1mjs - Revision history

OCA at 07:44, 14 February 2024

OCA — Wed, 14 Feb 2024 07:44:36 GMT

←Older revision		Revision as of 07:44, 14 February 2024
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	<StructureSection load='1mjs' size='340' side='right'caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>		<StructureSection load='1mjs' size='340' side='right'caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=1MJS FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1MJS 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;'>[[1mk2\|1mk2]]</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]] 1.91Å</td></tr>
-	~~<tr~~ id~~='gene'><td class~~="~~sblockLbl~~">~~<b>~~[[~~Gene~~\|~~Gene:~~]]~~</b></td><td class="sblockDat">SMAD3 ([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=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [https://pdbe.org/1mjs PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [https://www.ebi.ac.uk/pdbsum/1mjs PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1mjs ProSAT]</span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [~~http~~://pdbe.org/1mjs PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1mjs PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1mjs ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Defects in SMAD3 may be a cause of colorectal cancer (CRC) [MIM:[~~http~~://omim.org/entry/114500 114500]]. Defects in SMAD3 are the cause of Loeys-Dietz syndrome 3 (LDS3) [MIM:[~~http~~://omim.org/entry/613795 613795]]. An aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation. Note=SMAD3 mutations have been reported to be also associated with thoracic aortic aneurysms and dissection (TAAD) (PubMed:21778426). This phenotype is distinguised from LDS3 by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit aneurysms of other arteries, including abdominal aorta, iliac, and/or intracranial arteries (PubMed:21778426), they have been classified as LDS3 by the OMIM resource.<ref>PMID:21778426</ref> <ref>PMID:21217753</ref>	+	[https://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN] Defects in SMAD3 may be a cause of colorectal cancer (CRC) [MIM:[https://omim.org/entry/114500 114500]. Defects in SMAD3 are the cause of Loeys-Dietz syndrome 3 (LDS3) [MIM:[https://omim.org/entry/613795 613795]. An aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation. Note=SMAD3 mutations have been reported to be also associated with thoracic aortic aneurysms and dissection (TAAD) (PubMed:21778426). This phenotype is distinguised from LDS3 by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit aneurysms of other arteries, including abdominal aorta, iliac, and/or intracranial arteries (PubMed:21778426), they have been classified as LDS3 by the OMIM resource.<ref>PMID:21778426</ref> <ref>PMID:21217753</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures (By similarity). Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.<ref>PMID:9732876</ref> <ref>PMID:9892009</ref> <ref>PMID:10995748</ref> <ref>PMID:15241418</ref> <ref>PMID:15588252</ref> <ref>PMID:16156666</ref> <ref>PMID:16751101</ref> <ref>PMID:17327236</ref> <ref>PMID:16862174</ref> <ref>PMID:19289081</ref> <ref>PMID:19218245</ref>	+	[https://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN] Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures (By similarity). Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.<ref>PMID:9732876</ref> <ref>PMID:9892009</ref> <ref>PMID:10995748</ref> <ref>PMID:15241418</ref> <ref>PMID:15588252</ref> <ref>PMID:16156666</ref> <ref>PMID:16751101</ref> <ref>PMID:17327236</ref> <ref>PMID:16862174</ref> <ref>PMID:19289081</ref> <ref>PMID:19218245</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1mjs ConSurf].		</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1mjs ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	Smad3 transduces the signals of TGF-betas, coupling transmembrane receptor kinase activation to transcriptional control. The membrane-associated molecule SARA (Smad Anchor for Receptor Activation) recruits Smad3 for phosphorylation by the receptor kinase. Upon phosphorylation, Smad3 dissociates from SARA and enters the nucleus, in which its transcriptional activity can be repressed by Ski. Here, we show that SARA and Ski recognize specifically the monomeric and trimeric forms of Smad3, respectively. Thus, trimerization of Smad3, induced by phosphorylation, simultaneously activates the TGF-beta signal by driving Smad3 dissociation from SARA and sets up the negative feedback mechanism by Ski. Structural models of the Smad3/SARA/receptor kinase complex and Smad3/Ski complex provide insights into the molecular basis of regulation.
-
-	Smad3 allostery links TGF-beta receptor kinase activation to transcriptional control.,Qin BY, Lam SS, Correia JJ, Lin K Genes Dev. 2002 Aug 1;16(15):1950-63. PMID:12154125<ref>PMID:12154125</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 1mjs" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Correia~~, J J~~]]	+	[[Category: Correia JJ]]
-	[[Category: Lam~~, S S~~]]	+	[[Category: Lam SS]]
-	[[Category: Lin, K]]	+	[[Category: Lin K]]
-	[[Category: Qin~~, B Y]]~~	+	[[Category: Qin BY]]
-	~~[[Category: Beta sandwich]]~~	+
-	~~[[Category: Transcription~~]]	+

OCA at 08:38, 2 December 2020

OCA — Wed, 02 Dec 2020 08:38:00 GMT

←Older revision		Revision as of 08:38, 2 December 2020
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	==MH2 domain of transcriptional factor SMAD3==		==MH2 domain of transcriptional factor SMAD3==
-	<StructureSection load='1mjs' size='340' side='right' caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>	+	<StructureSection load='1mjs' size='340' side='right'caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1MJS FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=1MJS FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1mk2\|1mk2]]</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;'>[[1mk2\|1mk2]]</div></td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([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=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://pdbe.org/1mjs PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1mjs ProSAT]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://pdbe.org/1mjs PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1mjs ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 36:		Line 36:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Correia, J J]]		[[Category: Correia, J J]]
	[[Category: Lam, S S]]		[[Category: Lam, S S]]

OCA at 07:57, 31 January 2018

OCA — Wed, 31 Jan 2018 07:57:35 GMT

←Older revision		Revision as of 07:57, 31 January 2018
Line 1:		Line 1:
		+
	==MH2 domain of transcriptional factor SMAD3==		==MH2 domain of transcriptional factor SMAD3==
	<StructureSection load='1mjs' size='340' side='right' caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>		<StructureSection load='1mjs' size='340' side='right' caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>
Line 5:		Line 6:
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1mk2\|1mk2]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1mk2\|1mk2]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([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=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://pdbe.org/1mjs PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs 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=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://pdbe.org/1mjs PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1mjs ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
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	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/mj/1mjs_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/mj/1mjs_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>

OCA at 11:40, 9 February 2016

OCA — Tue, 09 Feb 2016 11:40:22 GMT

←Older revision		Revision as of 11:40, 9 February 2016
Line 19:		Line 19:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1mjs ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 21:51, 10 September 2015

OCA — Thu, 10 Sep 2015 21:51:49 GMT

←Older revision		Revision as of 21:51, 10 September 2015
Line 2:		Line 2:
	<StructureSection load='1mjs' size='340' side='right' caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>		<StructureSection load='1mjs' size='340' side='right' caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1MJS FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1MJS FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1mk2\|1mk2]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1mk2\|1mk2]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([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=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs 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=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://pdbe.org/1mjs PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 29:		Line 29:
	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 1mjs" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Correia, J J]]		[[Category: Correia, J J]]
	[[Category: Lam, S S]]		[[Category: Lam, S S]]

OCA at 16:45, 5 January 2015

OCA — Mon, 05 Jan 2015 16:45:49 GMT

←Older revision		Revision as of 16:45, 5 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1MJS FirstGlance]. <br>		<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1MJS FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1mk2\|1mk2]]</td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1mk2\|1mk2]]</td></tr>
-	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
-	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs 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=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Defects in SMAD3 may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]]. Defects in SMAD3 are the cause of Loeys-Dietz syndrome 3 (LDS3) [MIM:[http://omim.org/entry/613795 613795]]. An aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation. Note=SMAD3 mutations have been reported to be also associated with thoracic aortic aneurysms and dissection (TAAD) (PubMed:21778426). This phenotype is distinguised from LDS3 by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit aneurysms of other arteries, including abdominal aorta, iliac, and/or intracranial arteries (PubMed:21778426), they have been classified as LDS3 by the OMIM resource.<ref>PMID:21778426</ref> <ref>PMID:21217753</ref>		[[http://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Defects in SMAD3 may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]]. Defects in SMAD3 are the cause of Loeys-Dietz syndrome 3 (LDS3) [MIM:[http://omim.org/entry/613795 613795]]. An aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation. Note=SMAD3 mutations have been reported to be also associated with thoracic aortic aneurysms and dissection (TAAD) (PubMed:21778426). This phenotype is distinguised from LDS3 by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit aneurysms of other arteries, including abdominal aorta, iliac, and/or intracranial arteries (PubMed:21778426), they have been classified as LDS3 by the OMIM resource.<ref>PMID:21778426</ref> <ref>PMID:21217753</ref>
Line 34:		Line 34:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Correia, J J.]]	+	[[Category: Correia, J J]]
-	[[Category: Lam, S S.]]	+	[[Category: Lam, S S]]
-	[[Category: Lin, K.]]	+	[[Category: Lin, K]]
-	[[Category: Qin, B Y.]]	+	[[Category: Qin, B Y]]
	[[Category: Beta sandwich]]		[[Category: Beta sandwich]]
	[[Category: Transcription]]		[[Category: Transcription]]

OCA at 17:27, 29 September 2014

OCA — Mon, 29 Sep 2014 17:27:59 GMT

←Older revision		Revision as of 17:27, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1mjs~~\| ~~PDB~~=1mjs \| ~~SCENE~~= }}	+	==MH2 domain of transcriptional factor SMAD3==
-	===~~MH2 domain of~~ transcriptional factor SMAD3===	+	<StructureSection load='1mjs' size='340' side='right' caption='[[1mjs]], [[Resolution\|resolution]] 1.91Å' scene=''>
-	~~{{ABSTRACT_PUBMED_12154125}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1mjs]] is a 1 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=1MJS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1MJS FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1mk2\|1mk2]]</td></tr>
		+	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">SMAD3 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1mjs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1mjs OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1mjs RCSB], [http://www.ebi.ac.uk/pdbsum/1mjs PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Defects in SMAD3 may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]]. Defects in SMAD3 are the cause of Loeys-Dietz syndrome 3 (LDS3) [MIM:[http://omim.org/entry/613795 613795]]. An aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation. Note=SMAD3 mutations have been reported to be also associated with thoracic aortic aneurysms and dissection (TAAD) (PubMed:21778426). This phenotype is distinguised from LDS3 by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit aneurysms of other arteries, including abdominal aorta, iliac, and/or intracranial arteries (PubMed:21778426), they have been classified as LDS3 by the OMIM resource.<ref>PMID:21778426</ref> <ref>PMID:21217753</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures (By similarity). Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.<ref>PMID:9732876</ref> <ref>PMID:9892009</ref> <ref>PMID:10995748</ref> <ref>PMID:15241418</ref> <ref>PMID:15588252</ref> <ref>PMID:16156666</ref> <ref>PMID:16751101</ref> <ref>PMID:17327236</ref> <ref>PMID:16862174</ref> <ref>PMID:19289081</ref> <ref>PMID:19218245</ref>
		+	== Evolutionary Conservation ==
		+	[[Image:Consurf_key_small.gif\|200px\|right]]
		+	Check<jmol>
		+	<jmolCheckbox>
		+	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/mj/1mjs_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Smad3 transduces the signals of TGF-betas, coupling transmembrane receptor kinase activation to transcriptional control. The membrane-associated molecule SARA (Smad Anchor for Receptor Activation) recruits Smad3 for phosphorylation by the receptor kinase. Upon phosphorylation, Smad3 dissociates from SARA and enters the nucleus, in which its transcriptional activity can be repressed by Ski. Here, we show that SARA and Ski recognize specifically the monomeric and trimeric forms of Smad3, respectively. Thus, trimerization of Smad3, induced by phosphorylation, simultaneously activates the TGF-beta signal by driving Smad3 dissociation from SARA and sets up the negative feedback mechanism by Ski. Structural models of the Smad3/SARA/receptor kinase complex and Smad3/Ski complex provide insights into the molecular basis of regulation.

-	~~==Disease==~~	+	Smad3 allostery links TGF-beta receptor kinase activation to transcriptional control.,Qin BY, Lam SS, Correia JJ, Lin K Genes Dev. 2002 Aug 1;16(15):1950-63. PMID:12154125<ref>PMID:12154125</ref>
-	[[http://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Defects in SMAD3 may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]]. Defects in SMAD3 are the cause of Loeys-~~Dietz syndrome 3 (LDS3) [MIM:[http://omim.org/entry/613795 613795]]. An aortic aneurysm syndrome with widespread systemic involvement~~. ~~The disorder is characterized by the triad of arterial tortuosity and aneurysms~~, ~~hypertelorism~~, ~~and bifid uvula or cleft palate~~. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation. Note=SMAD3 mutations have been reported to be also associated with thoracic aortic aneurysms and dissection (~~TAAD~~) ~~(PubMed~~:~~21778426)~~. This phenotype is distinguised from LDS3 by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit aneurysms of other arteries, including abdominal aorta, iliac, and/or intracranial arteries (PubMed:21778426), they have been classified as LDS3 by the OMIM resource.<ref>PMID:~~21778426</ref>~~<ref>PMID:~~21217753~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~//www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, ~~on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form~~ a ~~SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration~~ of ~~primary keratinocytes and by altering~~ the ~~TGF-mediated chemotaxis of monocytes~~. ~~This effect on wound healing appears to be hormone-sensitive~~. ~~Regulator~~ of chondrogenesis and osteogenesis and inhibits early healing of bone fractures (By similarity). Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.<~~ref~~>~~PMID:9732876~~</~~ref~~><ref>PMID:9892009</ref><ref>PMID:10995748</ref><ref>PMID:15241418</ref><ref>PMID:15588252</ref><ref>PMID:16156666</ref><ref>PMID:16751101</ref><ref>PMID:17327236</ref><ref>PMID:16862174</ref><ref>PMID:19289081</ref><ref>PMID:19218245</ref>	+	</div>
-		+	== References ==
-	==~~About this Structure==~~	+	<references/>
-	[[1mjs]] is a 1 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=1MJS OCA].	+	__TOC__
-		+	</StructureSection>
-	~~==Reference~~==	+
-	~~<ref group="xtra">PMID:012154125</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Correia, J J.]]		[[Category: Correia, J J.]]

OCA at 06:50, 25 March 2013

OCA — Mon, 25 Mar 2013 06:50:57 GMT

←Older revision		Revision as of 06:50, 25 March 2013
Line 1:		Line 1:
-	[[Image:1mjs.png\|left\|200px]]
-
	{{STRUCTURE_1mjs\| PDB=1mjs \| SCENE= }}		{{STRUCTURE_1mjs\| PDB=1mjs \| SCENE= }}
-
	===MH2 domain of transcriptional factor SMAD3===		===MH2 domain of transcriptional factor SMAD3===
		+	{{ABSTRACT_PUBMED_12154125}}

-	~~{{ABSTRACT_PUBMED_12154125}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Defects in SMAD3 may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]]. Defects in SMAD3 are the cause of Loeys-Dietz syndrome 3 (LDS3) [MIM:[http://omim.org/entry/613795 613795]]. An aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation. Note=SMAD3 mutations have been reported to be also associated with thoracic aortic aneurysms and dissection (TAAD) (PubMed:21778426). This phenotype is distinguised from LDS3 by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit aneurysms of other arteries, including abdominal aorta, iliac, and/or intracranial arteries (PubMed:21778426), they have been classified as LDS3 by the OMIM resource.<ref>PMID:21778426</ref><ref>PMID:21217753</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/SMAD3_HUMAN SMAD3_HUMAN]] Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures (By similarity). Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.<ref>PMID:9732876</ref><ref>PMID:9892009</ref><ref>PMID:10995748</ref><ref>PMID:15241418</ref><ref>PMID:15588252</ref><ref>PMID:16156666</ref><ref>PMID:16751101</ref><ref>PMID:17327236</ref><ref>PMID:16862174</ref><ref>PMID:19289081</ref><ref>PMID:19218245</ref>

	==About this Structure==		==About this Structure==
Line 11:		Line 13:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:012154125</ref><references group="xtra"/>	+	<ref group="xtra">PMID:012154125</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Correia, J J.]]		[[Category: Correia, J J.]]

OCA: Protected "1mjs" [edit=sysop:move=sysop]

OCA — Wed, 05 Dec 2012 21:03:23 GMT

Protected "1mjs" [edit=sysop:move=sysop]

←Older revision

Revision as of 21:03, 5 December 2012

OCA at 21:03, 5 December 2012

OCA — Wed, 05 Dec 2012 21:03:21 GMT

←Older revision		Revision as of 21:03, 5 December 2012
Line 1:		Line 1:
-	{{Seed}}
	[[Image:1mjs.png\|left\|200px]]		[[Image:1mjs.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_1mjs", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_1mjs\| PDB=1mjs \| SCENE= }}		{{STRUCTURE_1mjs\| PDB=1mjs \| SCENE= }}

	===MH2 domain of transcriptional factor SMAD3===		===MH2 domain of transcriptional factor SMAD3===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_12154125}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 12154125 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_12154125}}		{{ABSTRACT_PUBMED_12154125}}

	==About this Structure==		==About this Structure==
-	~~1MJS~~ is a 1 chain structure of 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=1MJS OCA].	+	[[1mjs]] is a 1 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=1MJS OCA].

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~12154125~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:012154125</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Correia, J J.]]		[[Category: Correia, J J.]]
Line 30:		Line 18:
	[[Category: Qin, B Y.]]		[[Category: Qin, B Y.]]
	[[Category: Beta sandwich]]		[[Category: Beta sandwich]]
-		+	[[Category: Transcription]]
-	~~''Page seeded by~~ [~~http~~:~~//oca.weizmann.ac.il/oca OCA~~ ] ~~on Tue Feb 17 09:29:23 2009''~~	+