1klc - Revision history

OCA at 08:01, 3 April 2024

OCA — Wed, 03 Apr 2024 08:01:22 GMT

←Older revision		Revision as of 08:01, 3 April 2024
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	==SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE==		==SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE==
-	<StructureSection load='1klc' size='340' side='right'caption='[[1klc~~]], [[NMR_Ensembles_of_Models \| 1 NMR models~~]]' scene=''>	+	<StructureSection load='1klc' size='340' side='right'caption='[[1klc]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1KLC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1KLC 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;'>[[1kla\|1kla]], [[1kld\|1kld]]</div~~></td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [https://pdbe.org/1klc PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [https://www.ebi.ac.uk/pdbsum/1klc PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1klc 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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [https://pdbe.org/1klc PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [https://www.ebi.ac.uk/pdbsum/1klc PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1klc ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[https://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>	+	[https://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[https://omim.org/entry/131300 131300]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.	+	[https://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.
	== 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=1klc 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=1klc ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	The three-dimensional solution structure of human transforming growth factor beta 1 (TGF-beta 1) has been determined using multinuclear magnetic resonance spectroscopy and a hybrid distance geometry/ simulated annealing algorithm. It represents one of the first examples of a mammalian protein structure that has been solved by isotopic labeling of the protein in a eukaryotic cell line and multinuclear NMR spectroscopy. The solution structure of the 25 kDa disulfide-linked TGF-beta 1 homodimer was calculated from over 3200 distance and dihedral angle restraints. The final ensemble of 33 accepted structures had no NOE or dihedral angle violations greater than 0.30 A and 5.0 degrees, respectively. The RMSD of backbone atoms for the ensemble of 33 structures relative to their mean structure was 1.1 A when all residues were used in the alignment and 0.7 A when loop regions were omitted. The solution structure of TGF-beta 1 follows two independently determined crystal structures of TGF-beta 2 (Daopin et al., 1992, 1993; Schlunegger & Grutter, 1992, 1993), providing the first opportunity to examine structural differences between the two isoforms at the molecular level. Although the structures are very similar, with an RMSD in backbone atom positions of 1.4 A when loop regions are omitted in the alignment and 1.9 A when all residues are considered, there are several notable differences in structure and flexibility which may be related to function. The clearest example of these is in the beta-turn from residues 69-72: the turn type found in the solution structure of TGF-beta 1 falls into the category of type II, whereas that present in the X-ray crystal structure of TGF-beta 2 is more consistent with a type I turn conformation. This may be of functional significance as studies using TGF-beta chimeras and deletion mutants indicate that this portion of the molecule may be important in receptor binding.
-
-	Transforming growth factor beta 1: three-dimensional structure in solution and comparison with the X-ray structure of transforming growth factor beta 2.,Hinck AP, Archer SJ, Qian SW, Roberts AB, Sporn MB, Weatherbee JA, Tsang ML, Lucas R, Zhang BL, Wenker J, Torchia DA Biochemistry. 1996 Jul 2;35(26):8517-34. PMID:8679613<ref>PMID:8679613</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 1klc" 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: Archer~~, S J~~]]	+	[[Category: Archer SJ]]
-	[[Category: Hinck~~, A P~~]]	+	[[Category: Hinck AP]]
-	[[Category: Lucas, R]]	+	[[Category: Lucas R]]
-	[[Category: Qian~~, S W~~]]	+	[[Category: Qian SW]]
-	[[Category: Roberts~~, A B~~]]	+	[[Category: Roberts AB]]
-	[[Category: Sporn~~, M B~~]]	+	[[Category: Sporn MB]]
-	[[Category: Torchia~~, D A~~]]	+	[[Category: Torchia DA]]
-	[[Category: Tsang~~, M L.~~S]]	+	[[Category: Tsang ML-S]]
-	[[Category: Weatherbee~~, J A~~]]	+	[[Category: Weatherbee JA]]
-	[[Category: Wenker, J]]	+	[[Category: Wenker J]]
-	[[Category: Zhang, B L]]	+	[[Category: Zhang B-L]]
-	~~[[Category: Glycoprotein]]~~	+
-	~~[[Category: Growth factor]]~~	+
-	~~[[Category: Mitogen~~]]	+

OCA at 06:32, 18 August 2021

OCA — Wed, 18 Aug 2021 06:32:48 GMT

←Older revision		Revision as of 06:32, 18 August 2021
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	<StructureSection load='1klc' size='340' side='right'caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>		<StructureSection load='1klc' size='340' side='right'caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1KLC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1KLC FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1kla\|1kla]], [[1kld\|1kld]]</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;'>[[1kla\|1kla]], [[1kld\|1kld]]</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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [~~http~~://pdbe.org/1klc PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1klc PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1klc 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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [https://pdbe.org/1klc PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [https://www.ebi.ac.uk/pdbsum/1klc PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1klc ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[~~http~~://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>	+	[[https://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[https://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.	+	[[https://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]

OCA at 09:33, 6 November 2019

OCA — Wed, 06 Nov 2019 09:33:05 GMT

←Older revision		Revision as of 09:33, 6 November 2019
Line 1:		Line 1:

	==SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE==		==SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE==
-	<StructureSection load='1klc' size='340' side='right' caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>	+	<StructureSection load='1klc' size='340' side='right'caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>		<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>
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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/kl/1klc_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/kl/1klc_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>
Line 35:		Line 35:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Archer, S J]]		[[Category: Archer, S J]]
	[[Category: Hinck, A P]]		[[Category: Hinck, A P]]

OCA at 06:41, 29 November 2017

OCA — Wed, 29 Nov 2017 06:41:02 GMT

←Older revision		Revision as of 06:41, 29 November 2017
Line 1:		Line 1:
		+
	==SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE==		==SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE==
	<StructureSection load='1klc' size='340' side='right' caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>		<StructureSection load='1klc' size='340' side='right' caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>
Line 4:		Line 5:
	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>		<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1kla\|1kla]], [[1kld\|1kld]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1kla\|1kla]], [[1kld\|1kld]]</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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [http://pdbe.org/1klc PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [http://www.ebi.ac.uk/pdbsum/1klc 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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [http://pdbe.org/1klc PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [http://www.ebi.ac.uk/pdbsum/1klc PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1klc ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 13:34, 8 February 2016

OCA — Mon, 08 Feb 2016 13:34:49 GMT

←Older revision		Revision as of 13:34, 8 February 2016
Line 18:		Line 18:
	<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=1klc ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 12:04, 10 September 2015

OCA — Thu, 10 Sep 2015 12:04:22 GMT

←Older revision		Revision as of 12:04, 10 September 2015
Line 2:		Line 2:
	<StructureSection load='1klc' size='340' side='right' caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>		<StructureSection load='1klc' size='340' side='right' caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1kla\|1kla]], [[1kld\|1kld]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1kla\|1kla]], [[1kld\|1kld]]</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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [http://www.ebi.ac.uk/pdbsum/1klc 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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [http://pdbe.org/1klc PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [http://www.ebi.ac.uk/pdbsum/1klc PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
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	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 1klc" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Archer, S J]]		[[Category: Archer, S J]]
	[[Category: Hinck, A P]]		[[Category: Hinck, A P]]

OCA at 15:59, 5 January 2015

OCA — Mon, 05 Jan 2015 15:59:11 GMT

←Older revision		Revision as of 15:59, 5 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>		<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1kla\|1kla]], [[1kld\|1kld]]</td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1kla\|1kla]], [[1kld\|1kld]]</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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [http://www.ebi.ac.uk/pdbsum/1klc 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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [http://www.ebi.ac.uk/pdbsum/1klc PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[http://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>		[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[http://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>
Line 33:		Line 33:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Archer, S J.]]	+	[[Category: Archer, S J]]
-	[[Category: Hinck, A P.]]	+	[[Category: Hinck, A P]]
-	[[Category: Lucas, R.]]	+	[[Category: Lucas, R]]
-	[[Category: Qian, S W.]]	+	[[Category: Qian, S W]]
-	[[Category: Roberts, A B.]]	+	[[Category: Roberts, A B]]
-	[[Category: Sporn, M B.]]	+	[[Category: Sporn, M B]]
-	[[Category: Torchia, D A.]]	+	[[Category: Torchia, D A]]
-	[[Category: Tsang, M L.S.]]	+	[[Category: Tsang, M L.S]]
-	[[Category: Weatherbee, J A.]]	+	[[Category: Weatherbee, J A]]
-	[[Category: Wenker, J.]]	+	[[Category: Wenker, J]]
-	[[Category: Zhang, B L.]]	+	[[Category: Zhang, B L]]
	[[Category: Glycoprotein]]		[[Category: Glycoprotein]]
	[[Category: Growth factor]]		[[Category: Growth factor]]
	[[Category: Mitogen]]		[[Category: Mitogen]]

OCA at 15:11, 29 September 2014

OCA — Mon, 29 Sep 2014 15:11:55 GMT

←Older revision		Revision as of 15:11, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1klc\| PDB=1klc \| SCENE= }}~~	+	==SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE==
-	===SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE===	+	<StructureSection load='1klc' size='340' side='right' caption='[[1klc]], [[NMR_Ensembles_of_Models \| 1 NMR models]]' scene=''>
-	~~{{ABSTRACT_PUBMED_8679613}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[1klc]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1KLC FirstGlance]. <br>
-	==Disease==	+	</td></tr><tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1kla\|1kla]], [[1kld\|1kld]]</td></tr>
-	[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[http://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref><ref>PMID:11062463</ref><ref>PMID:12493741</ref><ref>PMID:12843182</ref><ref>PMID:15103729</ref>	+	<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=1klc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1klc OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1klc RCSB], [http://www.ebi.ac.uk/pdbsum/1klc PDBsum]</span></td></tr>
-		+	<table>
-	==Function==	+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[http://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref> <ref>PMID:11062463</ref> <ref>PMID:12493741</ref> <ref>PMID:12843182</ref> <ref>PMID:15103729</ref>
		+	== Function ==
	[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.		[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.
		+	== 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/kl/1klc_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 ==
		+	The three-dimensional solution structure of human transforming growth factor beta 1 (TGF-beta 1) has been determined using multinuclear magnetic resonance spectroscopy and a hybrid distance geometry/ simulated annealing algorithm. It represents one of the first examples of a mammalian protein structure that has been solved by isotopic labeling of the protein in a eukaryotic cell line and multinuclear NMR spectroscopy. The solution structure of the 25 kDa disulfide-linked TGF-beta 1 homodimer was calculated from over 3200 distance and dihedral angle restraints. The final ensemble of 33 accepted structures had no NOE or dihedral angle violations greater than 0.30 A and 5.0 degrees, respectively. The RMSD of backbone atoms for the ensemble of 33 structures relative to their mean structure was 1.1 A when all residues were used in the alignment and 0.7 A when loop regions were omitted. The solution structure of TGF-beta 1 follows two independently determined crystal structures of TGF-beta 2 (Daopin et al., 1992, 1993; Schlunegger & Grutter, 1992, 1993), providing the first opportunity to examine structural differences between the two isoforms at the molecular level. Although the structures are very similar, with an RMSD in backbone atom positions of 1.4 A when loop regions are omitted in the alignment and 1.9 A when all residues are considered, there are several notable differences in structure and flexibility which may be related to function. The clearest example of these is in the beta-turn from residues 69-72: the turn type found in the solution structure of TGF-beta 1 falls into the category of type II, whereas that present in the X-ray crystal structure of TGF-beta 2 is more consistent with a type I turn conformation. This may be of functional significance as studies using TGF-beta chimeras and deletion mutants indicate that this portion of the molecule may be important in receptor binding.

-	~~==About this Structure==~~	+	Transforming growth factor beta 1: three-dimensional structure in solution and comparison with the X-ray structure of transforming growth factor beta 2.,Hinck AP, Archer SJ, Qian SW, Roberts AB, Sporn MB, Weatherbee JA, Tsang ML, Lucas R, Zhang BL, Wenker J, Torchia DA Biochemistry. 1996 Jul 2;35(26):8517-34. PMID:8679613<ref>PMID:8679613</ref>
-	~~[[1klc]] is a 2 chain~~ structure with ~~sequence from [http://en~~.~~wikipedia~~.~~org/wiki/Homo_sapiens Homo sapiens]~~. ~~Full experimental information is available from [http~~:/~~/oca.weizmann.ac.il/oca-bin/ocashort?id=1KLC OCA].~~	+

-	==~~Reference~~==	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~<ref group="xtra">PMID:008679613</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	</div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Archer, S J.]]		[[Category: Archer, S J.]]

OCA at 16:35, 24 March 2013

OCA — Sun, 24 Mar 2013 16:35:46 GMT

←Older revision		Revision as of 16:35, 24 March 2013
Line 1:		Line 1:
-	[[Image:1klc.png\|left\|200px]]
-
	{{STRUCTURE_1klc\| PDB=1klc \| SCENE= }}		{{STRUCTURE_1klc\| PDB=1klc \| SCENE= }}
-
	===SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE===		===SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE===
		+	{{ABSTRACT_PUBMED_8679613}}

-	~~{{ABSTRACT_PUBMED_8679613}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[http://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref><ref>PMID:11062463</ref><ref>PMID:12493741</ref><ref>PMID:12843182</ref><ref>PMID:15103729</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts.

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

	==Reference==		==Reference==
-	<ref group="xtra">PMID:008679613</ref><references group="xtra"/>	+	<ref group="xtra">PMID:008679613</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Archer, S J.]]		[[Category: Archer, S J.]]

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

OCA — Wed, 05 Dec 2012 20:12:41 GMT

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

←Older revision

Revision as of 20:12, 5 December 2012