4ank - Revision history

OCA at 11:31, 20 December 2023

OCA — Wed, 20 Dec 2023 11:31:01 GMT

←Older revision		Revision as of 11:31, 20 December 2023
Line 3:		Line 3:
	<StructureSection load='4ank' size='340' side='right'caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>		<StructureSection load='4ank' size='340' side='right'caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4ank]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ANK OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4ANK FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4ank]] 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=4ANK OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4ANK FirstGlance]. <br>
-	</td></tr><tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat">~~<div style='overflow: auto; max~~-~~height: 3em;'>[[1bm7\|1bm7]]~~, [[~~1bmz~~\|~~1bmz~~]], [[1bz8\|1bz8]], [[1bzd\|1bzd]], [[1bze\|1bze]], [[1dvq\|1dvq]], [[1dvs\|1dvs]], [[1dvt\|1dvt]], [[1dvu\|1dvu]], [[1dvx\|1dvx]], [[1dvy\|1dvy]], [[1dvz\|1dvz]], [[1e3f\|1e3f]], [[1e4h\|1e4h]], [[1e5a\|1e5a]], [[1eta\|1eta]], [[1etb\|1etb]], [[1f41\|1f41]], [[1f64\|1f64]], [[1f86\|1f86]], [[1fh2\|1fh2]], [[1fhn\|1fhn]], [[1g1o\|1g1o]], [[1gko\|1gko]], [[1ict\|1ict]], [[1iii\|1iii]], [[1iik\|1iik]], [[1ijn\|1ijn]], [[1qab\|1qab]], [[1qwh\|1qwh]], [[1rlb\|1rlb]], [[1sok\|1sok]], [[1soq\|1soq]], [[1tha\|1tha]], [[1thc\|1thc]], [[1tlm\|1tlm]], [[1tsh\|1tsh]], [[1tt6\|1tt6]], [[1tta\|1tta]], [[1ttb\|1ttb]], [[1ttc\|1ttc]], [[1ttr\|1ttr]], [[1tyr\|1tyr]], [[1tz8\|1tz8]], [[1u21\|1u21]], [[1x7s\|1x7s]], [[1x7t\|1x7t]], [[1y1d\|1y1d]], [[1z7j\|1z7j]], [[1zcr\|1zcr]], [[1zd6\|1zd6]], [[2b14\|2b14]], [[2b15\|2b15]], [[2b16\|2b16]], [[2b77\|2b77]], [[2b9a\|2b9a]], [[2f7i\|2f7i]], [[2f8i\|2f8i]], [[2fbr\|2fbr]], [[2flm\|2flm]], [[2g5u\|2g5u]], [[2g9k\|2g9k]], [[2gab\|2gab]], [[2pab\|2pab]], [[2rox\|2rox]], [[2roy\|2roy]], [[2trh\|2trh]], [[2try\|2try]], [[2wqa\|2wqa]], [[4abq\|4abq]], [[4abu\|4abu]], [[4abv\|4abv]], [[4abw\|4abw]], [[4ac2\|4ac2]], [[4ac4\|4ac4]], [[4act\|4act]], [[5ttr\|5ttr]]</div></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]] 1.7Å</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=4ank FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ank OCA], [https://pdbe.org/4ank PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4ank RCSB], [https://www.ebi.ac.uk/pdbsum/4ank PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4ank 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=4ank FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ank OCA], [https://pdbe.org/4ank PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4ank RCSB], [https://www.ebi.ac.uk/pdbsum/4ank PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4ank ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[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>	+	[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 ==
-	[[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>	+	[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 27:		Line 27:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Gupta, S]]	+	[[Category: Gupta S]]
-	[[Category: Khan, T]]	+	[[Category: Khan T]]
-	[[Category: Mishra, S]]	+	[[Category: Mishra S]]
-	[[Category: Salunke~~, D M~~]]	+	[[Category: Salunke DM]]
-	[[Category: Singh~~, R R~~]]	+	[[Category: Singh RR]]
-	[[Category: Surolia, A]]	+	[[Category: Surolia A]]
-	[[Category: Tomar, D]]	+	[[Category: Tomar D]]
-	~~[[Category: Amyloidosis inhibition]]~~	+
-	~~[[Category: Hormone]]~~	+
-	~~[[Category: Hormone binding protein]]~~	+
-	~~[[Category: Thyroxine transport protein~~]]	+

OCA at 05:40, 25 August 2022

OCA — Thu, 25 Aug 2022 05:40:11 GMT

←Older revision		Revision as of 05:40, 25 August 2022
Line 3:		Line 3:
	<StructureSection load='4ank' size='340' side='right'caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>		<StructureSection load='4ank' size='340' side='right'caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4ank]] 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=4ANK OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=4ANK FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4ank]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ANK OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4ANK FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1bm7\|1bm7]], [[1bmz\|1bmz]], [[1bz8\|1bz8]], [[1bzd\|1bzd]], [[1bze\|1bze]], [[1dvq\|1dvq]], [[1dvs\|1dvs]], [[1dvt\|1dvt]], [[1dvu\|1dvu]], [[1dvx\|1dvx]], [[1dvy\|1dvy]], [[1dvz\|1dvz]], [[1e3f\|1e3f]], [[1e4h\|1e4h]], [[1e5a\|1e5a]], [[1eta\|1eta]], [[1etb\|1etb]], [[1f41\|1f41]], [[1f64\|1f64]], [[1f86\|1f86]], [[1fh2\|1fh2]], [[1fhn\|1fhn]], [[1g1o\|1g1o]], [[1gko\|1gko]], [[1ict\|1ict]], [[1iii\|1iii]], [[1iik\|1iik]], [[1ijn\|1ijn]], [[1qab\|1qab]], [[1qwh\|1qwh]], [[1rlb\|1rlb]], [[1sok\|1sok]], [[1soq\|1soq]], [[1tha\|1tha]], [[1thc\|1thc]], [[1tlm\|1tlm]], [[1tsh\|1tsh]], [[1tt6\|1tt6]], [[1tta\|1tta]], [[1ttb\|1ttb]], [[1ttc\|1ttc]], [[1ttr\|1ttr]], [[1tyr\|1tyr]], [[1tz8\|1tz8]], [[1u21\|1u21]], [[1x7s\|1x7s]], [[1x7t\|1x7t]], [[1y1d\|1y1d]], [[1z7j\|1z7j]], [[1zcr\|1zcr]], [[1zd6\|1zd6]], [[2b14\|2b14]], [[2b15\|2b15]], [[2b16\|2b16]], [[2b77\|2b77]], [[2b9a\|2b9a]], [[2f7i\|2f7i]], [[2f8i\|2f8i]], [[2fbr\|2fbr]], [[2flm\|2flm]], [[2g5u\|2g5u]], [[2g9k\|2g9k]], [[2gab\|2gab]], [[2pab\|2pab]], [[2rox\|2rox]], [[2roy\|2roy]], [[2trh\|2trh]], [[2try\|2try]], [[2wqa\|2wqa]], [[4abq\|4abq]], [[4abu\|4abu]], [[4abv\|4abv]], [[4abw\|4abw]], [[4ac2\|4ac2]], [[4ac4\|4ac4]], [[4act\|4act]], [[5ttr\|5ttr]]</td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1bm7\|1bm7]], [[1bmz\|1bmz]], [[1bz8\|1bz8]], [[1bzd\|1bzd]], [[1bze\|1bze]], [[1dvq\|1dvq]], [[1dvs\|1dvs]], [[1dvt\|1dvt]], [[1dvu\|1dvu]], [[1dvx\|1dvx]], [[1dvy\|1dvy]], [[1dvz\|1dvz]], [[1e3f\|1e3f]], [[1e4h\|1e4h]], [[1e5a\|1e5a]], [[1eta\|1eta]], [[1etb\|1etb]], [[1f41\|1f41]], [[1f64\|1f64]], [[1f86\|1f86]], [[1fh2\|1fh2]], [[1fhn\|1fhn]], [[1g1o\|1g1o]], [[1gko\|1gko]], [[1ict\|1ict]], [[1iii\|1iii]], [[1iik\|1iik]], [[1ijn\|1ijn]], [[1qab\|1qab]], [[1qwh\|1qwh]], [[1rlb\|1rlb]], [[1sok\|1sok]], [[1soq\|1soq]], [[1tha\|1tha]], [[1thc\|1thc]], [[1tlm\|1tlm]], [[1tsh\|1tsh]], [[1tt6\|1tt6]], [[1tta\|1tta]], [[1ttb\|1ttb]], [[1ttc\|1ttc]], [[1ttr\|1ttr]], [[1tyr\|1tyr]], [[1tz8\|1tz8]], [[1u21\|1u21]], [[1x7s\|1x7s]], [[1x7t\|1x7t]], [[1y1d\|1y1d]], [[1z7j\|1z7j]], [[1zcr\|1zcr]], [[1zd6\|1zd6]], [[2b14\|2b14]], [[2b15\|2b15]], [[2b16\|2b16]], [[2b77\|2b77]], [[2b9a\|2b9a]], [[2f7i\|2f7i]], [[2f8i\|2f8i]], [[2fbr\|2fbr]], [[2flm\|2flm]], [[2g5u\|2g5u]], [[2g9k\|2g9k]], [[2gab\|2gab]], [[2pab\|2pab]], [[2rox\|2rox]], [[2roy\|2roy]], [[2trh\|2trh]], [[2try\|2try]], [[2wqa\|2wqa]], [[4abq\|4abq]], [[4abu\|4abu]], [[4abv\|4abv]], [[4abw\|4abw]], [[4ac2\|4ac2]], [[4ac4\|4ac4]], [[4act\|4act]], [[5ttr\|5ttr]]</div></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=4ank FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ank OCA], [~~http~~://pdbe.org/4ank PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=4ank RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/4ank PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=4ank 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=4ank FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ank OCA], [https://pdbe.org/4ank PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4ank RCSB], [https://www.ebi.ac.uk/pdbsum/4ank PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4ank 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 22:		Line 22:

	==See Also==		==See Also==
-	*[[Transthyretin\|Transthyretin]]	+	*[[Transthyretin 3D structures\|Transthyretin 3D structures]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:47, 17 July 2019

OCA — Wed, 17 Jul 2019 11:47:42 GMT

←Older revision		Revision as of 11:47, 17 July 2019
Line 1:		Line 1:

	==Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.==		==Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.==
-	<StructureSection load='4ank' size='340' side='right' caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>	+	<StructureSection load='4ank' size='340' side='right'caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[4ank]] 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=4ANK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ANK FirstGlance]. <br>		<table><tr><td colspan='2'>[[4ank]] 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=4ANK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ANK FirstGlance]. <br>
Line 28:		Line 28:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Gupta, S]]		[[Category: Gupta, S]]
	[[Category: Khan, T]]		[[Category: Khan, T]]

OCA at 11:34, 11 August 2016

OCA — Thu, 11 Aug 2016 11:34:40 GMT

←Older revision		Revision as of 11:34, 11 August 2016
Line 1:		Line 1:
		+
	==Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.==		==Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.==
	<StructureSection load='4ank' size='340' side='right' caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>		<StructureSection load='4ank' size='340' side='right' caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4ank]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ANK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ANK FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4ank]] 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=4ANK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ANK FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1bm7\|1bm7]], [[1bmz\|1bmz]], [[1bz8\|1bz8]], [[1bzd\|1bzd]], [[1bze\|1bze]], [[1dvq\|1dvq]], [[1dvs\|1dvs]], [[1dvt\|1dvt]], [[1dvu\|1dvu]], [[1dvx\|1dvx]], [[1dvy\|1dvy]], [[1dvz\|1dvz]], [[1e3f\|1e3f]], [[1e4h\|1e4h]], [[1e5a\|1e5a]], [[1eta\|1eta]], [[1etb\|1etb]], [[1f41\|1f41]], [[1f64\|1f64]], [[1f86\|1f86]], [[1fh2\|1fh2]], [[1fhn\|1fhn]], [[1g1o\|1g1o]], [[1gko\|1gko]], [[1ict\|1ict]], [[1iii\|1iii]], [[1iik\|1iik]], [[1ijn\|1ijn]], [[1qab\|1qab]], [[1qwh\|1qwh]], [[1rlb\|1rlb]], [[1sok\|1sok]], [[1soq\|1soq]], [[1tha\|1tha]], [[1thc\|1thc]], [[1tlm\|1tlm]], [[1tsh\|1tsh]], [[1tt6\|1tt6]], [[1tta\|1tta]], [[1ttb\|1ttb]], [[1ttc\|1ttc]], [[1ttr\|1ttr]], [[1tyr\|1tyr]], [[1tz8\|1tz8]], [[1u21\|1u21]], [[1x7s\|1x7s]], [[1x7t\|1x7t]], [[1y1d\|1y1d]], [[1z7j\|1z7j]], [[1zcr\|1zcr]], [[1zd6\|1zd6]], [[2b14\|2b14]], [[2b15\|2b15]], [[2b16\|2b16]], [[2b77\|2b77]], [[2b9a\|2b9a]], [[2f7i\|2f7i]], [[2f8i\|2f8i]], [[2fbr\|2fbr]], [[2flm\|2flm]], [[2g5u\|2g5u]], [[2g9k\|2g9k]], [[2gab\|2gab]], [[2pab\|2pab]], [[2rox\|2rox]], [[2roy\|2roy]], [[2trh\|2trh]], [[2try\|2try]], [[2wqa\|2wqa]], [[4abq\|4abq]], [[4abu\|4abu]], [[4abv\|4abv]], [[4abw\|4abw]], [[4ac2\|4ac2]], [[4ac4\|4ac4]], [[4act\|4act]], [[5ttr\|5ttr]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1bm7\|1bm7]], [[1bmz\|1bmz]], [[1bz8\|1bz8]], [[1bzd\|1bzd]], [[1bze\|1bze]], [[1dvq\|1dvq]], [[1dvs\|1dvs]], [[1dvt\|1dvt]], [[1dvu\|1dvu]], [[1dvx\|1dvx]], [[1dvy\|1dvy]], [[1dvz\|1dvz]], [[1e3f\|1e3f]], [[1e4h\|1e4h]], [[1e5a\|1e5a]], [[1eta\|1eta]], [[1etb\|1etb]], [[1f41\|1f41]], [[1f64\|1f64]], [[1f86\|1f86]], [[1fh2\|1fh2]], [[1fhn\|1fhn]], [[1g1o\|1g1o]], [[1gko\|1gko]], [[1ict\|1ict]], [[1iii\|1iii]], [[1iik\|1iik]], [[1ijn\|1ijn]], [[1qab\|1qab]], [[1qwh\|1qwh]], [[1rlb\|1rlb]], [[1sok\|1sok]], [[1soq\|1soq]], [[1tha\|1tha]], [[1thc\|1thc]], [[1tlm\|1tlm]], [[1tsh\|1tsh]], [[1tt6\|1tt6]], [[1tta\|1tta]], [[1ttb\|1ttb]], [[1ttc\|1ttc]], [[1ttr\|1ttr]], [[1tyr\|1tyr]], [[1tz8\|1tz8]], [[1u21\|1u21]], [[1x7s\|1x7s]], [[1x7t\|1x7t]], [[1y1d\|1y1d]], [[1z7j\|1z7j]], [[1zcr\|1zcr]], [[1zd6\|1zd6]], [[2b14\|2b14]], [[2b15\|2b15]], [[2b16\|2b16]], [[2b77\|2b77]], [[2b9a\|2b9a]], [[2f7i\|2f7i]], [[2f8i\|2f8i]], [[2fbr\|2fbr]], [[2flm\|2flm]], [[2g5u\|2g5u]], [[2g9k\|2g9k]], [[2gab\|2gab]], [[2pab\|2pab]], [[2rox\|2rox]], [[2roy\|2roy]], [[2trh\|2trh]], [[2try\|2try]], [[2wqa\|2wqa]], [[4abq\|4abq]], [[4abu\|4abu]], [[4abv\|4abv]], [[4abw\|4abw]], [[4ac2\|4ac2]], [[4ac4\|4ac4]], [[4act\|4act]], [[5ttr\|5ttr]]</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=4ank FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ank OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4ank RCSB], [http://www.ebi.ac.uk/pdbsum/4ank 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=4ank FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ank OCA], [http://pdbe.org/4ank PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4ank RCSB], [http://www.ebi.ac.uk/pdbsum/4ank PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4ank ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 18:		Line 19:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 4ank" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 25:		Line 27:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Gupta, S]]		[[Category: Gupta, S]]
	[[Category: Khan, T]]		[[Category: Khan, T]]

OCA at 09:35, 25 January 2015

OCA — Sun, 25 Jan 2015 09:35:09 GMT

←Older revision		Revision as of 09:35, 25 January 2015
Line 1:		Line 1:
-	~~{{STRUCTURE_4ank\| PDB=4ank \| SCENE= }}~~	+	==Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.==
-	===Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.===	+	<StructureSection load='4ank' size='340' side='right' caption='[[4ank]], [[Resolution\|resolution]] 1.70Å' scene=''>
-	~~{{ABSTRACT_PUBMED_22973437}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[4ank]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ANK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ANK FirstGlance]. <br>
		+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1bm7\|1bm7]], [[1bmz\|1bmz]], [[1bz8\|1bz8]], [[1bzd\|1bzd]], [[1bze\|1bze]], [[1dvq\|1dvq]], [[1dvs\|1dvs]], [[1dvt\|1dvt]], [[1dvu\|1dvu]], [[1dvx\|1dvx]], [[1dvy\|1dvy]], [[1dvz\|1dvz]], [[1e3f\|1e3f]], [[1e4h\|1e4h]], [[1e5a\|1e5a]], [[1eta\|1eta]], [[1etb\|1etb]], [[1f41\|1f41]], [[1f64\|1f64]], [[1f86\|1f86]], [[1fh2\|1fh2]], [[1fhn\|1fhn]], [[1g1o\|1g1o]], [[1gko\|1gko]], [[1ict\|1ict]], [[1iii\|1iii]], [[1iik\|1iik]], [[1ijn\|1ijn]], [[1qab\|1qab]], [[1qwh\|1qwh]], [[1rlb\|1rlb]], [[1sok\|1sok]], [[1soq\|1soq]], [[1tha\|1tha]], [[1thc\|1thc]], [[1tlm\|1tlm]], [[1tsh\|1tsh]], [[1tt6\|1tt6]], [[1tta\|1tta]], [[1ttb\|1ttb]], [[1ttc\|1ttc]], [[1ttr\|1ttr]], [[1tyr\|1tyr]], [[1tz8\|1tz8]], [[1u21\|1u21]], [[1x7s\|1x7s]], [[1x7t\|1x7t]], [[1y1d\|1y1d]], [[1z7j\|1z7j]], [[1zcr\|1zcr]], [[1zd6\|1zd6]], [[2b14\|2b14]], [[2b15\|2b15]], [[2b16\|2b16]], [[2b77\|2b77]], [[2b9a\|2b9a]], [[2f7i\|2f7i]], [[2f8i\|2f8i]], [[2fbr\|2fbr]], [[2flm\|2flm]], [[2g5u\|2g5u]], [[2g9k\|2g9k]], [[2gab\|2gab]], [[2pab\|2pab]], [[2rox\|2rox]], [[2roy\|2roy]], [[2trh\|2trh]], [[2try\|2try]], [[2wqa\|2wqa]], [[4abq\|4abq]], [[4abu\|4abu]], [[4abv\|4abv]], [[4abw\|4abw]], [[4ac2\|4ac2]], [[4ac4\|4ac4]], [[4act\|4act]], [[5ttr\|5ttr]]</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=4ank FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ank OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4ank RCSB], [http://www.ebi.ac.uk/pdbsum/4ank PDBsum]</span></td></tr>
		+	</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>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	BACKGROUND: Transthyretin (TTR) is a homotetrameric serum and cerebrospinal fluid protein that transports thyroxine (T4) and retinol by binding to retinol binding protein. Rate-limiting tetramer dissociation and rapid monomer misfolding and disassembly of TTR lead to amyloid fibril formation in different tissues causing various amyloid diseases. Based on the current understanding of the pathogenesis of TTR amyloidosis, it is considered that the inhibition of amyloid fibril formation by stabilization of TTR in native tetrameric form is a viable approach for the treatment of TTR amyloidosis. METHODOLOGY AND PRINCIPAL FINDINGS: We have examined interactions of the wtTTR with a series of compounds containing various substitutions at biphenyl ether skeleton and a novel compound, previously evaluated for binding and inhibiting tetramer dissociation, by x-ray crystallographic approach. High resolution crystal structures of five ligands in complex with wtTTR provided snapshots of negatively cooperative binding of ligands in two T4 binding sites besides characterizing their binding orientations, conformations, and interactions with binding site residues. In all complexes, the ligand has better fit and more potent interactions in first T4 site i.e. (AC site) than the second T4 site (BD site). Together, these results suggest that AC site is a preferred ligand binding site and retention of ordered water molecules between the dimer interfaces further stabilizes the tetramer by bridging a hydrogen bond interaction between Ser117 and its symmetric copy. CONCLUSION: Novel biphenyl ether based compounds exhibit negative-cooperativity while binding to two T4 sites which suggests that binding of only single ligand molecule is sufficient to inhibit the TTR tetramer dissociation.

-	~~==Disease==~~	+	Crystallographic Study of Novel Transthyretin Ligands Exhibiting Negative-Cooperativity between Two Thyroxine Binding Sites.,Tomar D, Khan T, Singh RR, Mishra S, Gupta S, Surolia A, Salunke DM PLoS One. 2012;7(9):e43522. Epub 2012 Sep 4. PMID:22973437<ref>PMID:22973437</ref>
-	~~[[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==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[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>
-		+
-	~~==About this Structure==~~	+
-	[[4ank]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ANK OCA].	+

	==See Also==		==See Also==
	*[[Transthyretin\|Transthyretin]]		*[[Transthyretin\|Transthyretin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Gupta, S.]]	+	[[Category: Gupta, S]]
-	[[Category: Khan, T.]]	+	[[Category: Khan, T]]
-	[[Category: Mishra, S.]]	+	[[Category: Mishra, S]]
-	[[Category: Salunke, D M.]]	+	[[Category: Salunke, D M]]
-	[[Category: Singh, R R.]]	+	[[Category: Singh, R R]]
-	[[Category: Surolia, A.]]	+	[[Category: Surolia, A]]
-	[[Category: Tomar, D.]]	+	[[Category: Tomar, D]]
	[[Category: Amyloidosis inhibition]]		[[Category: Amyloidosis inhibition]]
	[[Category: Hormone]]		[[Category: Hormone]]
	[[Category: Hormone binding protein]]		[[Category: Hormone binding protein]]
	[[Category: Thyroxine transport protein]]		[[Category: Thyroxine transport protein]]

OCA at 19:24, 24 March 2013

OCA — Sun, 24 Mar 2013 19:24:28 GMT

←Older revision		Revision as of 19:24, 24 March 2013
Line 1:		Line 1:
-	[[Image:4ank.jpg\|left\|200px]]
-
	{{STRUCTURE_4ank\| PDB=4ank \| SCENE= }}		{{STRUCTURE_4ank\| PDB=4ank \| SCENE= }}
-
	===Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.===		===Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.===
-
	{{ABSTRACT_PUBMED_22973437}}		{{ABSTRACT_PUBMED_22973437}}
		+
		+	==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>

	==About this Structure==		==About this Structure==
	[[4ank]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ANK OCA].		[[4ank]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ANK OCA].
		+
		+	==See Also==
		+	*[[Transthyretin\|Transthyretin]]
		+
		+	==Reference==
		+	<references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Gupta, S.]]		[[Category: Gupta, S.]]

OCA at 20:35, 26 September 2012

OCA — Wed, 26 Sep 2012 20:35:02 GMT

←Older revision		Revision as of 20:35, 26 September 2012
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	[[Image:4ank.jpg\|left\|200px]]

-	~~The entry~~ 4ank ~~is ON HOLD~~ ~~until Paper Publication~~	+	{{STRUCTURE_4ank\| PDB=4ank \| SCENE= }}

-	~~Authors: TOMAR, D., KHAN, T., SINGH, R.R., MISHRA, S., GUPTA, S., SUROLIA, A., SALUNKE, D.M~~.	+	===Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.===

-	~~Description~~: ~~Crystallographic study of novel transthyretin ligands exhibiting negative~~-~~cooperativity between two T4 binding sites~~.	+	{{ABSTRACT_PUBMED_22973437}}
		+
		+	==About this Structure==
		+	[[4ank]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ANK OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Gupta, S.]]
		+	[[Category: Khan, T.]]
		+	[[Category: Mishra, S.]]
		+	[[Category: Salunke, D M.]]
		+	[[Category: Singh, R R.]]
		+	[[Category: Surolia, A.]]
		+	[[Category: Tomar, D.]]
		+	[[Category: Amyloidosis inhibition]]
		+	[[Category: Hormone]]
		+	[[Category: Hormone binding protein]]
		+	[[Category: Thyroxine transport protein]]

OCA at 04:33, 29 August 2012

OCA — Wed, 29 Aug 2012 04:33:59 GMT

←Older revision		Revision as of 04:33, 29 August 2012
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 4ank is ON HOLD	+	The entry 4ank is ON HOLD until Paper Publication

	Authors: TOMAR, D., KHAN, T., SINGH, R.R., MISHRA, S., GUPTA, S., SUROLIA, A., SALUNKE, D.M.		Authors: TOMAR, D., KHAN, T., SINGH, R.R., MISHRA, S., GUPTA, S., SUROLIA, A., SALUNKE, D.M.

	Description: Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.		Description: Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.

OCA: Protected "4ank" [edit=sysop:move=sysop]

OCA — Wed, 28 Mar 2012 07:17:29 GMT

Protected "4ank" [edit=sysop:move=sysop]

←Older revision

Revision as of 07:17, 28 March 2012

OCA: New page: '''Unreleased structure''' The entry 4ank is ON HOLD Authors: TOMAR, D., KHAN, T., SINGH, R.R., MISHRA, S., GUPTA, S., SUROLIA, A., SALUNKE, D.M. Description: Crystallographic study of...

OCA — Wed, 28 Mar 2012 07:17:29 GMT

New page: '''Unreleased structure''' The entry 4ank is ON HOLD Authors: TOMAR, D., KHAN, T., SINGH, R.R., MISHRA, S., GUPTA, S., SUROLIA, A., SALUNKE, D.M. Description: Crystallographic study of...

New page

'''Unreleased structure'''

The entry 4ank is ON HOLD

Authors: TOMAR, D., KHAN, T., SINGH, R.R., MISHRA, S., GUPTA, S., SUROLIA, A., SALUNKE, D.M.

Description: Crystallographic study of novel transthyretin ligands exhibiting negative-cooperativity between two T4 binding sites.