2zt7 - Revision history

OCA at 13:53, 1 November 2023

OCA — Wed, 01 Nov 2023 13:53:59 GMT

←Older revision		Revision as of 13:53, 1 November 2023
Line 3:		Line 3:
	<StructureSection load='2zt7' size='340' side='right'caption='[[2zt7]], [[Resolution\|resolution]] 2.70Å' scene=''>		<StructureSection load='2zt7' size='340' side='right'caption='[[2zt7]], [[Resolution\|resolution]] 2.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2zt7]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2zt7]] 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=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=ATP:ADENOSINE~~-~~5-TRIPHOSPHATE'>ATP</scene>~~, ~~<scene name='pdbligand=GLY:GLYCINE'>GLY</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]] 2.7Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>~~[[~~Related_structure~~\|~~Related:~~]]~~</b></td><td class="sblockDat"><div style='overflow: auto~~; ~~max-height: 3em;'>[[2pme\|2pme]], [[2pmf\|2pmf]], [[2zt5\|2zt5]], [[2zt6\|2zt6]], [[2zt8\|2zt8]]</div>~~</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene></td></tr>
-	<tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat"~~>GARS ([https://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~~'>~~[https://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [https://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'>[https://proteopedia.org/fgij/fg.htm?mol=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [https://pdbe.org/2zt7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [https://www.ebi.ac.uk/pdbsum/2zt7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2zt7 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=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [https://pdbe.org/2zt7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [https://www.ebi.ac.uk/pdbsum/2zt7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2zt7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/~~SYG_HUMAN SYG_HUMAN~~]~~] Defects in GARS are the cause of~~ Charcot-Marie-Tooth disease type 2D (CMT2D) [MIM:[https://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:[https://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 ==
-	[[https://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>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Glycine--tRNA ligase]]~~	+	[[Category: Homo sapiens]]
-	~~[[Category: Human~~]]	+
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Guo~~, R T~~]]	+	[[Category: Guo RT]]
-	[[Category: Schimmel, P]]	+	[[Category: Schimmel P]]
-	[[Category: Yang~~, X L]]~~	+	[[Category: Yang XL]]
-	~~[[Category: Aminoacyl-trna synthetase]]~~	+
-	~~[[Category: Ap4a]]~~	+
-	~~[[Category: Atp]]~~	+
-	~~[[Category: Atp-binding]]~~	+
-	~~[[Category: Charcot-marie-tooth disease]]~~	+
-	~~[[Category: Disease mutation]]~~	+
-	~~[[Category: Gly-amp]]~~	+
-	~~[[Category: Glycine]]~~	+
-	~~[[Category: Ligase]]~~	+
-	~~[[Category: Nucleotide-binding]]~~	+
-	~~[[Category: Phosphoprotein]]~~	+
-	~~[[Category: Protein biosynthesis]]~~	+
-	~~[[Category: Trna~~]]	+

OCA at 17:37, 15 December 2021

OCA — Wed, 15 Dec 2021 17:37:24 GMT

←Older revision		Revision as of 17:37, 15 December 2021
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	==Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP==		==Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP==
-	<StructureSection load='2zt7' size='340' side='right' caption='[[2zt7]], [[Resolution\|resolution]] 2.70Å' scene=''>	+	<StructureSection load='2zt7' size='340' side='right'caption='[[2zt7]], [[Resolution\|resolution]] 2.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2zt7]] 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=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2zt7]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2pme\|2pme]], [[2pmf\|2pmf]], [[2zt5\|2zt5]], [[2zt6\|2zt6]], [[2zt8\|2zt8]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2pme\|2pme]], [[2pmf\|2pmf]], [[2zt5\|2zt5]], [[2zt6\|2zt6]], [[2zt8\|2zt8]]</div></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='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GARS ([https://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'>[https://en.wikipedia.org/wiki/Glycine--tRNA_ligase Glycine--tRNA ligase], with EC number [https://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=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [~~http~~://pdbe.org/2zt7 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2zt7 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2zt7 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=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [https://pdbe.org/2zt7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [https://www.ebi.ac.uk/pdbsum/2zt7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2zt7 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/SYG_HUMAN SYG_HUMAN]] Defects in GARS are the cause of Charcot-Marie-Tooth disease type 2D (CMT2D) [MIM:[https://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:[https://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 ==		== 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/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>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 26:		Line 26:

	==See Also==		==See Also==
-	*[[Aminoacyl tRNA ~~Synthetase~~\|Aminoacyl tRNA ~~Synthetase~~]]	+	*[[Aminoacyl tRNA synthetase 3D structures\|Aminoacyl tRNA synthetase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 33:		Line 33:
	[[Category: Glycine--tRNA ligase]]		[[Category: Glycine--tRNA ligase]]
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Guo, R T]]		[[Category: Guo, R T]]
	[[Category: Schimmel, P]]		[[Category: Schimmel, P]]

OCA at 07:13, 18 October 2018

OCA — Thu, 18 Oct 2018 07:13:04 GMT

←Older revision		Revision as of 07:13, 18 October 2018
Line 18:		Line 18:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/zt/2zt7_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/zt/2zt7_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 38:		Line 38:
	[[Category: Aminoacyl-trna synthetase]]		[[Category: Aminoacyl-trna synthetase]]
	[[Category: Ap4a]]		[[Category: Ap4a]]
		+	[[Category: Atp]]
	[[Category: Atp-binding]]		[[Category: Atp-binding]]
	[[Category: Charcot-marie-tooth disease]]		[[Category: Charcot-marie-tooth disease]]

OCA at 09:24, 11 August 2016

OCA — Thu, 11 Aug 2016 09:24:45 GMT

←Older revision		Revision as of 09:24, 11 August 2016
Line 1:		Line 1:
		+
	==Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP==		==Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP==
	<StructureSection load='2zt7' size='340' side='right' caption='[[2zt7]], [[Resolution\|resolution]] 2.70Å' scene=''>		<StructureSection load='2zt7' size='340' side='right' caption='[[2zt7]], [[Resolution\|resolution]] 2.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2zt7]] 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=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2zt7]] 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=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2pme\|2pme]], [[2pmf\|2pmf]], [[2zt5\|2zt5]], [[2zt6\|2zt6]], [[2zt8\|2zt8]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2pme\|2pme]], [[2pmf\|2pmf]], [[2zt5\|2zt5]], [[2zt6\|2zt6]], [[2zt8\|2zt8]]</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 ~~Homo sapiens~~])</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=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [http://www.ebi.ac.uk/pdbsum/2zt7 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=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [http://pdbe.org/2zt7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [http://www.ebi.ac.uk/pdbsum/2zt7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2zt7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 21:		Line 22:
	<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=2zt7 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>

Line 31:		Line 32:
	</StructureSection>		</StructureSection>
	[[Category: Glycine--tRNA ligase]]		[[Category: Glycine--tRNA ligase]]
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Guo, R T]]		[[Category: Guo, R T]]
	[[Category: Schimmel, P]]		[[Category: Schimmel, P]]

OCA at 10:26, 20 January 2015

OCA — Tue, 20 Jan 2015 10:26:46 GMT

←Older revision		Revision as of 10:26, 20 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2zt7]] 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=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2zt7]] 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=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2pme\|2pme]], [[2pmf\|2pmf]], [[2zt5\|2zt5]], [[2zt6\|2zt6]], [[2zt8\|2zt8]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2pme\|2pme]], [[2pmf\|2pmf]], [[2zt5\|2zt5]], [[2zt6\|2zt6]], [[2zt8\|2zt8]]</td></tr>
-	<tr><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 Homo sapiens])</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 Homo sapiens])</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=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [http://www.ebi.ac.uk/pdbsum/2zt7 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=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [http://www.ebi.ac.uk/pdbsum/2zt7 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 32:		Line 32:
	[[Category: Glycine--tRNA ligase]]		[[Category: Glycine--tRNA ligase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Guo, R T.]]	+	[[Category: Guo, R T]]
-	[[Category: Schimmel, P.]]	+	[[Category: Schimmel, P]]
-	[[Category: Yang, X L.]]	+	[[Category: Yang, X L]]
	[[Category: Aminoacyl-trna synthetase]]		[[Category: Aminoacyl-trna synthetase]]
	[[Category: Ap4a]]		[[Category: Ap4a]]

OCA at 04:57, 2 October 2014

OCA — Thu, 02 Oct 2014 04:57:42 GMT

←Older revision		Revision as of 04:57, 2 October 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2zt7\| PDB=2zt7 \| SCENE= }}~~	+	==Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP==
-	===Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP===	+	<StructureSection load='2zt7' size='340' side='right' caption='[[2zt7]], [[Resolution\|resolution]] 2.70Å' scene=''>
-	~~{{ABSTRACT_PUBMED_019710017}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[2zt7]] 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=2ZT7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2ZT7 FirstGlance]. <br>
-	==Disease==	+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene><br>
-	[[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>	+	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2pme\|2pme]], [[2pmf\|2pmf]], [[2zt5\|2zt5]], [[2zt6\|2zt6]], [[2zt8\|2zt8]]</td></tr>
-		+	<tr><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 Homo sapiens])</td></tr>
-	==Function==	+	<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>
-	[[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>	+	<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=2zt7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2zt7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2zt7 RCSB], [http://www.ebi.ac.uk/pdbsum/2zt7 PDBsum]</span></td></tr>
-		+	<table>
-	==~~About this Structure~~==	+	== Disease ==
-	[[~~2zt7~~]] ~~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=~~2ZT7 OCA~~].	+	[[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>
		+	== 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/zt/2zt7_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>

	==See Also==		==See Also==
	*[[Aminoacyl tRNA Synthetase\|Aminoacyl tRNA Synthetase]]		*[[Aminoacyl tRNA Synthetase\|Aminoacyl tRNA Synthetase]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:019710017</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Glycine--tRNA ligase]]		[[Category: Glycine--tRNA ligase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]

OCA at 16:19, 24 March 2013

OCA — Sun, 24 Mar 2013 16:19:45 GMT

←Older revision		Revision as of 16:19, 24 March 2013
Line 1:		Line 1:
-	[[Image:2zt7.png\|left\|200px]]
-
	{{STRUCTURE_2zt7\| PDB=2zt7 \| SCENE= }}		{{STRUCTURE_2zt7\| PDB=2zt7 \| SCENE= }}
-
	===Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP===		===Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP===
		+	{{ABSTRACT_PUBMED_019710017}}

-	~~{{ABSTRACT_PUBMED_019710017}}~~	+	==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>

	==About this Structure==		==About this Structure==
Line 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:019710017</ref><references group="xtra"/>	+	<ref group="xtra">PMID:019710017</ref><references group="xtra"/><references/>
	[[Category: Glycine--tRNA ligase]]		[[Category: Glycine--tRNA ligase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]

OCA at 18:48, 20 October 2012

OCA — Sat, 20 Oct 2012 18:48:34 GMT

←Older revision		Revision as of 18:48, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[2zt7]] is a 1 chain structure ~~of [[Aminoacyl tRNA Synthetase]]~~ 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=2ZT7 OCA].	+	[[2zt7]] 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=2ZT7 OCA].

	==See Also==		==See Also==

OCA: Protected "2zt7" [edit=sysop:move=sysop]

OCA — Fri, 27 Jul 2012 05:18:36 GMT

Protected "2zt7" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:18, 27 July 2012

OCA at 05:18, 27 July 2012

OCA — Fri, 27 Jul 2012 05:18:35 GMT

←Older revision		Revision as of 05:18, 27 July 2012
Line 1:		Line 1:
-	{{Seed}}
	[[Image:2zt7.png\|left\|200px]]		[[Image:2zt7.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_2zt7", 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_2zt7\| PDB=2zt7 \| SCENE= }}		{{STRUCTURE_2zt7\| PDB=2zt7 \| SCENE= }}

	===Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP===		===Crystal structure of human Glycyl-tRNA synthetase (GlyRS) in complex with Glycine and ATP===

-		+	{{ABSTRACT_PUBMED_019710017}}
-	~~==Disease==~~	+
-	Known disease associated with this structure: Charcot-Marie-Tooth disease, type 2D OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600287 600287]], Neuropathy, distal hereditary motor, type V OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600287 600287]]	+

	==About this Structure==		==About this Structure==
-	~~2ZT7~~ 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=2ZT7 OCA].	+	[[2zt7]] is a 1 chain structure of [[Aminoacyl tRNA Synthetase]] 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=2ZT7 OCA].
		+
		+	==See Also==
		+	*[[Aminoacyl tRNA Synthetase\|Aminoacyl tRNA Synthetase]]
		+
		+	==Reference==
		+	<ref group="xtra">PMID:019710017</ref><references group="xtra"/>
	[[Category: Glycine--tRNA ligase]]		[[Category: Glycine--tRNA ligase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
Line 25:		Line 22:
	[[Category: Aminoacyl-trna synthetase]]		[[Category: Aminoacyl-trna synthetase]]
	[[Category: Ap4a]]		[[Category: Ap4a]]
-	[[Category: Atp]]
	[[Category: Atp-binding]]		[[Category: Atp-binding]]
	[[Category: Charcot-marie-tooth disease]]		[[Category: Charcot-marie-tooth disease]]
Line 36:		Line 32:
	[[Category: Protein biosynthesis]]		[[Category: Protein biosynthesis]]
	[[Category: Trna]]		[[Category: Trna]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Mon Sep 21 16:41:53 2009''