3ktr - Revision history

OCA at 08:22, 6 September 2023

2023-09-06T08:22:55Z

←Older revision		Revision as of 08:22, 6 September 2023
Line 1:		Line 1:

	==Structural basis of ataxin-2 recognition by poly(A)-binding protein==		==Structural basis of ataxin-2 recognition by poly(A)-binding protein==
-	<StructureSection load='3ktr' size='340' side='right' caption='[[3ktr]], [[Resolution\|resolution]] 1.70Å' scene=''>	+	<StructureSection load='3ktr' size='340' side='right'caption='[[3ktr]], [[Resolution\|resolution]] 1.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3ktr]] is a 2 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KTR OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3KTR FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3ktr]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KTR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3KTR FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat"~~><scene name~~=~~'pdbligand=CD:CADMIUM+ION'>CD</scene~~>, ~~<scene name='pdbligand=SO4:SULFATE+ION'>SO4</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]] 1.7Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat">~~[[3ktp\|3ktp]]~~<~~/td~~></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CD:CADMIUM+ION'>CD</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	<~~tr id~~='~~gene'><td class~~=~~"sblockLbl"><b>[[Gene\|Gene~~:~~]]</b~~></td>~~<td class="sblockDat">PABPC1, PAB1, PABP1, PABPC2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])~~</td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3ktr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ktr OCA], [https://pdbe.org/3ktr PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3ktr RCSB], [https://www.ebi.ac.uk/pdbsum/3ktr PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3ktr ProSAT]</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=3ktr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ktr OCA], [~~http~~://pdbe.org/3ktr PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3ktr RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3ktr PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3ktr ProSAT]</span></td></tr>	+
	</table>		</table>
-	== Disease ==
-	[[http://www.uniprot.org/uniprot/ATX2_HUMAN ATX2_HUMAN]] Amyotrophic lateral sclerosis;Spinocerebellar ataxia type 2. Defects in ATXN2 are the cause of spinocerebellar ataxia type 2 (SCA2) [MIM:[http://omim.org/entry/183090 183090]]; also known as olivopontocerebellar atrophy II (OPCA II or OPCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to cerebellum degeneration with variable involvement of the brainstem and spinal cord. SCA2 belongs to the autosomal dominant cerebellar ataxias type I (ADCA I) which are characterized by cerebellar ataxia in combination with additional clinical features like optic atrophy, ophthalmoplegia, bulbar and extrapyramidal signs, peripheral neuropathy and dementia. SCA2 is characterized by hyporeflexia, myoclonus and action tremor and dopamine-responsive parkinsonism. Note=SCA2 is caused by expansion of a CAG repeat resulting in about 36 to 52 repeats in some patients. Longer expansions result in earlier the expansion, onset of the disease.<ref>PMID:8896555</ref> <ref>PMID:8896556</ref> <ref>PMID:8896557</ref> Defects in ATXN2 are a cause of susceptibility to amyotrophic lateral sclerosis type 13 (ALS13) [MIM:[http://omim.org/entry/183090 183090]]. It is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Note=An increased risk for developing amyotrophic lateral sclerosis is seems to be conferred by CAG repeat intermediate expansions greater than 23 but below the threshold for developing spinocerebellar ataxia.<ref>PMID:20740007</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/PABP1_HUMAN PABP1_HUMAN]] Binds the poly(A) tail of mRNA. May be involved in cytoplasmic regulatory processes of mRNA metabolism such as pre-mRNA splicing. Its function in translational initiation regulation can either be enhanced by PAIP1 or repressed by PAIP2. Can probably bind to cytoplasmic RNA sequences other than poly(A) in vivo. Involved in translationally coupled mRNA turnover. Implicated with other RNA-binding proteins in the cytoplasmic deadenylation/translational and decay interplay of the FOS mRNA mediated by the major coding-region determinant of instability (mCRD) domain. Involved in regulation of nonsense-mediated decay (NMD) of mRNAs containing premature stop codons; for the recognition of premature termination codons (PTC) and initiation of NMD a competitive interaction between UPF1 and PABPC1 with the ribosome-bound release factors is proposed.<ref>PMID:11051545</ref> <ref>PMID:18447585</ref> ~~[[http://www.uniprot.org/uniprot/ATX2_HUMAN ATX2_HUMAN]] Involved in EGFR trafficking, acting as negative regulator of endocytic EGFR internalization at the plasma membrane.<ref>PMID:18602463</ref>~~	+	[https://www.uniprot.org/uniprot/PABP1_HUMAN PABP1_HUMAN] Binds the poly(A) tail of mRNA. May be involved in cytoplasmic regulatory processes of mRNA metabolism such as pre-mRNA splicing. Its function in translational initiation regulation can either be enhanced by PAIP1 or repressed by PAIP2. Can probably bind to cytoplasmic RNA sequences other than poly(A) in vivo. Involved in translationally coupled mRNA turnover. Implicated with other RNA-binding proteins in the cytoplasmic deadenylation/translational and decay interplay of the FOS mRNA mediated by the major coding-region determinant of instability (mCRD) domain. Involved in regulation of nonsense-mediated decay (NMD) of mRNAs containing premature stop codons; for the recognition of premature termination codons (PTC) and initiation of NMD a competitive interaction between UPF1 and PABPC1 with the ribosome-bound release factors is proposed.<ref>PMID:11051545</ref> <ref>PMID:18447585</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: ~~Human~~]]	+	[[Category: Homo sapiens]]
-	[[Category: ~~Gehring, K~~]]	+	[[Category: Large Structures]]
-	[[Category: ~~Kozlov, G~~]]	+	[[Category: Gehring K]]
-	[[Category: ~~Acetylation]]~~	+	[[Category: Kozlov G]]
-	~~[[Category: Alternative splicing]]~~	+
-	~~[[Category: Cytoplasm]]~~	+
-	~~[[Category: Methylation]]~~	+
-	~~[[Category: Mrna processing]]~~	+
-	~~[[Category: Mrna splicing]]~~	+
-	~~[[Category: Neurodegeneration]]~~	+
-	~~[[Category: Nucleus]]~~	+
-	~~[[Category: Parkinsonism]]~~	+
-	~~[[Category: Phosphoprotein]]~~	+
-	~~[[Category: Polymorphism]]~~	+
-	~~[[Category: Protein binding]]~~	+
-	~~[[Category: Protein-protein complex]]~~	+
-	~~[[Category: Rna-binding]]~~	+
-	~~[[Category: Spinocerebellar ataxia]]~~	+
-	~~[[Category: Spliceosome]]~~	+
-	~~[[Category: Triplet repeat expansion~~]]	+

OCA at 06:59, 2 January 2019

2019-01-02T06:59:44Z

←Older revision		Revision as of 06:59, 2 January 2019
Line 1:		Line 1:
		+
	==Structural basis of ataxin-2 recognition by poly(A)-binding protein==		==Structural basis of ataxin-2 recognition by poly(A)-binding protein==
	<StructureSection load='3ktr' size='340' side='right' caption='[[3ktr]], [[Resolution\|resolution]] 1.70Å' scene=''>		<StructureSection load='3ktr' size='340' side='right' caption='[[3ktr]], [[Resolution\|resolution]] 1.70Å' scene=''>
Line 6:		Line 7:
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3ktp\|3ktp]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3ktp\|3ktp]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PABPC1, PAB1, PABP1, PABPC2 ([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">PABPC1, PAB1, PABP1, PABPC2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3ktr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ktr OCA], [http://pdbe.org/3ktr PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3ktr RCSB], [http://www.ebi.ac.uk/pdbsum/3ktr 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=3ktr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ktr OCA], [http://pdbe.org/3ktr PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3ktr RCSB], [http://www.ebi.ac.uk/pdbsum/3ktr PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3ktr ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 16:		Line 17:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/kt/3ktr_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/kt/3ktr_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 39:
	[[Category: Gehring, K]]		[[Category: Gehring, K]]
	[[Category: Kozlov, G]]		[[Category: Kozlov, G]]
		+	[[Category: Acetylation]]
		+	[[Category: Alternative splicing]]
		+	[[Category: Cytoplasm]]
	[[Category: Methylation]]		[[Category: Methylation]]
	[[Category: Mrna processing]]		[[Category: Mrna processing]]
Line 45:		Line 49:
	[[Category: Parkinsonism]]		[[Category: Parkinsonism]]
	[[Category: Phosphoprotein]]		[[Category: Phosphoprotein]]
		+	[[Category: Polymorphism]]
	[[Category: Protein binding]]		[[Category: Protein binding]]
	[[Category: Protein-protein complex]]		[[Category: Protein-protein complex]]
Line 50:		Line 55:
	[[Category: Spinocerebellar ataxia]]		[[Category: Spinocerebellar ataxia]]
	[[Category: Spliceosome]]		[[Category: Spliceosome]]
		+	[[Category: Triplet repeat expansion]]

OCA at 01:38, 10 February 2016

2016-02-10T01:38:43Z

←Older revision		Revision as of 01:38, 10 February 2016
Line 2:		Line 2:
	<StructureSection load='3ktr' size='340' side='right' caption='[[3ktr]], [[Resolution\|resolution]] 1.70Å' scene=''>		<StructureSection load='3ktr' size='340' side='right' caption='[[3ktr]], [[Resolution\|resolution]] 1.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3ktr]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KTR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3KTR FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3ktr]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KTR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3KTR FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CD:CADMIUM+ION'>CD</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CD:CADMIUM+ION'>CD</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3ktp\|3ktp]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3ktp\|3ktp]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PABPC1, PAB1, PABP1, PABPC2 ([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">PABPC1, PAB1, PABP1, PABPC2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3ktr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ktr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3ktr RCSB], [http://www.ebi.ac.uk/pdbsum/3ktr 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=3ktr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ktr OCA], [http://pdbe.org/3ktr PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3ktr RCSB], [http://www.ebi.ac.uk/pdbsum/3ktr PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 20:
	<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=3ktr ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
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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 3ktr" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Gehring, K]]		[[Category: Gehring, K]]
	[[Category: Kozlov, G]]		[[Category: Kozlov, G]]

OCA at 17:43, 18 December 2014

2014-12-18T17:43:34Z

←Older revision		Revision as of 17:43, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3ktr\| PDB=3ktr \| SCENE= }}~~	+	==Structural basis of ataxin-2 recognition by poly(A)-binding protein==
-	===Structural basis of ataxin-2 recognition by poly(A)-binding protein===	+	<StructureSection load='3ktr' size='340' side='right' caption='[[3ktr]], [[Resolution\|resolution]] 1.70Å' scene=''>
-	~~{{ABSTRACT_PUBMED_20181956}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[3ktr]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KTR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3KTR FirstGlance]. <br>
-	==Disease==	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CD:CADMIUM+ION'>CD</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3ktp\|3ktp]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PABPC1, PAB1, PABP1, PABPC2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=3ktr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ktr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3ktr RCSB], [http://www.ebi.ac.uk/pdbsum/3ktr PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
	[[http://www.uniprot.org/uniprot/ATX2_HUMAN ATX2_HUMAN]] Amyotrophic lateral sclerosis;Spinocerebellar ataxia type 2. Defects in ATXN2 are the cause of spinocerebellar ataxia type 2 (SCA2) [MIM:[http://omim.org/entry/183090 183090]]; also known as olivopontocerebellar atrophy II (OPCA II or OPCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to cerebellum degeneration with variable involvement of the brainstem and spinal cord. SCA2 belongs to the autosomal dominant cerebellar ataxias type I (ADCA I) which are characterized by cerebellar ataxia in combination with additional clinical features like optic atrophy, ophthalmoplegia, bulbar and extrapyramidal signs, peripheral neuropathy and dementia. SCA2 is characterized by hyporeflexia, myoclonus and action tremor and dopamine-responsive parkinsonism. Note=SCA2 is caused by expansion of a CAG repeat resulting in about 36 to 52 repeats in some patients. Longer expansions result in earlier the expansion, onset of the disease.<ref>PMID:8896555</ref> <ref>PMID:8896556</ref> <ref>PMID:8896557</ref> Defects in ATXN2 are a cause of susceptibility to amyotrophic lateral sclerosis type 13 (ALS13) [MIM:[http://omim.org/entry/183090 183090]]. It is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Note=An increased risk for developing amyotrophic lateral sclerosis is seems to be conferred by CAG repeat intermediate expansions greater than 23 but below the threshold for developing spinocerebellar ataxia.<ref>PMID:20740007</ref>		[[http://www.uniprot.org/uniprot/ATX2_HUMAN ATX2_HUMAN]] Amyotrophic lateral sclerosis;Spinocerebellar ataxia type 2. Defects in ATXN2 are the cause of spinocerebellar ataxia type 2 (SCA2) [MIM:[http://omim.org/entry/183090 183090]]; also known as olivopontocerebellar atrophy II (OPCA II or OPCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to cerebellum degeneration with variable involvement of the brainstem and spinal cord. SCA2 belongs to the autosomal dominant cerebellar ataxias type I (ADCA I) which are characterized by cerebellar ataxia in combination with additional clinical features like optic atrophy, ophthalmoplegia, bulbar and extrapyramidal signs, peripheral neuropathy and dementia. SCA2 is characterized by hyporeflexia, myoclonus and action tremor and dopamine-responsive parkinsonism. Note=SCA2 is caused by expansion of a CAG repeat resulting in about 36 to 52 repeats in some patients. Longer expansions result in earlier the expansion, onset of the disease.<ref>PMID:8896555</ref> <ref>PMID:8896556</ref> <ref>PMID:8896557</ref> Defects in ATXN2 are a cause of susceptibility to amyotrophic lateral sclerosis type 13 (ALS13) [MIM:[http://omim.org/entry/183090 183090]]. It is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Note=An increased risk for developing amyotrophic lateral sclerosis is seems to be conferred by CAG repeat intermediate expansions greater than 23 but below the threshold for developing spinocerebellar ataxia.<ref>PMID:20740007</ref>
-		+	== Function ==
-	==Function==	+
	[[http://www.uniprot.org/uniprot/PABP1_HUMAN PABP1_HUMAN]] Binds the poly(A) tail of mRNA. May be involved in cytoplasmic regulatory processes of mRNA metabolism such as pre-mRNA splicing. Its function in translational initiation regulation can either be enhanced by PAIP1 or repressed by PAIP2. Can probably bind to cytoplasmic RNA sequences other than poly(A) in vivo. Involved in translationally coupled mRNA turnover. Implicated with other RNA-binding proteins in the cytoplasmic deadenylation/translational and decay interplay of the FOS mRNA mediated by the major coding-region determinant of instability (mCRD) domain. Involved in regulation of nonsense-mediated decay (NMD) of mRNAs containing premature stop codons; for the recognition of premature termination codons (PTC) and initiation of NMD a competitive interaction between UPF1 and PABPC1 with the ribosome-bound release factors is proposed.<ref>PMID:11051545</ref> <ref>PMID:18447585</ref> [[http://www.uniprot.org/uniprot/ATX2_HUMAN ATX2_HUMAN]] Involved in EGFR trafficking, acting as negative regulator of endocytic EGFR internalization at the plasma membrane.<ref>PMID:18602463</ref>		[[http://www.uniprot.org/uniprot/PABP1_HUMAN PABP1_HUMAN]] Binds the poly(A) tail of mRNA. May be involved in cytoplasmic regulatory processes of mRNA metabolism such as pre-mRNA splicing. Its function in translational initiation regulation can either be enhanced by PAIP1 or repressed by PAIP2. Can probably bind to cytoplasmic RNA sequences other than poly(A) in vivo. Involved in translationally coupled mRNA turnover. Implicated with other RNA-binding proteins in the cytoplasmic deadenylation/translational and decay interplay of the FOS mRNA mediated by the major coding-region determinant of instability (mCRD) domain. Involved in regulation of nonsense-mediated decay (NMD) of mRNAs containing premature stop codons; for the recognition of premature termination codons (PTC) and initiation of NMD a competitive interaction between UPF1 and PABPC1 with the ribosome-bound release factors is proposed.<ref>PMID:11051545</ref> <ref>PMID:18447585</ref> [[http://www.uniprot.org/uniprot/ATX2_HUMAN ATX2_HUMAN]] Involved in EGFR trafficking, acting as negative regulator of endocytic EGFR internalization at the plasma membrane.<ref>PMID:18602463</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/kt/3ktr_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 ==
		+	Poly(A)-binding protein (PABPC1) is involved in multiple aspects of mRNA processing and translation. It is a component of RNA stress granules and binds the RNA-induced silencing complex to promote degradation of silenced mRNAs. Here, we report the crystal structures of the C-terminal Mlle (or PABC) domain in complex with peptides from GW182 (TNRC6C) and Ataxin-2. The structures reveal overlapping binding sites but with unexpected diversity in the peptide conformation and residues involved in binding. The mutagenesis and binding studies show low to submicromolar binding affinity with overlapping but distinct specificity determinants. These results rationalize the role of the Mlle domain of PABPC1 in microRNA-mediated mRNA deadenylation and suggest a more general function in the assembly of cytoplasmic RNA granules.

-	~~==About this Structure==~~	+	Structural basis of binding of P-body-associated proteins GW182 and ataxin-2 by the Mlle domain of poly(A)-binding protein.,Kozlov G, Safaee N, Rosenauer A, Gehring K J Biol Chem. 2010 Apr 30;285(18):13599-606. Epub 2010 Feb 24. PMID:20181956<ref>PMID:20181956</ref>
-	~~[[3ktr]] is a~~ 2 ~~chain structure with sequence from [http://en~~.~~wikipedia~~.~~org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http~~:~~//oca~~.~~weizmann~~.~~ac.il~~/~~oca-bin/ocashort?id=3KTR OCA].~~	+

-	==~~Reference~~==	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~<ref group="xtra">PMID:020181956</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	</div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Gehring, K.]]	+	[[Category: Gehring, K]]
-	[[Category: Kozlov, G.]]	+	[[Category: Kozlov, G]]
	[[Category: Methylation]]		[[Category: Methylation]]
	[[Category: Mrna processing]]		[[Category: Mrna processing]]

OCA: Protected "3ktr" [edit=sysop:move=sysop]

2013-04-04T19:59:49Z

Protected "3ktr" [edit=sysop:move=sysop]

←Older revision

Revision as of 19:59, 4 April 2013

OCA at 19:59, 4 April 2013

2013-04-04T19:59:44Z

←Older revision		Revision as of 19:59, 4 April 2013
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-	{{Seed}}
-	[[Image:3ktr.png\|left\|200px]]
-
-	<!--
-	The line below this paragraph, containing "STRUCTURE_3ktr", 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_3ktr\| PDB=3ktr \| SCENE= }}		{{STRUCTURE_3ktr\| PDB=3ktr \| SCENE= }}
-
	===Structural basis of ataxin-2 recognition by poly(A)-binding protein===		===Structural basis of ataxin-2 recognition by poly(A)-binding protein===
		+	{{ABSTRACT_PUBMED_20181956}}

		+	==Disease==
		+	[[http://www.uniprot.org/uniprot/ATX2_HUMAN ATX2_HUMAN]] Amyotrophic lateral sclerosis;Spinocerebellar ataxia type 2. Defects in ATXN2 are the cause of spinocerebellar ataxia type 2 (SCA2) [MIM:[http://omim.org/entry/183090 183090]]; also known as olivopontocerebellar atrophy II (OPCA II or OPCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to cerebellum degeneration with variable involvement of the brainstem and spinal cord. SCA2 belongs to the autosomal dominant cerebellar ataxias type I (ADCA I) which are characterized by cerebellar ataxia in combination with additional clinical features like optic atrophy, ophthalmoplegia, bulbar and extrapyramidal signs, peripheral neuropathy and dementia. SCA2 is characterized by hyporeflexia, myoclonus and action tremor and dopamine-responsive parkinsonism. Note=SCA2 is caused by expansion of a CAG repeat resulting in about 36 to 52 repeats in some patients. Longer expansions result in earlier the expansion, onset of the disease.<ref>PMID:8896555</ref> <ref>PMID:8896556</ref> <ref>PMID:8896557</ref> Defects in ATXN2 are a cause of susceptibility to amyotrophic lateral sclerosis type 13 (ALS13) [MIM:[http://omim.org/entry/183090 183090]]. It is a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Note=An increased risk for developing amyotrophic lateral sclerosis is seems to be conferred by CAG repeat intermediate expansions greater than 23 but below the threshold for developing spinocerebellar ataxia.<ref>PMID:20740007</ref>

-	~~<!--~~	+	==Function==
-	~~The line below this paragraph, {{ABSTRACT_PUBMED_20181956}}, adds~~ the ~~Publication Abstract~~ to the ~~page~~	+	[[http://www.uniprot.org/uniprot/PABP1_HUMAN PABP1_HUMAN]] Binds the poly(A) tail of mRNA. May be involved in cytoplasmic regulatory processes of mRNA metabolism such as pre-mRNA splicing. Its function in translational initiation regulation can either be enhanced by PAIP1 or repressed by PAIP2. Can probably bind to cytoplasmic RNA sequences other than poly(A) in vivo. Involved in translationally coupled mRNA turnover. Implicated with other RNA-binding proteins in the cytoplasmic deadenylation/translational and decay interplay of the FOS mRNA mediated by the major coding-region determinant of instability (mCRD) domain. Involved in regulation of nonsense-mediated decay (NMD) of mRNAs containing premature stop codons; for the recognition of premature termination codons (PTC) and initiation of NMD a competitive interaction between UPF1 and PABPC1 with the ribosome-bound release factors is proposed.<ref>PMID:11051545</ref> <ref>PMID:18447585</ref> [[http://www.uniprot.org/uniprot/ATX2_HUMAN ATX2_HUMAN]] Involved in EGFR trafficking, acting as negative regulator of endocytic EGFR internalization at the plasma membrane.<ref>PMID:18602463</ref>
-	(~~as it appears on PubMed at~~ http://www.~~pubmed~~.~~gov)~~, ~~where 20181956 is~~ the ~~PubMed ID number~~.	+
-	-->	+
-	~~{{ABSTRACT_PUBMED_20181956}}~~	+

	==About this Structure==		==About this Structure==
-	~~3KTR~~ is a 2 ~~chains~~ structure with ~~sequences~~ 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=3KTR OCA].	+	[[3ktr]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KTR OCA].

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~20181956~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020181956</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Gehring, K.]]		[[Category: Gehring, K.]]
	[[Category: Kozlov, G.]]		[[Category: Kozlov, G.]]
-	[[Category: Acetylation]]
-	[[Category: Alternative splicing]]
-	[[Category: Cytoplasm]]
	[[Category: Methylation]]		[[Category: Methylation]]
	[[Category: Mrna processing]]		[[Category: Mrna processing]]
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	[[Category: Parkinsonism]]		[[Category: Parkinsonism]]
	[[Category: Phosphoprotein]]		[[Category: Phosphoprotein]]
-	[[Category: Polymorphism]]
	[[Category: Protein binding]]		[[Category: Protein binding]]
	[[Category: Protein-protein complex]]		[[Category: Protein-protein complex]]
Line 43:		Line 29:
	[[Category: Spinocerebellar ataxia]]		[[Category: Spinocerebellar ataxia]]
	[[Category: Spliceosome]]		[[Category: Spliceosome]]
-	[[Category: Triplet repeat expansion]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Mar 10 13:41:16 2010''

OCA at 11:41, 10 March 2010

2010-03-10T11:41:17Z

←Older revision		Revision as of 11:41, 10 March 2010
Line 1:		Line 1:
	{{Seed}}		{{Seed}}
-	[[Image:3ktr.~~jpg~~\|left\|200px]]	+	[[Image:3ktr.png\|left\|200px]]

	<!--		<!--
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	===Structural basis of ataxin-2 recognition by poly(A)-binding protein===		===Structural basis of ataxin-2 recognition by poly(A)-binding protein===

		+
		+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_20181956}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 20181956 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_20181956}}

	==About this Structure==		==About this Structure==
	3KTR is a 2 chains structure with sequences 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=3KTR OCA].		3KTR is a 2 chains structure with sequences 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=3KTR OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:20181956</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Gehring, K.]]		[[Category: Gehring, K.]]
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	[[Category: Triplet repeat expansion]]		[[Category: Triplet repeat expansion]]

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on ~~Thu Feb 25 14~~:09:33 2010''	+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Mar 10 13:41:16 2010''

OCA at 12:09, 25 February 2010

2010-02-25T12:09:35Z

←Older revision		Revision as of 12:09, 25 February 2010
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-	~~'''Unreleased structure'''~~	+	{{Seed}}
		+	[[Image:3ktr.jpg\|left\|200px]]

-	The ~~entry 3ktr~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3ktr", 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_3ktr\| PDB=3ktr \| SCENE= }}

-	~~Authors: Kozlov, G., Gehring, K.~~	+	===Structural basis of ataxin-2 recognition by poly(A)-binding protein===

-	Description: Structural basis of ataxin-2 recognition by poly(A)-binding protein

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on ~~Wed Dec 16 12~~:36:~~42 2009~~''	+	==About this Structure==
		+	3KTR is a 2 chains structure with sequences 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=3KTR OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Gehring, K.]]
		+	[[Category: Kozlov, G.]]
		+	[[Category: Acetylation]]
		+	[[Category: Alternative splicing]]
		+	[[Category: Cytoplasm]]
		+	[[Category: Methylation]]
		+	[[Category: Mrna processing]]
		+	[[Category: Mrna splicing]]
		+	[[Category: Neurodegeneration]]
		+	[[Category: Nucleus]]
		+	[[Category: Parkinsonism]]
		+	[[Category: Phosphoprotein]]
		+	[[Category: Polymorphism]]
		+	[[Category: Protein binding]]
		+	[[Category: Protein-protein complex]]
		+	[[Category: Rna-binding]]
		+	[[Category: Spinocerebellar ataxia]]
		+	[[Category: Spliceosome]]
		+	[[Category: Triplet repeat expansion]]
		+
		+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 25 14:09:33 2010''

OCA at 10:36, 16 December 2009

2009-12-16T10:36:43Z

←Older revision		Revision as of 10:36, 16 December 2009
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 3ktr is ON HOLD	+	The entry 3ktr is ON HOLD until Paper Publication

	Authors: Kozlov, G., Gehring, K.		Authors: Kozlov, G., Gehring, K.
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	Description: Structural basis of ataxin-2 recognition by poly(A)-binding protein		Description: Structural basis of ataxin-2 recognition by poly(A)-binding protein

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Dec ~~9 14~~:44:32 2009''	+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Dec 16 12:36:42 2009''

OCA at 12:44, 9 December 2009

2009-12-09T12:44:32Z

←Older revision		Revision as of 12:44, 9 December 2009
Line 3:		Line 3:
	The entry 3ktr is ON HOLD		The entry 3ktr is ON HOLD

-	Authors: Kozlov, G~~., Safaee, N., Rosenauer, A~~., Gehring, K.	+	Authors: Kozlov, G., Gehring, K.

	Description: Structural basis of ataxin-2 recognition by poly(A)-binding protein		Description: Structural basis of ataxin-2 recognition by poly(A)-binding protein

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Dec ~~2 09~~:40:00 2009''	+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Dec 9 14:44:32 2009''