6xyp - Revision history

OCA at 10:20, 22 May 2024

2024-05-22T10:20:18Z

←Older revision		Revision as of 10:20, 22 May 2024
Line 3:		Line 3:
	<SX load='6xyp' size='340' side='right' viewer='molstar' caption='[[6xyp]], [[Resolution\|resolution]] 3.29Å' scene=''>		<SX load='6xyp' size='340' side='right' viewer='molstar' caption='[[6xyp]], [[Resolution\|resolution]] 3.29Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6xyp]] is a 10 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=6XYP OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=6XYP FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6xyp]] is a 10 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=6XYP OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6XYP FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=6xyp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6xyp OCA], [~~http~~://pdbe.org/6xyp PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6xyp RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6xyp PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6xyp ProSAT]</span></td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution\|Resolution]] 3.29Å</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=6xyp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6xyp OCA], [https://pdbe.org/6xyp PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6xyp RCSB], [https://www.ebi.ac.uk/pdbsum/6xyp PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6xyp ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN]] Note=Genetic alterations of SNCA resulting in aberrant polymerization into fibrils, are associated with several neurodegenerative diseases (synucleinopathies). SNCA fibrillar aggregates represent the major non A-beta component of Alzheimer disease amyloid plaque, and a major component of Lewy body inclusions. They are also found within Lewy body (LB)-like intraneuronal inclusions, glial inclusions and axonal spheroids in neurodegeneration with brain iron accumulation type 1. Defects in SNCA are the cause of Parkinson disease type 1 (PARK1) [MIM:[~~http~~://omim.org/entry/168601 168601]]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia. The pathology of Parkinson disease involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins), in surviving neurons in various areas of the brain. The disease is progressive and usually manifests after the age of 50 years, although early-onset cases (before 50 years) are known. The majority of the cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, some patients present with a positive family history for the disease. Familial forms of the disease usually begin at earlier ages and are associated with atypical clinical features.<ref>PMID:9197268</ref> <ref>PMID:9462735</ref> <ref>PMID:14755719</ref> Defects in SNCA are the cause of Parkinson disease type 4 (PARK4) [MIM:[~~http~~://omim.org/entry/605543 605543]]. A complex neurodegenerative disorder with manifestations ranging from typical Parkinson disease to dementia with Lewy bodies. Clinical features include parkinsonian symptoms (tremor, rigidity, postural instability and bradykinesia), dementia, diffuse Lewy body pathology, autonomic dysfunction, hallucinations and paranoia. Defects in SNCA are the cause of dementia Lewy body (DLB) [MIM:[~~http~~://omim.org/entry/127750 127750]]. A neurodegenerative disorder clinically characterized by mental impairment leading to dementia, parkinsonism, often with fluctuating cognitive function, visual hallucinations, falls, syncopal episodes, and sensitivity to neuroleptic medication. Brainstem or cortical intraneuronal accumulations of aggregated proteins (Lewy bodies) are the only essential pathologic features. Patients may also have hippocampal and neocortical senile plaques, sometimes in sufficient number to fulfill the diagnostic criteria for Alzheimer disease.	+	[https://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN] Note=Genetic alterations of SNCA resulting in aberrant polymerization into fibrils, are associated with several neurodegenerative diseases (synucleinopathies). SNCA fibrillar aggregates represent the major non A-beta component of Alzheimer disease amyloid plaque, and a major component of Lewy body inclusions. They are also found within Lewy body (LB)-like intraneuronal inclusions, glial inclusions and axonal spheroids in neurodegeneration with brain iron accumulation type 1. Defects in SNCA are the cause of Parkinson disease type 1 (PARK1) [MIM:[https://omim.org/entry/168601 168601]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia. The pathology of Parkinson disease involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins), in surviving neurons in various areas of the brain. The disease is progressive and usually manifests after the age of 50 years, although early-onset cases (before 50 years) are known. The majority of the cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, some patients present with a positive family history for the disease. Familial forms of the disease usually begin at earlier ages and are associated with atypical clinical features.<ref>PMID:9197268</ref> <ref>PMID:9462735</ref> <ref>PMID:14755719</ref> Defects in SNCA are the cause of Parkinson disease type 4 (PARK4) [MIM:[https://omim.org/entry/605543 605543]. A complex neurodegenerative disorder with manifestations ranging from typical Parkinson disease to dementia with Lewy bodies. Clinical features include parkinsonian symptoms (tremor, rigidity, postural instability and bradykinesia), dementia, diffuse Lewy body pathology, autonomic dysfunction, hallucinations and paranoia. Defects in SNCA are the cause of dementia Lewy body (DLB) [MIM:[https://omim.org/entry/127750 127750]. A neurodegenerative disorder clinically characterized by mental impairment leading to dementia, parkinsonism, often with fluctuating cognitive function, visual hallucinations, falls, syncopal episodes, and sensitivity to neuroleptic medication. Brainstem or cortical intraneuronal accumulations of aggregated proteins (Lewy bodies) are the only essential pathologic features. Patients may also have hippocampal and neocortical senile plaques, sometimes in sufficient number to fulfill the diagnostic criteria for Alzheimer disease.
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN]] May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation.	+	[https://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN] May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 28:		Line 29:
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Ando, T]]	+	[[Category: Ando T]]
-	[[Category: Ghetti, B]]	+	[[Category: Ghetti B]]
-	[[Category: Goedert, M]]	+	[[Category: Goedert M]]
-	[[Category: Hasegawa, K]]	+	[[Category: Hasegawa K]]
-	[[Category: Hasegawa, M]]	+	[[Category: Hasegawa M]]
-	[[Category: Kametani, F]]	+	[[Category: Kametani F]]
-	[[Category: Matsubara, T]]	+	[[Category: Matsubara T]]
-	[[Category: Murayama, S]]	+	[[Category: Murayama S]]
-	[[Category: Murzin~~, A G~~]]	+	[[Category: Murzin AG]]
-	[[Category: Scheres~~, S H.W~~]]	+	[[Category: Scheres SHW]]
-	[[Category: Schweighauser, M]]	+	[[Category: Schweighauser M]]
-	[[Category: Shi, Y]]	+	[[Category: Shi Y]]
-	[[Category: Tarutani, A]]	+	[[Category: Tarutani A]]
-	[[Category: Tomita, T]]	+	[[Category: Tomita T]]
-	[[Category: Yoshida, M]]	+	[[Category: Yoshida M]]
-	~~[[Category: Alpha-synuclein filament]]~~	+
-	~~[[Category: Multiple system atrophy]]~~	+
-	~~[[Category: Protein fibril~~]]	+

OCA at 06:52, 10 June 2020

2020-06-10T06:52:15Z

←Older revision		Revision as of 06:52, 10 June 2020
Line 10:		Line 10:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN]] May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation.		[[http://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN]] May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Synucleinopathies, which include multiple system atrophy (MSA), Parkinson's disease, Parkinson's disease with dementia and dementia with Lewy bodies (DLB), are human neurodegenerative diseases(1). Existing treatments are at best symptomatic. These diseases are characterized by the presence of, and believed to be caused by the formation of, filamentous inclusions of alpha-synuclein in brain cells(2,3). However, the structures of alpha-synuclein filaments from the human brain are unknown. Here, using cryo-electron microscopy, we show that alpha-synuclein inclusions from the brains of individuals with MSA are made of two types of filament, each of which consists of two different protofilaments. In each type of filament, non-proteinaceous molecules are present at the interface of the two protofilaments. Using two-dimensional class averaging, we show that alpha-synuclein filaments from the brains of individuals with MSA differ from those of individuals with DLB, which suggests that distinct conformers or strains characterize specific synucleinopathies. As is the case with tau assemblies(4-9), the structures of alpha-synuclein filaments extracted from the brains of individuals with MSA differ from those formed in vitro using recombinant proteins, which has implications for understanding the mechanisms of aggregate propagation and neurodegeneration in the human brain. These findings have diagnostic and potential therapeutic relevance, especially because of the unmet clinical need to be able to image filamentous alpha-synuclein inclusions in the human brain.
		+
		+	Structures of alpha-synuclein filaments from multiple system atrophy.,Schweighauser M, Shi Y, Tarutani A, Kametani F, Murzin AG, Ghetti B, Matsubara T, Tomita T, Ando T, Hasegawa K, Murayama S, Yoshida M, Hasegawa M, Scheres SHW, Goedert M Nature. 2020 May 27. pii: 10.1038/s41586-020-2317-6. doi:, 10.1038/s41586-020-2317-6. PMID:32461689<ref>PMID:32461689</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 6xyp" style="background-color:#fffaf0;"></div>

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

OCA at 07:13, 11 April 2020

2020-04-11T07:13:05Z

←Older revision		Revision as of 07:13, 11 April 2020
Line 3:		Line 3:
	<SX load='6xyp' size='340' side='right' viewer='molstar' caption='[[6xyp]], [[Resolution\|resolution]] 3.29Å' scene=''>		<SX load='6xyp' size='340' side='right' viewer='molstar' caption='[[6xyp]], [[Resolution\|resolution]] 3.29Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6xyp]] is a 10 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=6XYP OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6XYP FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6xyp]] is a 10 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=6XYP OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=6XYP FirstGlance]. <br>
-	</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=6xyp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6xyp OCA], [http://pdbe.org/6xyp PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6xyp RCSB], [http://www.ebi.ac.uk/pdbsum/6xyp PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6xyp ProSAT]</span></td></tr>	+	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=6xyp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6xyp OCA], [http://pdbe.org/6xyp PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6xyp RCSB], [http://www.ebi.ac.uk/pdbsum/6xyp PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6xyp ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 10:		Line 10:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN]] May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation.		[[http://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN]] May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation.
		+
		+	==See Also==
		+	*[[Alpha-synuclein\|Alpha-synuclein]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 01:27, 7 March 2020

2020-03-07T01:27:28Z

←Older revision		Revision as of 01:27, 7 March 2020
Line 1:		Line 1:

	==Multiple system atrophy Type II-1 alpha-synuclein filament==		==Multiple system atrophy Type II-1 alpha-synuclein filament==
-	<~~StructureSection~~ load='6xyp' size='340' side='right'caption='[[6xyp]], [[Resolution\|resolution]] 3.29Å' scene=''>	+	<SX load='6xyp' size='340' side='right' viewer='molstar' caption='[[6xyp]], [[Resolution\|resolution]] 3.29Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[6xyp]] is a 10 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=6XYP OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6XYP FirstGlance]. <br>		<table><tr><td colspan='2'>[[6xyp]] is a 10 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=6XYP OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6XYP FirstGlance]. <br>
Line 13:		Line 13:
	<references/>		<references/>
	__TOC__		__TOC__
-	</~~StructureSection~~>	+	</SX>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]

OCA at 04:31, 13 February 2020

2020-02-13T04:31:37Z

←Older revision		Revision as of 04:31, 13 February 2020
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 6xyp ~~is ON HOLD~~	+	==Multiple system atrophy Type II-1 alpha-synuclein filament==
-		+	<StructureSection load='6xyp' size='340' side='right'caption='[[6xyp]], [[Resolution\|resolution]] 3.29Å' scene=''>
-	~~Authors~~: ~~Schweighauser~~, M., ~~Shi~~, Y., ~~Tarutani~~, A., ~~Kametani, F~~., ~~Murzin~~, A.G., ~~Ghetti~~, B., ~~Matsubara~~, T., ~~Tomita, T~~., ~~Hasegawa, K~~., ~~Murayama, S~~., ~~Yoshida~~, M., ~~Hasegawa~~, M., ~~Scheres~~, S.H.W., ~~Goedert~~, M.	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[6xyp]] is a 10 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=6XYP OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6XYP FirstGlance]. <br>
-	~~Description~~: ~~Multiple system atrophy Type II~~-~~1 alpha~~-~~synuclein filament~~	+	</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=6xyp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6xyp OCA], [http://pdbe.org/6xyp PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6xyp RCSB], [http://www.ebi.ac.uk/pdbsum/6xyp PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6xyp ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	</table>
-	[[Category: ~~Yoshida, M~~]]	+	== Disease ==
-	[[Category: ~~Tomita~~, T]]	+	[[http://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN]] Note=Genetic alterations of SNCA resulting in aberrant polymerization into fibrils, are associated with several neurodegenerative diseases (synucleinopathies). SNCA fibrillar aggregates represent the major non A-beta component of Alzheimer disease amyloid plaque, and a major component of Lewy body inclusions. They are also found within Lewy body (LB)-like intraneuronal inclusions, glial inclusions and axonal spheroids in neurodegeneration with brain iron accumulation type 1. Defects in SNCA are the cause of Parkinson disease type 1 (PARK1) [MIM:[http://omim.org/entry/168601 168601]]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia. The pathology of Parkinson disease involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins), in surviving neurons in various areas of the brain. The disease is progressive and usually manifests after the age of 50 years, although early-onset cases (before 50 years) are known. The majority of the cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, some patients present with a positive family history for the disease. Familial forms of the disease usually begin at earlier ages and are associated with atypical clinical features.<ref>PMID:9197268</ref> <ref>PMID:9462735</ref> <ref>PMID:14755719</ref> Defects in SNCA are the cause of Parkinson disease type 4 (PARK4) [MIM:[http://omim.org/entry/605543 605543]]. A complex neurodegenerative disorder with manifestations ranging from typical Parkinson disease to dementia with Lewy bodies. Clinical features include parkinsonian symptoms (tremor, rigidity, postural instability and bradykinesia), dementia, diffuse Lewy body pathology, autonomic dysfunction, hallucinations and paranoia. Defects in SNCA are the cause of dementia Lewy body (DLB) [MIM:[http://omim.org/entry/127750 127750]]. A neurodegenerative disorder clinically characterized by mental impairment leading to dementia, parkinsonism, often with fluctuating cognitive function, visual hallucinations, falls, syncopal episodes, and sensitivity to neuroleptic medication. Brainstem or cortical intraneuronal accumulations of aggregated proteins (Lewy bodies) are the only essential pathologic features. Patients may also have hippocampal and neocortical senile plaques, sometimes in sufficient number to fulfill the diagnostic criteria for Alzheimer disease.
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/SYUA_HUMAN SYUA_HUMAN]] May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation.
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Homo sapiens]]
		+	[[Category: Large Structures]]
		+	[[Category: Ando, T]]
	[[Category: Ghetti, B]]		[[Category: Ghetti, B]]
		+	[[Category: Goedert, M]]
		+	[[Category: Hasegawa, K]]
		+	[[Category: Hasegawa, M]]
	[[Category: Kametani, F]]		[[Category: Kametani, F]]
-	[[Category: Goedert, M]]
	[[Category: Matsubara, T]]		[[Category: Matsubara, T]]
-	[[Category: Tarutani, A]]
	[[Category: Murayama, S]]		[[Category: Murayama, S]]
		+	[[Category: Murzin, A G]]
		+	[[Category: Scheres, S H.W]]
	[[Category: Schweighauser, M]]		[[Category: Schweighauser, M]]
-	[[Category: Hasegawa, K]]
-	[[Category: Hasegawa, M]]
-	[[Category: Scheres, S.H.W]]
-	[[Category: Murzin, A.G]]
	[[Category: Shi, Y]]		[[Category: Shi, Y]]
		+	[[Category: Tarutani, A]]
		+	[[Category: Tomita, T]]
		+	[[Category: Yoshida, M]]
		+	[[Category: Alpha-synuclein filament]]
		+	[[Category: Multiple system atrophy]]
		+	[[Category: Protein fibril]]

OCA: Protected "6xyp" [edit=sysop:move=sysop]

2020-02-05T06:31:43Z

Protected "6xyp" [edit=sysop:move=sysop]

←Older revision

Revision as of 06:31, 5 February 2020

OCA: New page: '''Unreleased structure''' The entry 6xyp is ON HOLD Authors: Schweighauser, M., Shi, Y., Tarutani, A., Kametani, F., Murzin, A.G., Ghetti, B., Matsubara, T., Tomita, T., Hasegawa, K., ...

2020-02-05T06:31:41Z

New page: '''Unreleased structure''' The entry 6xyp is ON HOLD Authors: Schweighauser, M., Shi, Y., Tarutani, A., Kametani, F., Murzin, A.G., Ghetti, B., Matsubara, T., Tomita, T., Hasegawa, K., ...

New page

'''Unreleased structure'''

The entry 6xyp is ON HOLD

Authors: Schweighauser, M., Shi, Y., Tarutani, A., Kametani, F., Murzin, A.G., Ghetti, B., Matsubara, T., Tomita, T., Hasegawa, K., Murayama, S., Yoshida, M., Hasegawa, M., Scheres, S.H.W., Goedert, M.

Description: Multiple system atrophy Type II-1 alpha-synuclein filament
[[Category: Unreleased Structures]]
[[Category: Yoshida, M]]
[[Category: Tomita, T]]
[[Category: Ghetti, B]]
[[Category: Kametani, F]]
[[Category: Goedert, M]]
[[Category: Matsubara, T]]
[[Category: Tarutani, A]]
[[Category: Murayama, S]]
[[Category: Schweighauser, M]]
[[Category: Hasegawa, K]]
[[Category: Hasegawa, M]]
[[Category: Scheres, S.H.W]]
[[Category: Murzin, A.G]]
[[Category: Shi, Y]]