580007<ref>PMID:26580007</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 5bo1" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 18:58, 1 December 2015

OCA — Tue, 01 Dec 2015 18:58:52 GMT

←Older revision		Revision as of 18:58, 1 December 2015
Line 1:		Line 1:
-	'''~~Unreleased structure~~'''	+	==Crystal structure of a human Jag1 fragment in complex with an anti-Jag1 Fab==
-		+	<StructureSection load='5bo1' size='340' side='right' caption='[[5bo1]], [[Resolution\|resolution]] 2.56Å' scene=''>
-	~~The entry~~ 5bo1 is ~~ON HOLD until Paper Publication~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[5bo1]] is a 6 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5BO1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5BO1 FirstGlance]. <br>
-	~~Authors~~: ~~Payandeh, J~~., ~~de Leon~~-~~Boenig~~, G.	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</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=5bo1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bo1 OCA], [http://pdbe.org/5bo1 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5bo1 RCSB], [http://www.ebi.ac.uk/pdbsum/5bo1 PDBsum]</span></td></tr>
-	~~Description~~:	+	</table>
-	[[Category: ~~Unreleased Structures~~]]	+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Defects in JAG1 are the cause of Alagille syndrome type 1 (ALGS1) [MIM:[http://omim.org/entry/118450 118450]]. Alagille syndrome is an autosomal dominant multisystem disorder defined clinically by hepatic bile duct paucity and cholestasis in association with cardiac, skeletal, and ophthalmologic manifestations. There are characteristic facial features and less frequent clinical involvement of the renal and vascular systems.<ref>PMID:9207788</ref> <ref>PMID:9207787</ref> <ref>PMID:9585603</ref> <ref>PMID:10220506</ref> <ref>PMID:10533065</ref> <ref>PMID:11058898</ref> <ref>PMID:11157803</ref> <ref>PMID:11139247</ref> <ref>PMID:11180599</ref> <ref>PMID:12442286</ref> <ref>PMID:12497640</ref> <ref>PMID:15712272</ref> <ref>PMID:16575836</ref> Defects in JAG1 are a cause of tetralogy of Fallot (TOF) [MIM:[http://omim.org/entry/187500 187500]]. TOF is a congenital heart anomaly which consists of pulmonary stenosis, ventricular septal defect, dextroposition of the aorta (aorta is on the right side instead of the left) and hypertrophy of the right ventricle. This condition results in a blue baby at birth due to inadequate oxygenation. Surgical correction is emergent.<ref>PMID:9207787</ref> <ref>PMID:11152664</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Ligand for multiple Notch receptors and involved in the mediation of Notch signaling. May be involved in cell-fate decisions during hematopoiesis. Seems to be involved in early and late stages of mammalian cardiovascular development. Inhibits myoblast differentiation (By similarity). Enhances fibroblast growth factor-induced angiogenesis (in vitro).<ref>PMID:9462510</ref> <ref>PMID:18660822</ref>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Leon-Boenig, G de]]
	[[Category: Payandeh, J]]		[[Category: Payandeh, J]]
-	[[Category: ~~De Leon~~-~~Boenig, G~~]]	+	[[Category: Antagonist]]
		+	[[Category: Jag]]
		+	[[Category: Notch]]
		+	[[Category: Signaling protein-immune system complex]]

OCA at 10:53, 7 October 2015

OCA — Wed, 07 Oct 2015 10:53:51 GMT

←Older revision		Revision as of 10:53, 7 October 2015
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5bo1 is ON HOLD	+	The entry 5bo1 is ON HOLD until Paper Publication

	Authors: Payandeh, J., de Leon-Boenig, G.		Authors: Payandeh, J., de Leon-Boenig, G.

OCA: Protected "5bo1" [edit=sysop:move=sysop]

OCA — Wed, 03 Jun 2015 11:41:42 GMT

Protected "5bo1" [edit=sysop:move=sysop]

←Older revision

Revision as of 11:41, 3 June 2015

OCA: New page: '''Unreleased structure''' The entry 5bo1 is ON HOLD Authors: Payandeh, J., de Leon-Boenig, G. Description: Category: Unreleased Structures Category: Payandeh, J [[Category: D...

OCA — Wed, 03 Jun 2015 11:41:40 GMT

New page: '''Unreleased structure''' The entry 5bo1 is ON HOLD Authors: Payandeh, J., de Leon-Boenig, G. Description: Category: Unreleased Structures Category: Payandeh, J [[Category: D...

New page

'''Unreleased structure'''

The entry 5bo1 is ON HOLD

Authors: Payandeh, J., de Leon-Boenig, G.

Description:
[[Category: Unreleased Structures]]
[[Category: Payandeh, J]]
[[Category: De Leon-Boenig, G]]