4kqe - Revision history

OCA at 14:31, 8 November 2023

OCA — Wed, 08 Nov 2023 14:31:27 GMT

←Older revision		Revision as of 14:31, 8 November 2023
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	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[4kqe]] 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=4KQE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4KQE FirstGlance]. <br>		<table><tr><td colspan='2'>[[4kqe]] 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=4KQE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4KQE FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 2.739Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [https://pdbe.org/4kqe PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [https://www.ebi.ac.uk/pdbsum/4kqe PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4kqe 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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [https://pdbe.org/4kqe PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [https://www.ebi.ac.uk/pdbsum/4kqe PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4kqe ProSAT]</span></td></tr>
	</table>		</table>

OCA at 09:07, 7 December 2022

OCA — Wed, 07 Dec 2022 09:07:33 GMT

←Older revision		Revision as of 09:07, 7 December 2022
Line 3:		Line 3:
	<StructureSection load='4kqe' size='340' side='right'caption='[[4kqe]], [[Resolution\|resolution]] 2.74Å' scene=''>		<StructureSection load='4kqe' size='340' side='right'caption='[[4kqe]], [[Resolution\|resolution]] 2.74Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4kqe]] 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=4KQE OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=4KQE FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4kqe]] 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=4KQE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4KQE FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene~~></td></tr>~~	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4kr2\|4kr2]], [[4kr3\|4kr3]]</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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [https://pdbe.org/4kqe PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [https://www.ebi.ac.uk/pdbsum/4kqe PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4kqe ProSAT]</span></td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GARS ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>~~	+
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=6.1.1.14 6.1.1.14] </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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [~~http~~://pdbe.org/4kqe PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/4kqe PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=4kqe ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/~~SYG_HUMAN SYG_HUMAN~~]~~] Defects in GARS are the cause of~~ Charcot-Marie-Tooth disease type 2D (CMT2D) [MIM:[http://omim.org/entry/601472 601472]]. CMT2D is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT2 group are characterized by signs of axonal regeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. CMT2D is characterized by a more severe phenotype in the upper extremities (severe weakness and atrophy, absence of tendon reflexes) than in the lower limbs. CMT2D inheritance is autosomal dominant.<ref>PMID:12690580</ref> Defects in GARS are a cause of distal hereditary motor neuronopathy type 5A (HMN5A) [MIM:[http://omim.org/entry/600794 600794]]; ~~also known as distal~~ hereditary motor neuropathy type ~~V (DSMAV)~~. ~~A disorder characterized~~ by ~~distal muscular atrophy mainly~~ affecting the ~~upper extremities,~~ in ~~contrast to other distal motor neuronopathies~~. ~~These constitute a heterogeneous group of neuromuscular diseases~~ caused by ~~selective degeneration of motor neurons in~~ the ~~anterior horn of the spinal cord, without sensory deficit~~ in ~~the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss~~. The disease ~~starts with weakness and wasting of distal muscles of~~ the ~~anterior tibial and peroneal compartments of the legs~~. ~~Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs.<ref>PMID:12690580</ref>~~	+	[https://www.uniprot.org/uniprot/GARS_HUMAN GARS_HUMAN] Autosomal dominant Charcot-Marie-Tooth disease type 2D;Distal hereditary motor neuropathy type 5. The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry.
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/~~SYG_HUMAN SYG_HUMAN]~~] Catalyzes the ~~attachment~~ of glycine to tRNA(Gly). ~~Is also able produce~~ diadenosine tetraphosphate (Ap4A), a universal pleiotropic signaling molecule needed for cell regulation pathways, by direct condensation of 2 ATPs.<ref>PMID:19710017</ref>	+	[https://www.uniprot.org/uniprot/GARS_HUMAN GARS_HUMAN] Catalyzes the ATP-dependent ligation of glycine to the 3'-end of its cognate tRNA, via the formation of an aminoacyl-adenylate intermediate (Gly-AMP) (PubMed:17544401, PubMed:28675565, PubMed:24898252). Also produces diadenosine tetraphosphate (Ap4A), a universal pleiotropic signaling molecule needed for cell regulation pathways, by direct condensation of 2 ATPs. Thereby, may play a special role in Ap4A homeostasis (PubMed:19710017).<ref>PMID:17544401</ref> <ref>PMID:19710017</ref> <ref>PMID:24898252</ref> <ref>PMID:28675565</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Glycine--tRNA ligase]]~~	+	[[Category: Homo sapiens]]
-	~~[[Category: Human~~]]	+
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Hao, Z]]	+	[[Category: Hao Z]]
-	[[Category: Qin, X]]	+	[[Category: Qin X]]
-	[[Category: Tian, Q]]	+	[[Category: Tian Q]]
-	[[Category: Xie, W]]	+	[[Category: Xie W]]
-	[[Category: Zhang, Z]]	+	[[Category: Zhang Z]]
-	[[Category: Zhou, C]]	+	[[Category: Zhou C]]
-	~~[[Category: Aminoacylation]]~~	+
-	~~[[Category: Ligase]]~~	+
-	~~[[Category: Rossmann fold]]~~	+
-	~~[[Category: Trna-gly~~]]	+

OCA at 09:21, 3 April 2019

OCA — Wed, 03 Apr 2019 09:21:09 GMT

←Older revision		Revision as of 09:21, 3 April 2019
Line 1:		Line 1:

	==The mutant structure of the human glycyl-tRNA synthetase E71G==		==The mutant structure of the human glycyl-tRNA synthetase E71G==
-	<StructureSection load='4kqe' size='340' side='right' caption='[[4kqe]], [[Resolution\|resolution]] 2.74Å' scene=''>	+	<StructureSection load='4kqe' size='340' side='right'caption='[[4kqe]], [[Resolution\|resolution]] 2.74Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4kqe]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4KQE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4KQE FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4kqe]] 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=4KQE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4KQE FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4kr2\|4kr2]], [[4kr3\|4kr3]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4kr2\|4kr2]], [[4kr3\|4kr3]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GARS ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=6.1.1.14 6.1.1.14] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=6.1.1.14 6.1.1.14] </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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [http://pdbe.org/4kqe PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [http://www.ebi.ac.uk/pdbsum/4kqe 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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [http://pdbe.org/4kqe PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [http://www.ebi.ac.uk/pdbsum/4kqe PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4kqe ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 22:		Line 23:
	</div>		</div>
	<div class="pdbe-citations 4kqe" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 4kqe" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Aminoacyl tRNA synthetase 3D structures\|Aminoacyl tRNA synthetase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 27:		Line 31:
	</StructureSection>		</StructureSection>
	[[Category: Glycine--tRNA ligase]]		[[Category: Glycine--tRNA ligase]]
		+	[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Hao, Z]]		[[Category: Hao, Z]]
	[[Category: Qin, X]]		[[Category: Qin, X]]

OCA at 16:57, 10 May 2016

OCA — Tue, 10 May 2016 16:57:20 GMT

←Older revision		Revision as of 16:57, 10 May 2016
Line 1:		Line 1:
-	==~~Complex~~ structure ~~reveals multiple conformations~~ of glycyl-tRNA synthetase ~~in glycylation~~==	+
		+	==The mutant structure of the human glycyl-tRNA synthetase E71G==
	<StructureSection load='4kqe' size='340' side='right' caption='[[4kqe]], [[Resolution\|resolution]] 2.74Å' scene=''>		<StructureSection load='4kqe' size='340' side='right' caption='[[4kqe]], [[Resolution\|resolution]] 2.74Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
Line 6:		Line 7:
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4kr2\|4kr2]], [[4kr3\|4kr3]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4kr2\|4kr2]], [[4kr3\|4kr3]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=6.1.1.14 6.1.1.14] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=6.1.1.14 6.1.1.14] </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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [http://www.ebi.ac.uk/pdbsum/4kqe 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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [http://pdbe.org/4kqe PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [http://www.ebi.ac.uk/pdbsum/4kqe PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 12:		Line 13:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/SYG_HUMAN SYG_HUMAN]] Catalyzes the attachment of glycine to tRNA(Gly). Is also able produce diadenosine tetraphosphate (Ap4A), a universal pleiotropic signaling molecule needed for cell regulation pathways, by direct condensation of 2 ATPs.<ref>PMID:19710017</ref>		[[http://www.uniprot.org/uniprot/SYG_HUMAN SYG_HUMAN]] Catalyzes the attachment of glycine to tRNA(Gly). Is also able produce diadenosine tetraphosphate (Ap4A), a universal pleiotropic signaling molecule needed for cell regulation pathways, by direct condensation of 2 ATPs.<ref>PMID:19710017</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Glycyl-tRNA synthetase (GlyRS) is the enzyme that covalently links glycine to cognate tRNA for translation. It is of great research interest because of its nonconserved quaternary structures, unique species-specific aminoacylation properties, and noncanonical functions in neurological diseases, but none of these is fully understood. We report two crystal structures of human GlyRS variants, in the free form and in complex with tRNA(Gly) respectively, and reveal new aspects of the glycylation mechanism. We discover that insertion 3 differs considerably in conformation in catalysis and that it acts like a "switch" and fully opens to allow tRNA to bind in a cross-subunit fashion. The flexibility of the protein is supported by molecular dynamics simulation, as well as enzymatic activity assays. The biophysical and biochemical studies suggest that human GlyRS may utilize its flexibility for both the traditional function (regulate tRNA binding) and alternative functions (roles in diseases).
		+
		+	Large Conformational Changes of Insertion 3 in Human Glycyl-tRNA Synthetase (hGlyRS) during Catalysis.,Deng X, Qin X, Chen L, Jia Q, Zhang Y, Zhang Z, Lei D, Ren G, Zhou Z, Wang Z, Li Q, Xie W J Biol Chem. 2016 Mar 11;291(11):5740-52. doi: 10.1074/jbc.M115.679126. Epub 2016, Jan 21. PMID:26797133<ref>PMID:26797133</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 4kqe" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 13:04, 4 January 2015

OCA — Sun, 04 Jan 2015 13:04:21 GMT

←Older revision		Revision as of 13:04, 4 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[4kqe]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4KQE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4KQE FirstGlance]. <br>		<table><tr><td colspan='2'>[[4kqe]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4KQE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4KQE FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4kr2\|4kr2]], [[4kr3\|4kr3]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4kr2\|4kr2]], [[4kr3\|4kr3]]</td></tr>
-	<tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=6.1.1.14 6.1.1.14] </span></td></tr>	+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=6.1.1.14 6.1.1.14] </span></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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [http://www.ebi.ac.uk/pdbsum/4kqe 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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [http://www.ebi.ac.uk/pdbsum/4kqe PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/SYG_HUMAN SYG_HUMAN]] Defects in GARS are the cause of Charcot-Marie-Tooth disease type 2D (CMT2D) [MIM:[http://omim.org/entry/601472 601472]]. CMT2D is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT2 group are characterized by signs of axonal regeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. CMT2D is characterized by a more severe phenotype in the upper extremities (severe weakness and atrophy, absence of tendon reflexes) than in the lower limbs. CMT2D inheritance is autosomal dominant.<ref>PMID:12690580</ref> Defects in GARS are a cause of distal hereditary motor neuronopathy type 5A (HMN5A) [MIM:[http://omim.org/entry/600794 600794]]; also known as distal hereditary motor neuropathy type V (DSMAV). A disorder characterized by distal muscular atrophy mainly affecting the upper extremities, in contrast to other distal motor neuronopathies. These constitute a heterogeneous group of neuromuscular diseases caused by selective degeneration of motor neurons in the anterior horn of the spinal cord, without sensory deficit in the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss. The disease starts with weakness and wasting of distal muscles of the anterior tibial and peroneal compartments of the legs. Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs.<ref>PMID:12690580</ref>		[[http://www.uniprot.org/uniprot/SYG_HUMAN SYG_HUMAN]] Defects in GARS are the cause of Charcot-Marie-Tooth disease type 2D (CMT2D) [MIM:[http://omim.org/entry/601472 601472]]. CMT2D is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT2 group are characterized by signs of axonal regeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. CMT2D is characterized by a more severe phenotype in the upper extremities (severe weakness and atrophy, absence of tendon reflexes) than in the lower limbs. CMT2D inheritance is autosomal dominant.<ref>PMID:12690580</ref> Defects in GARS are a cause of distal hereditary motor neuronopathy type 5A (HMN5A) [MIM:[http://omim.org/entry/600794 600794]]; also known as distal hereditary motor neuropathy type V (DSMAV). A disorder characterized by distal muscular atrophy mainly affecting the upper extremities, in contrast to other distal motor neuronopathies. These constitute a heterogeneous group of neuromuscular diseases caused by selective degeneration of motor neurons in the anterior horn of the spinal cord, without sensory deficit in the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss. The disease starts with weakness and wasting of distal muscles of the anterior tibial and peroneal compartments of the legs. Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs.<ref>PMID:12690580</ref>
Line 17:		Line 17:
	</StructureSection>		</StructureSection>
	[[Category: Glycine--tRNA ligase]]		[[Category: Glycine--tRNA ligase]]
-	[[Category: Hao, Z.]]	+	[[Category: Hao, Z]]
-	[[Category: Qin, X.]]	+	[[Category: Qin, X]]
-	[[Category: Tian, Q.]]	+	[[Category: Tian, Q]]
-	[[Category: Xie, W.]]	+	[[Category: Xie, W]]
-	[[Category: Zhang, Z.]]	+	[[Category: Zhang, Z]]
-	[[Category: Zhou, C.]]	+	[[Category: Zhou, C]]
	[[Category: Aminoacylation]]		[[Category: Aminoacylation]]
	[[Category: Ligase]]		[[Category: Ligase]]
	[[Category: Rossmann fold]]		[[Category: Rossmann fold]]
	[[Category: Trna-gly]]		[[Category: Trna-gly]]

OCA at 09:19, 21 May 2014

OCA — Wed, 21 May 2014 09:19:00 GMT

←Older revision		Revision as of 09:19, 21 May 2014
Line 1:		Line 1:
-	'''~~Unreleased~~ structure'''	+	==Complex structure reveals multiple conformations of glycyl-tRNA synthetase in glycylation==
-		+	<StructureSection load='4kqe' size='340' side='right' caption='[[4kqe]], [[Resolution\|resolution]] 2.74Å' scene=''>
-	~~The~~ entry ~~4kqe~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[4kqe]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4KQE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4KQE FirstGlance]. <br>
-	~~Authors~~: ~~Qin, X~~., Hao, Z., Tian, Q., Zhang, Z., Zhou, C.~~, Xie, W.~~	+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene><br>
-		+	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4kr2\|4kr2]], [[4kr3\|4kr3]]</td></tr>
-	~~Description~~: ~~Complex structure reveals multiple conformations of glycyl~~-~~tRNA synthetase in glycylation~~	+	<tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=6.1.1.14 6.1.1.14] </span></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=4kqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kqe OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4kqe RCSB], [http://www.ebi.ac.uk/pdbsum/4kqe PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/SYG_HUMAN SYG_HUMAN]] Defects in GARS are the cause of Charcot-Marie-Tooth disease type 2D (CMT2D) [MIM:[http://omim.org/entry/601472 601472]]. CMT2D is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT2 group are characterized by signs of axonal regeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. CMT2D is characterized by a more severe phenotype in the upper extremities (severe weakness and atrophy, absence of tendon reflexes) than in the lower limbs. CMT2D inheritance is autosomal dominant.<ref>PMID:12690580</ref> Defects in GARS are a cause of distal hereditary motor neuronopathy type 5A (HMN5A) [MIM:[http://omim.org/entry/600794 600794]]; also known as distal hereditary motor neuropathy type V (DSMAV). A disorder characterized by distal muscular atrophy mainly affecting the upper extremities, in contrast to other distal motor neuronopathies. These constitute a heterogeneous group of neuromuscular diseases caused by selective degeneration of motor neurons in the anterior horn of the spinal cord, without sensory deficit in the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss. The disease starts with weakness and wasting of distal muscles of the anterior tibial and peroneal compartments of the legs. Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs.<ref>PMID:12690580</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/SYG_HUMAN SYG_HUMAN]] Catalyzes the attachment of glycine to tRNA(Gly). Is also able produce diadenosine tetraphosphate (Ap4A), a universal pleiotropic signaling molecule needed for cell regulation pathways, by direct condensation of 2 ATPs.<ref>PMID:19710017</ref>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Glycine--tRNA ligase]]
		+	[[Category: Hao, Z.]]
		+	[[Category: Qin, X.]]
		+	[[Category: Tian, Q.]]
		+	[[Category: Xie, W.]]
		+	[[Category: Zhang, Z.]]
		+	[[Category: Zhou, C.]]
		+	[[Category: Aminoacylation]]
		+	[[Category: Ligase]]
		+	[[Category: Rossmann fold]]
		+	[[Category: Trna-gly]]

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

OCA — Wed, 19 Jun 2013 11:54:14 GMT

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

←Older revision

Revision as of 11:54, 19 June 2013

OCA: New page: '''Unreleased structure''' The entry 4kqe is ON HOLD until Paper Publication Authors: Qin, X., Hao, Z., Tian, Q., Zhang, Z., Zhou, C., Xie, W. Description: Complex structure reveals mu...

OCA — Wed, 19 Jun 2013 11:54:13 GMT

New page: '''Unreleased structure''' The entry 4kqe is ON HOLD until Paper Publication Authors: Qin, X., Hao, Z., Tian, Q., Zhang, Z., Zhou, C., Xie, W. Description: Complex structure reveals mu...

New page

'''Unreleased structure'''

The entry 4kqe is ON HOLD until Paper Publication

Authors: Qin, X., Hao, Z., Tian, Q., Zhang, Z., Zhou, C., Xie, W.

Description: Complex structure reveals multiple conformations of glycyl-tRNA synthetase in glycylation