5akv - Revision history

OCA at 11:12, 10 January 2024

OCA — Wed, 10 Jan 2024 11:12:05 GMT

←Older revision		Revision as of 11:12, 10 January 2024
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5akv]] 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=5AKV OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5AKV FirstGlance]. <br>		<table><tr><td colspan='2'>[[5akv]] 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=5AKV OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5AKV FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=G7G:GENISTEIN-7-O-GLUCURONIDE'>G7G</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]] 1.52Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=G7G:GENISTEIN-7-O-GLUCURONIDE'>G7G</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=5akv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5akv OCA], [https://pdbe.org/5akv PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5akv RCSB], [https://www.ebi.ac.uk/pdbsum/5akv PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5akv 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=5akv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5akv OCA], [https://pdbe.org/5akv PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5akv RCSB], [https://www.ebi.ac.uk/pdbsum/5akv PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5akv ProSAT]</span></td></tr>
	</table>		</table>

OCA at 05:06, 25 May 2023

OCA — Thu, 25 May 2023 05:06:53 GMT

←Older revision		Revision as of 05:06, 25 May 2023
Line 3:		Line 3:
	<StructureSection load='5akv' size='340' side='right'caption='[[5akv]], [[Resolution\|resolution]] 1.52Å' scene=''>		<StructureSection load='5akv' size='340' side='right'caption='[[5akv]], [[Resolution\|resolution]] 1.52Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5akv]] 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=5AKV OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5AKV FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5akv]] 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=5AKV OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5AKV FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=G7G:GENISTEIN-7-O-GLUCURONIDE'>G7G</scene>~~</td></tr>~~	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=G7G:GENISTEIN-7-O-GLUCURONIDE'>G7G</scene></td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5aks\|5aks]], [[5akt\|5akt]], [[5al0\|5al0]], [[5al8\|5al8]]~~</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=5akv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5akv OCA], [https://pdbe.org/5akv PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5akv RCSB], [https://www.ebi.ac.uk/pdbsum/5akv PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5akv 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=5akv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5akv OCA], [~~http~~://pdbe.org/5akv PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5akv RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5akv PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5akv ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/TTHY_HUMAN TTHY_HUMAN]] Defects in TTR are the cause of amyloidosis transthyretin-related (AMYL-TTR) [MIM:[~~http~~://omim.org/entry/105210 105210]]. A hereditary generalized amyloidosis due to transthyretin amyloid deposition. Protein fibrils can form in different tissues leading to amyloid polyneuropathies, amyloidotic cardiomyopathy, carpal tunnel syndrome, systemic senile amyloidosis. The disease includes leptomeningeal amyloidosis that is characterized by primary involvement of the central nervous system. Neuropathologic examination shows amyloid in the walls of leptomeningeal vessels, in pia arachnoid, and subpial deposits. Some patients also develop vitreous amyloid deposition that leads to visual impairment (oculoleptomeningeal amyloidosis). Clinical features include seizures, stroke-like episodes, dementia, psychomotor deterioration, variable amyloid deposition in the vitreous humor.<ref>PMID:11243784</ref> <ref>PMID:15735344</ref> <ref>PMID:19167329</ref> <ref>PMID:3818577</ref> <ref>PMID:3022108</ref> <ref>PMID:6651852</ref> <ref>PMID:6583672</ref> <ref>PMID:3135807</ref> <ref>PMID:1517749</ref> <ref>PMID:1932142</ref> <ref>PMID:7923855</ref> <ref>PMID:8382610</ref> <ref>PMID:8428915</ref> <ref>PMID:9733771</ref> <ref>PMID:12403615</ref> <ref>PMID:16185074</ref> <ref>PMID:16627944</ref> <ref>PMID:6487335</ref> <ref>PMID:3722385</ref> <ref>PMID:2891727</ref> <ref>PMID:2161654</ref> <ref>PMID:2363717</ref> <ref>PMID:1656975</ref> <ref>PMID:2046936</ref> <ref>PMID:1570831</ref> <ref>PMID:1734866</ref> <ref>PMID:1520326</ref> <ref>PMID:1520336</ref> <ref>PMID:1544214</ref> <ref>PMID:1351039</ref> <ref>PMID:1301926</ref> <ref>PMID:1362222</ref> <ref>PMID:1436517</ref> <ref>PMID:8352764</ref> <ref>PMID:8038017</ref> <ref>PMID:8257997</ref> <ref>PMID:8095302</ref> <ref>PMID:1997217</ref> <ref>PMID:8019560</ref> <ref>PMID:8081397</ref> <ref>PMID:7914929</ref> <ref>PMID:8133316</ref> <ref>PMID:7910950</ref> <ref>PMID:7655883</ref> <ref>PMID:7850982</ref> <ref>PMID:8579098</ref> <ref>PMID:9066351</ref> <ref>PMID:8990019</ref> <ref>PMID:9605286</ref> <ref>PMID:10036587</ref> <ref>PMID:10627135</ref> <ref>PMID:10694917</ref> <ref>PMID:10211412</ref> <ref>PMID:10439117</ref> <ref>PMID:10611950</ref> <ref>PMID:10071047</ref> <ref>PMID:10436378</ref> <ref>PMID:10842705</ref> <ref>PMID:10842718</ref> <ref>PMID:10882995</ref> <ref>PMID:11445644</ref> <ref>PMID:12557757</ref> <ref>PMID:11866053</ref> <ref>PMID:12050338</ref> <ref>PMID:12771253</ref> <ref>PMID:15214015</ref> <ref>PMID:15478468</ref> <ref>PMID:15217993</ref> <ref>PMID:17453626</ref> <ref>PMID:17577687</ref> <ref>PMID:17503405</ref> <ref>PMID:17635579</ref> Defects in TTR are a cause of hyperthyroxinemia dystransthyretinemic euthyroidal (HTDE) [MIM:[~~http~~://omim.org/entry/145680 145680]]. It is a condition characterized by elevation of total and free thyroxine in healthy, euthyroid persons without detectable binding protein abnormalities.<ref>PMID:1979335</ref> Defects in TTR are a cause of carpal tunnel syndrome type 1 (CTS1) [MIM:[~~http~~://omim.org/entry/115430 115430]]. It is a condition characterized by entrapment of the median nerve within the carpal tunnel. Symptoms include burning pain and paresthesias involving the ventral surface of the hand and fingers which may radiate proximally. Impairment of sensation in the distribution of the median nerve and thenar muscle atrophy may occur. This condition may be associated with repetitive occupational trauma, wrist injuries, amyloid neuropathies, rheumatoid arthritis.<ref>PMID:8309582</ref>	+	[https://www.uniprot.org/uniprot/TTHY_HUMAN TTHY_HUMAN] Defects in TTR are the cause of amyloidosis transthyretin-related (AMYL-TTR) [MIM:[https://omim.org/entry/105210 105210]. A hereditary generalized amyloidosis due to transthyretin amyloid deposition. Protein fibrils can form in different tissues leading to amyloid polyneuropathies, amyloidotic cardiomyopathy, carpal tunnel syndrome, systemic senile amyloidosis. The disease includes leptomeningeal amyloidosis that is characterized by primary involvement of the central nervous system. Neuropathologic examination shows amyloid in the walls of leptomeningeal vessels, in pia arachnoid, and subpial deposits. Some patients also develop vitreous amyloid deposition that leads to visual impairment (oculoleptomeningeal amyloidosis). Clinical features include seizures, stroke-like episodes, dementia, psychomotor deterioration, variable amyloid deposition in the vitreous humor.<ref>PMID:11243784</ref> <ref>PMID:15735344</ref> <ref>PMID:19167329</ref> <ref>PMID:3818577</ref> <ref>PMID:3022108</ref> <ref>PMID:6651852</ref> <ref>PMID:6583672</ref> <ref>PMID:3135807</ref> <ref>PMID:1517749</ref> <ref>PMID:1932142</ref> <ref>PMID:7923855</ref> <ref>PMID:8382610</ref> <ref>PMID:8428915</ref> <ref>PMID:9733771</ref> <ref>PMID:12403615</ref> <ref>PMID:16185074</ref> <ref>PMID:16627944</ref> <ref>PMID:6487335</ref> <ref>PMID:3722385</ref> <ref>PMID:2891727</ref> <ref>PMID:2161654</ref> <ref>PMID:2363717</ref> <ref>PMID:1656975</ref> <ref>PMID:2046936</ref> <ref>PMID:1570831</ref> <ref>PMID:1734866</ref> <ref>PMID:1520326</ref> <ref>PMID:1520336</ref> <ref>PMID:1544214</ref> <ref>PMID:1351039</ref> <ref>PMID:1301926</ref> <ref>PMID:1362222</ref> <ref>PMID:1436517</ref> <ref>PMID:8352764</ref> <ref>PMID:8038017</ref> <ref>PMID:8257997</ref> <ref>PMID:8095302</ref> <ref>PMID:1997217</ref> <ref>PMID:8019560</ref> <ref>PMID:8081397</ref> <ref>PMID:7914929</ref> <ref>PMID:8133316</ref> <ref>PMID:7910950</ref> <ref>PMID:7655883</ref> <ref>PMID:7850982</ref> <ref>PMID:8579098</ref> <ref>PMID:9066351</ref> <ref>PMID:8990019</ref> <ref>PMID:9605286</ref> <ref>PMID:10036587</ref> <ref>PMID:10627135</ref> <ref>PMID:10694917</ref> <ref>PMID:10211412</ref> <ref>PMID:10439117</ref> <ref>PMID:10611950</ref> <ref>PMID:10071047</ref> <ref>PMID:10436378</ref> <ref>PMID:10842705</ref> <ref>PMID:10842718</ref> <ref>PMID:10882995</ref> <ref>PMID:11445644</ref> <ref>PMID:12557757</ref> <ref>PMID:11866053</ref> <ref>PMID:12050338</ref> <ref>PMID:12771253</ref> <ref>PMID:15214015</ref> <ref>PMID:15478468</ref> <ref>PMID:15217993</ref> <ref>PMID:17453626</ref> <ref>PMID:17577687</ref> <ref>PMID:17503405</ref> <ref>PMID:17635579</ref> Defects in TTR are a cause of hyperthyroxinemia dystransthyretinemic euthyroidal (HTDE) [MIM:[https://omim.org/entry/145680 145680]. It is a condition characterized by elevation of total and free thyroxine in healthy, euthyroid persons without detectable binding protein abnormalities.<ref>PMID:1979335</ref> Defects in TTR are a cause of carpal tunnel syndrome type 1 (CTS1) [MIM:[https://omim.org/entry/115430 115430]. It is a condition characterized by entrapment of the median nerve within the carpal tunnel. Symptoms include burning pain and paresthesias involving the ventral surface of the hand and fingers which may radiate proximally. Impairment of sensation in the distribution of the median nerve and thenar muscle atrophy may occur. This condition may be associated with repetitive occupational trauma, wrist injuries, amyloid neuropathies, rheumatoid arthritis.<ref>PMID:8309582</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/TTHY_HUMAN TTHY_HUMAN]] Thyroid hormone-binding protein. Probably transports thyroxine from the bloodstream to the brain.<ref>PMID:3714052</ref>	+	[https://www.uniprot.org/uniprot/TTHY_HUMAN TTHY_HUMAN] Thyroid hormone-binding protein. Probably transports thyroxine from the bloodstream to the brain.<ref>PMID:3714052</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 23:		Line 22:

	==See Also==		==See Also==
-	*[[Transthyretin\|Transthyretin]]	+	*[[Transthyretin 3D structures\|Transthyretin 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Berni, R]]	+	[[Category: Berni R]]
-	[[Category: Cianci, M]]	+	[[Category: Cianci M]]
-	[[Category: ~~Florio, P~~]]	+	[[Category: Del Rio D]]
-	[[Category: ~~Foll, C~~]]	+	[[Category: Florio P]]
-	[[Category: ~~Rio, D Del~~]]	+	[[Category: Foll C]]
-	[[Category: Zanotti, G]]	+	[[Category: Zanotti G]]
-	~~[[Category: Amyloid]]~~	+
-	~~[[Category: Fibrillogenesis]]~~	+
-	~~[[Category: Fibrillogenesis inhibitor]]~~	+
-	~~[[Category: Negative cooperativity]]~~	+
-	~~[[Category: Polyphenol]]~~	+
-	~~[[Category: Polyphenol metabolite]]~~	+
-	~~[[Category: Transport protein]]~~	+
-	~~[[Category: Transthyretin~~]]	+

OCA at 08:02, 21 May 2019

OCA — Tue, 21 May 2019 08:02:14 GMT

←Older revision		Revision as of 08:02, 21 May 2019
Line 1:		Line 1:

	==Transthyretin binding heterogeneity and anti-amyloidogenic activity of natural polyphenols and their metabolites: genistein-7-O- glucuronide==		==Transthyretin binding heterogeneity and anti-amyloidogenic activity of natural polyphenols and their metabolites: genistein-7-O- glucuronide==
-	<StructureSection load='5akv' size='340' side='right' caption='[[5akv]], [[Resolution\|resolution]] 1.52Å' scene=''>	+	<StructureSection load='5akv' size='340' side='right'caption='[[5akv]], [[Resolution\|resolution]] 1.52Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5akv]] 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=5AKV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5AKV FirstGlance]. <br>		<table><tr><td colspan='2'>[[5akv]] 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=5AKV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5AKV FirstGlance]. <br>
Line 29:		Line 29:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Berni, R]]		[[Category: Berni, R]]
	[[Category: Cianci, M]]		[[Category: Cianci, M]]

OCA at 06:00, 8 March 2018

OCA — Thu, 08 Mar 2018 06:00:55 GMT

←Older revision		Revision as of 06:00, 8 March 2018
Line 1:		Line 1:
		+
	==Transthyretin binding heterogeneity and anti-amyloidogenic activity of natural polyphenols and their metabolites: genistein-7-O- glucuronide==		==Transthyretin binding heterogeneity and anti-amyloidogenic activity of natural polyphenols and their metabolites: genistein-7-O- glucuronide==
	<StructureSection load='5akv' size='340' side='right' caption='[[5akv]], [[Resolution\|resolution]] 1.52Å' scene=''>		<StructureSection load='5akv' size='340' side='right' caption='[[5akv]], [[Resolution\|resolution]] 1.52Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5akv]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5AKV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5AKV FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5akv]] 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=5AKV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5AKV FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=G7G:GENISTEIN-7-O-GLUCURONIDE'>G7G</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=G7G:GENISTEIN-7-O-GLUCURONIDE'>G7G</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5aks\|5aks]], [[5akt\|5akt]], [[5al0\|5al0]], [[5al8\|5al8]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5aks\|5aks]], [[5akt\|5akt]], [[5al0\|5al0]], [[5al8\|5al8]]</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=5akv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5akv OCA], [http://pdbe.org/5akv PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5akv RCSB], [http://www.ebi.ac.uk/pdbsum/5akv PDBsum]</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=5akv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5akv OCA], [http://pdbe.org/5akv PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5akv RCSB], [http://www.ebi.ac.uk/pdbsum/5akv PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5akv ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 21:
	</div>		</div>
	<div class="pdbe-citations 5akv" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5akv" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Transthyretin\|Transthyretin]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Berni, R]]		[[Category: Berni, R]]
	[[Category: Cianci, M]]		[[Category: Cianci, M]]
Line 34:		Line 39:
	[[Category: Fibrillogenesis inhibitor]]		[[Category: Fibrillogenesis inhibitor]]
	[[Category: Negative cooperativity]]		[[Category: Negative cooperativity]]
-	[[Category: Polyphenol metabolite]]
	[[Category: Polyphenol]]		[[Category: Polyphenol]]
		+	[[Category: Polyphenol metabolite]]
	[[Category: Transport protein]]		[[Category: Transport protein]]
	[[Category: Transthyretin]]		[[Category: Transthyretin]]

OCA at 22:04, 30 November 2015

OCA — Mon, 30 Nov 2015 22:04:47 GMT

←Older revision		Revision as of 22:04, 30 November 2015
Line 11:		Line 11:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/TTHY_HUMAN TTHY_HUMAN]] Thyroid hormone-binding protein. Probably transports thyroxine from the bloodstream to the brain.<ref>PMID:3714052</ref>		[[http://www.uniprot.org/uniprot/TTHY_HUMAN TTHY_HUMAN]] Thyroid hormone-binding protein. Probably transports thyroxine from the bloodstream to the brain.<ref>PMID:3714052</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Transthyretin (TTR) is an amyloidogenic protein, whose amyloidogenic potential is enhanced by a number of specific point mutations. The ability to inhibit TTR fibrillogenesis is known for several classes of compounds, including natural polyphenols, which protect the native state of TTR by specifically interacting with its thyroxine binding sites. Comparative analyses of the interaction and of the ability to protect the TTR native state for polyphenols, both stilbenoids and flavonoids, and some of their main metabolites have been carried out. A main finding of this investigation was the highly preferential binding of resveratrol and thyroxine, both characterized by negative binding cooperativity, to distinct sites in TTR, consistent with the data of X-ray analysis of TTR in complex with both ligands. While revealing the ability of the two thyroxine binding sites of TTR to discriminate between different ligands, this feature has allowed us to evaluate the interactions of polyphenols with both resveratrol and thyroxine preferential binding sites, by using resveratrol and radiolabeled T4 as probes. Among flavonoids, genistein and apigenin were able to effectively displace resveratrol from its preferential binding site, while genistein also showed the ability to interact, albeit weakly, with the preferential thyroxine binding site. Several glucuronidated polyphenol metabolites did not exhibit significant competition for resveratrol and thyroxine preferential binding sites, and lacked the ability to stabilize TTR. However, resveratrol-3-O-sulphate was able to significantly protect the protein native state. A rationale for the in vitro properties found for polyphenol metabolites was provided by X-ray analysis of their complexes with TTR.
		+
		+	Transthyretin Binding Heterogeneity and Anti-amyloidogenic Activity of Natural Polyphenols and their Metabolites.,Florio P, Folli C, Cianci M, Del Rio D, Zanotti G, Berni R J Biol Chem. 2015 Oct 14. pii: jbc.M115.690172. PMID:26468275<ref>PMID:26468275</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 5akv" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 05:32, 22 October 2015

OCA — Thu, 22 Oct 2015 05:32:04 GMT

←Older revision		Revision as of 05:32, 22 October 2015
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-	'''~~Unreleased structure~~'''	+	==Transthyretin binding heterogeneity and anti-amyloidogenic activity of natural polyphenols and their metabolites: genistein-7-O- glucuronide==
-		+	<StructureSection load='5akv' size='340' side='right' caption='[[5akv]], [[Resolution\|resolution]] 1.52Å' scene=''>
-	~~The entry~~ 5akv is ~~ON HOLD until Paper Publication~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[5akv]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5AKV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5AKV FirstGlance]. <br>
-	~~Authors~~: ~~Florio~~, P., ~~Foll~~, C., ~~Cianci~~, M., ~~Del Rio~~, D., ~~Zanotti~~, G., ~~Berni~~, R.	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=G7G:GENISTEIN-7-O-GLUCURONIDE'>G7G</scene></td></tr>
-		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5aks\|5aks]], [[5akt\|5akt]], [[5al0\|5al0]], [[5al8\|5al8]]</td></tr>
-	~~Description~~: ~~Transthyretin~~ binding ~~heterogeneity~~ and ~~anti-amyloidogenic activity~~ of ~~natural polyphenols~~ and ~~their metabolites~~: ~~genistein-7-O-glucuronide~~	+	<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=5akv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5akv OCA], [http://pdbe.org/5akv PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5akv RCSB], [http://www.ebi.ac.uk/pdbsum/5akv PDBsum]</span></td></tr>
-	[[~~Category~~: ~~Unreleased Structures~~]]	+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/TTHY_HUMAN TTHY_HUMAN]] Defects in TTR are the cause of amyloidosis transthyretin-related (AMYL-TTR) [MIM:[http://omim.org/entry/105210 105210]]. A hereditary generalized amyloidosis due to transthyretin amyloid deposition. Protein fibrils can form in different tissues leading to amyloid polyneuropathies, amyloidotic cardiomyopathy, carpal tunnel syndrome, systemic senile amyloidosis. The disease includes leptomeningeal amyloidosis that is characterized by primary involvement of the central nervous system. Neuropathologic examination shows amyloid in the walls of leptomeningeal vessels, in pia arachnoid, and subpial deposits. Some patients also develop vitreous amyloid deposition that leads to visual impairment (oculoleptomeningeal amyloidosis). Clinical features include seizures, stroke-like episodes, dementia, psychomotor deterioration, variable amyloid deposition in the vitreous humor.<ref>PMID:11243784</ref> <ref>PMID:15735344</ref> <ref>PMID:19167329</ref> <ref>PMID:3818577</ref> <ref>PMID:3022108</ref> <ref>PMID:6651852</ref> <ref>PMID:6583672</ref> <ref>PMID:3135807</ref> <ref>PMID:1517749</ref> <ref>PMID:1932142</ref> <ref>PMID:7923855</ref> <ref>PMID:8382610</ref> <ref>PMID:8428915</ref> <ref>PMID:9733771</ref> <ref>PMID:12403615</ref> <ref>PMID:16185074</ref> <ref>PMID:16627944</ref> <ref>PMID:6487335</ref> <ref>PMID:3722385</ref> <ref>PMID:2891727</ref> <ref>PMID:2161654</ref> <ref>PMID:2363717</ref> <ref>PMID:1656975</ref> <ref>PMID:2046936</ref> <ref>PMID:1570831</ref> <ref>PMID:1734866</ref> <ref>PMID:1520326</ref> <ref>PMID:1520336</ref> <ref>PMID:1544214</ref> <ref>PMID:1351039</ref> <ref>PMID:1301926</ref> <ref>PMID:1362222</ref> <ref>PMID:1436517</ref> <ref>PMID:8352764</ref> <ref>PMID:8038017</ref> <ref>PMID:8257997</ref> <ref>PMID:8095302</ref> <ref>PMID:1997217</ref> <ref>PMID:8019560</ref> <ref>PMID:8081397</ref> <ref>PMID:7914929</ref> <ref>PMID:8133316</ref> <ref>PMID:7910950</ref> <ref>PMID:7655883</ref> <ref>PMID:7850982</ref> <ref>PMID:8579098</ref> <ref>PMID:9066351</ref> <ref>PMID:8990019</ref> <ref>PMID:9605286</ref> <ref>PMID:10036587</ref> <ref>PMID:10627135</ref> <ref>PMID:10694917</ref> <ref>PMID:10211412</ref> <ref>PMID:10439117</ref> <ref>PMID:10611950</ref> <ref>PMID:10071047</ref> <ref>PMID:10436378</ref> <ref>PMID:10842705</ref> <ref>PMID:10842718</ref> <ref>PMID:10882995</ref> <ref>PMID:11445644</ref> <ref>PMID:12557757</ref> <ref>PMID:11866053</ref> <ref>PMID:12050338</ref> <ref>PMID:12771253</ref> <ref>PMID:15214015</ref> <ref>PMID:15478468</ref> <ref>PMID:15217993</ref> <ref>PMID:17453626</ref> <ref>PMID:17577687</ref> <ref>PMID:17503405</ref> <ref>PMID:17635579</ref> Defects in TTR are a cause of hyperthyroxinemia dystransthyretinemic euthyroidal (HTDE) [MIM:[http://omim.org/entry/145680 145680]]. It is a condition characterized by elevation of total and free thyroxine in healthy, euthyroid persons without detectable binding protein abnormalities.<ref>PMID:1979335</ref> Defects in TTR are a cause of carpal tunnel syndrome type 1 (CTS1) [MIM:[http://omim.org/entry/115430 115430]]. It is a condition characterized by entrapment of the median nerve within the carpal tunnel. Symptoms include burning pain and paresthesias involving the ventral surface of the hand and fingers which may radiate proximally. Impairment of sensation in the distribution of the median nerve and thenar muscle atrophy may occur. This condition may be associated with repetitive occupational trauma, wrist injuries, amyloid neuropathies, rheumatoid arthritis.<ref>PMID:8309582</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/TTHY_HUMAN TTHY_HUMAN]] Thyroid hormone-binding protein. Probably transports thyroxine from the bloodstream to the brain.<ref>PMID:3714052</ref>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Berni, R]]		[[Category: Berni, R]]
		+	[[Category: Cianci, M]]
	[[Category: Florio, P]]		[[Category: Florio, P]]
	[[Category: Foll, C]]		[[Category: Foll, C]]
-	[[Category: ~~Del~~ Rio, D]]	+	[[Category: Rio, D Del]]
-	~~[[Category: Cianci, M~~]]	+
	[[Category: Zanotti, G]]		[[Category: Zanotti, G]]
		+	[[Category: Amyloid]]
		+	[[Category: Fibrillogenesis]]
		+	[[Category: Fibrillogenesis inhibitor]]
		+	[[Category: Negative cooperativity]]
		+	[[Category: Polyphenol metabolite]]
		+	[[Category: Polyphenol]]
		+	[[Category: Transport protein]]
		+	[[Category: Transthyretin]]

OCA at 13:38, 17 June 2015

OCA — Wed, 17 Jun 2015 13:38:29 GMT

←Older revision		Revision as of 13:38, 17 June 2015
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

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

	Authors: Florio, P., Foll, C., Cianci, M., Del Rio, D., Zanotti, G., Berni, R.		Authors: Florio, P., Foll, C., Cianci, M., Del Rio, D., Zanotti, G., Berni, R.

OCA at 13:05, 26 March 2015

OCA — Thu, 26 Mar 2015 13:05:51 GMT

←Older revision		Revision as of 13:05, 26 March 2015
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5akv is ON HOLD ~~until sometime in the future~~	+	The entry 5akv is ON HOLD

	Authors: Florio, P., Foll, C., Cianci, M., Del Rio, D., Zanotti, G., Berni, R.		Authors: Florio, P., Foll, C., Cianci, M., Del Rio, D., Zanotti, G., Berni, R.

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

OCA — Wed, 11 Mar 2015 11:03:42 GMT

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

←Older revision

Revision as of 11:03, 11 March 2015

OCA: New page: '''Unreleased structure''' The entry 5akv is ON HOLD until sometime in the future Authors: Florio, P., Foll, C., Cianci, M., Del Rio, D., Zanotti, G., Berni, R. Description: Transthyre...

OCA — Wed, 11 Mar 2015 11:03:41 GMT

New page: '''Unreleased structure''' The entry 5akv is ON HOLD until sometime in the future Authors: Florio, P., Foll, C., Cianci, M., Del Rio, D., Zanotti, G., Berni, R. Description: Transthyre...

New page

'''Unreleased structure'''

The entry 5akv is ON HOLD until sometime in the future

Authors: Florio, P., Foll, C., Cianci, M., Del Rio, D., Zanotti, G., Berni, R.

Description: Transthyretin binding heterogeneity and anti-amyloidogenic activity of natural polyphenols and their metabolites: genistein-7-O-glucuronide
[[Category: Unreleased Structures]]
[[Category: Berni, R]]
[[Category: Florio, P]]
[[Category: Foll, C]]
[[Category: Del Rio, D]]
[[Category: Cianci, M]]
[[Category: Zanotti, G]]