5e6a - Revision history

OCA at 12:27, 6 March 2024

2024-03-06T12:27:27Z

←Older revision		Revision as of 12:27, 6 March 2024
Line 12:		Line 12:
	== Function ==		== Function ==
	[https://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>		[https://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	Glucocorticoids (GCs) are potent repressors of NF-kappaB activity, making them a preferred choice for treatment of inflammation-driven conditions. Despite the widespread use of GCs in the clinic, current models are inadequate to explain the role of the glucocorticoid receptor (GR) within this critical signaling pathway. GR binding directly to NF-kappaB itself-tethering in a DNA binding-independent manner-represents the standing model of how GCs inhibit NF-kappaB-driven transcription. We demonstrate that direct binding of GR to genomic NF-kappaB response elements (kappaBREs) mediates GR-driven repression of inflammatory gene expression. We report five crystal structures and solution NMR data of GR DBD-kappaBRE complexes, which reveal that GR recognizes a cryptic response element between the binding footprints of NF-kappaB subunits within kappaBREs. These cryptic sequences exhibit high sequence and functional conservation, suggesting that GR binding to kappaBREs is an evolutionarily conserved mechanism of controlling the inflammatory response.
-
-	Cryptic glucocorticoid receptor-binding sites pervade genomic NF-kappaB response elements.,Hudson WH, Vera IMS, Nwachukwu JC, Weikum ER, Herbst AG, Yang Q, Bain DL, Nettles KW, Kojetin DJ, Ortlund EA Nat Commun. 2018 Apr 6;9(1):1337. doi: 10.1038/s41467-018-03780-1. PMID:29626214<ref>PMID:29626214</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 5e6a" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==

OCA at 06:14, 5 July 2023

2023-07-05T06:14:27Z

←Older revision		Revision as of 06:14, 5 July 2023
Line 1:		Line 1:

	==Glucocorticoid receptor DNA binding domain - PLAU NF-kB response element complex==		==Glucocorticoid receptor DNA binding domain - PLAU NF-kB response element complex==
-	<StructureSection load='5e6a' size='340' side='right' caption='[[5e6a]], [[Resolution\|resolution]] 2.20Å' scene=''>	+	<StructureSection load='5e6a' size='340' side='right'caption='[[5e6a]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5e6a]] 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=5E6A OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5E6A FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5e6a]] is a 4 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=5E6A OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5E6A FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat"~~><scene name='pdbligand=ZN:ZINC+ION'>ZN</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]] 2.197Å</td></tr>
-	~~<tr~~ id~~='related'><td class~~="~~sblockLbl~~">~~<b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5e69\|5e69]]~~, [[~~5e6b~~\|~~5e6b]], [[5e6d\|5e6d~~]]</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	<tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat">~~NR3C1, GRL ([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=5e6a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e6a OCA], [https://pdbe.org/5e6a PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5e6a RCSB], [https://www.ebi.ac.uk/pdbsum/5e6a PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5e6a 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=5e6a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e6a OCA], [~~http~~://pdbe.org/5e6a PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5e6a RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5e6a PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5e6a ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Defects in NR3C1 are a cause of glucocorticoid resistance (GCRES) [MIM:[~~http~~://omim.org/entry/138040 138040]]; also known as cortisol resistance. It is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations. Inheritance is autosomal dominant.<ref>PMID:12050230</ref> <ref>PMID:1704018</ref> <ref>PMID:7683692</ref> <ref>PMID:11589680</ref> <ref>PMID:11701741</ref>	+	[https://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN] Defects in NR3C1 are a cause of glucocorticoid resistance (GCRES) [MIM:[https://omim.org/entry/138040 138040]; also known as cortisol resistance. It is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations. Inheritance is autosomal dominant.<ref>PMID:12050230</ref> <ref>PMID:1704018</ref> <ref>PMID:7683692</ref> <ref>PMID:11589680</ref> <ref>PMID:11701741</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>	+	[https://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 24:		Line 23:

	==See Also==		==See Also==
-	*[[Glucocorticoid receptor\|Glucocorticoid receptor]]	+	*[[Glucocorticoid receptor 3D structures\|Glucocorticoid receptor 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
-	[[Category: ~~Herbst, A G~~]]	+	[[Category: Large Structures]]
-	[[Category: ~~Hudson, W H~~]]	+	[[Category: Herbst AG]]
-	[[Category: ~~Ortlund, E A~~]]	+	[[Category: Hudson WH]]
-	[[Category: ~~Rye, E A~~]]	+	[[Category: Ortlund EA]]
-	[[Category: ~~Dna binding protein]]~~	+	[[Category: Rye EA]]
-	~~[[Category: Dna binding protein-dna complex~~]]	+

OCA at 06:17, 24 October 2018

2018-10-24T06:17:58Z

←Older revision		Revision as of 06:17, 24 October 2018
Line 3:		Line 3:
	<StructureSection load='5e6a' size='340' side='right' caption='[[5e6a]], [[Resolution\|resolution]] 2.20Å' scene=''>		<StructureSection load='5e6a' size='340' side='right' caption='[[5e6a]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5e6a]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E6A OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5E6A FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5e6a]] 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=5E6A OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5E6A FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5e69\|5e69]], [[5e6b\|5e6b]], [[5e6d\|5e6d]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5e69\|5e69]], [[5e6b\|5e6b]], [[5e6d\|5e6d]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">NR3C1, GRL ([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=5e6a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e6a OCA], [http://pdbe.org/5e6a PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5e6a RCSB], [http://www.ebi.ac.uk/pdbsum/5e6a PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5e6a 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=5e6a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e6a OCA], [http://pdbe.org/5e6a PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5e6a RCSB], [http://www.ebi.ac.uk/pdbsum/5e6a PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5e6a ProSAT]</span></td></tr>
	</table>		</table>
Line 12:		Line 13:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>		[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Glucocorticoids (GCs) are potent repressors of NF-kappaB activity, making them a preferred choice for treatment of inflammation-driven conditions. Despite the widespread use of GCs in the clinic, current models are inadequate to explain the role of the glucocorticoid receptor (GR) within this critical signaling pathway. GR binding directly to NF-kappaB itself-tethering in a DNA binding-independent manner-represents the standing model of how GCs inhibit NF-kappaB-driven transcription. We demonstrate that direct binding of GR to genomic NF-kappaB response elements (kappaBREs) mediates GR-driven repression of inflammatory gene expression. We report five crystal structures and solution NMR data of GR DBD-kappaBRE complexes, which reveal that GR recognizes a cryptic response element between the binding footprints of NF-kappaB subunits within kappaBREs. These cryptic sequences exhibit high sequence and functional conservation, suggesting that GR binding to kappaBREs is an evolutionarily conserved mechanism of controlling the inflammatory response.
		+
		+	Cryptic glucocorticoid receptor-binding sites pervade genomic NF-kappaB response elements.,Hudson WH, Vera IMS, Nwachukwu JC, Weikum ER, Herbst AG, Yang Q, Bain DL, Nettles KW, Kojetin DJ, Ortlund EA Nat Commun. 2018 Apr 6;9(1):1337. doi: 10.1038/s41467-018-03780-1. PMID:29626214<ref>PMID:29626214</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 5e6a" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Glucocorticoid receptor\|Glucocorticoid receptor]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Herbst, A G]]		[[Category: Herbst, A G]]
	[[Category: Hudson, W H]]		[[Category: Hudson, W H]]

OCA at 09:21, 10 March 2017

2017-03-10T09:21:05Z

←Older revision		Revision as of 09:21, 10 March 2017
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 5e6a is ~~ON HOLD~~ ~~until Feb 05 2018~~	+	==Glucocorticoid receptor DNA binding domain - PLAU NF-kB response element complex==
-		+	<StructureSection load='5e6a' size='340' side='right' caption='[[5e6a]], [[Resolution\|resolution]] 2.20Å' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[5e6a]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E6A OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5E6A FirstGlance]. <br>
-	~~Description~~:	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5e69\|5e69]], [[5e6b\|5e6b]], [[5e6d\|5e6d]]</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=5e6a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e6a OCA], [http://pdbe.org/5e6a PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5e6a RCSB], [http://www.ebi.ac.uk/pdbsum/5e6a PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5e6a ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Defects in NR3C1 are a cause of glucocorticoid resistance (GCRES) [MIM:[http://omim.org/entry/138040 138040]]; also known as cortisol resistance. It is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations. Inheritance is autosomal dominant.<ref>PMID:12050230</ref> <ref>PMID:1704018</ref> <ref>PMID:7683692</ref> <ref>PMID:11589680</ref> <ref>PMID:11701741</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Herbst, A G]]
		+	[[Category: Hudson, W H]]
		+	[[Category: Ortlund, E A]]
		+	[[Category: Rye, E A]]
		+	[[Category: Dna binding protein]]
		+	[[Category: Dna binding protein-dna complex]]

OCA at 08:57, 18 January 2017

2017-01-18T08:57:30Z

←Older revision		Revision as of 08:57, 18 January 2017
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5e6a is ON HOLD until ~~Jan 09~~ 2018	+	The entry 5e6a is ON HOLD until Feb 05 2018

	Authors:		Authors:

OCA at 10:41, 19 October 2016

2016-10-19T10:41:11Z

←Older revision		Revision as of 10:41, 19 October 2016
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5e6a is ON HOLD until ~~Paper Publication~~	+	The entry 5e6a is ON HOLD until Jan 09 2018

	Authors:		Authors:

OCA at 12:14, 15 May 2016

2016-05-15T12:14:29Z

←Older revision		Revision as of 12:14, 15 May 2016
Line 3:		Line 3:
	The entry 5e6a is ON HOLD until Paper Publication		The entry 5e6a is ON HOLD until Paper Publication

-	Authors: ~~Hudson, W.H., Rye, E.A., Herbst, A.G., Ortlund, E.A.~~	+	Authors:

	Description:		Description:
	[[Category: Unreleased Structures]]		[[Category: Unreleased Structures]]
-	[[Category: Herbst, A.G]]
-	[[Category: Hudson, W.H]]
-	[[Category: Rye, E.A]]
-	[[Category: Ortlund, E.A]]

OCA at 02:27, 1 December 2015

2015-12-01T02:27:31Z

←Older revision		Revision as of 02:27, 1 December 2015
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5e6a is ON HOLD	+	The entry 5e6a is ON HOLD until Paper Publication

	Authors: Hudson, W.H., Rye, E.A., Herbst, A.G., Ortlund, E.A.		Authors: Hudson, W.H., Rye, E.A., Herbst, A.G., Ortlund, E.A.

OCA: Protected "5e6a" [edit=sysop:move=sysop]

2015-10-22T04:24:02Z

Protected "5e6a" [edit=sysop:move=sysop]

←Older revision

Revision as of 04:24, 22 October 2015

OCA: New page: '''Unreleased structure''' The entry 5e6a is ON HOLD Authors: Hudson, W.H., Rye, E.A., Herbst, A.G., Ortlund, E.A. Description: Category: Unreleased Structures [[Category: Herbst,...

2015-10-22T04:24:01Z

New page: '''Unreleased structure''' The entry 5e6a is ON HOLD Authors: Hudson, W.H., Rye, E.A., Herbst, A.G., Ortlund, E.A. Description: Category: Unreleased Structures [[Category: Herbst,...

New page

'''Unreleased structure'''

The entry 5e6a is ON HOLD

Authors: Hudson, W.H., Rye, E.A., Herbst, A.G., Ortlund, E.A.

Description:
[[Category: Unreleased Structures]]
[[Category: Herbst, A.G]]
[[Category: Hudson, W.H]]
[[Category: Rye, E.A]]
[[Category: Ortlund, E.A]]