5e2w - Revision history

OCA at 06:11, 5 July 2023

OCA — Wed, 05 Jul 2023 06:11:15 GMT

←Older revision		Revision as of 06:11, 5 July 2023
Line 3:		Line 3:
	<StructureSection load='5e2w' size='340' side='right'caption='[[5e2w]], [[Resolution\|resolution]] 1.50Å' scene=''>		<StructureSection load='5e2w' size='340' side='right'caption='[[5e2w]], [[Resolution\|resolution]] 1.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5e2w]] is a 3 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/~~Lk3_transgenic_mice Lk3 transgenic mice~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E2W OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=5E2W FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5e2w]] is a 3 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E2W OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5E2W FirstGlance]. <br>
-	</td></tr><tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"~~><scene name~~=~~'pdbligand=SEP:PHOSPHOSERINE'>SEP</scene~~>, ~~<scene name='pdbligand=TPO:PHOSPHOTHREONINE'>TPO</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]] 1.5Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat">~~[[5e2v\|5e2v]]~~, ~~[[5e2u\|5e2u]], [[5e2t\|5e2t]]~~</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene>, <scene name='pdbligand=TPO:PHOSPHOTHREONINE'>TPO</scene></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=5e2w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e2w OCA], [~~http~~://pdbe.org/5e2w PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5e2w RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5e2w PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5e2w 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=5e2w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e2w OCA], [https://pdbe.org/5e2w PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5e2w RCSB], [https://www.ebi.ac.uk/pdbsum/5e2w PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5e2w ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[https://www.uniprot.org/uniprot/TAU_HUMAN TAU_HUMAN] Note=In Alzheimer disease, the neuronal cytoskeleton in the brain is progressively disrupted and replaced by tangles of paired helical filaments (PHF) and straight filaments, mainly composed of hyperphosphorylated forms of TAU (PHF-TAU or AD P-TAU). O-GlcNAcylation is greatly reduced in Alzheimer disease brain cerebral cortex leading to an increase in TAU/MAPT phosphorylations.<ref>PMID:19451179</ref> <ref>PMID:2484340</ref> <ref>PMID:14517953</ref> Defects in MAPT are a cause of frontotemporal dementia (FTD) [MIM:[https://omim.org/entry/600274 600274]; also called frontotemporal dementia (FTD), pallido-ponto-nigral degeneration (PPND) or historically termed Pick complex. This form of frontotemporal dementia is characterized by presenile dementia with behavioral changes, deterioration of cognitive capacities and loss of memory. In some cases, parkinsonian symptoms are prominent. Neuropathological changes include frontotemporal atrophy often associated with atrophy of the basal ganglia, substantia nigra, amygdala. In most cases, protein tau deposits are found in glial cells and/or neurons.<ref>PMID:19451179</ref> <ref>PMID:2484340</ref> <ref>PMID:14517953</ref> <ref>PMID:9629852</ref> <ref>PMID:9736786</ref> <ref>PMID:9641683</ref> <ref>PMID:9789048</ref> <ref>PMID:9973279</ref> <ref>PMID:10553987</ref> <ref>PMID:10214944</ref> <ref>PMID:10374757</ref> <ref>PMID:10489057</ref> <ref>PMID:10208578</ref> <ref>PMID:11117541</ref> <ref>PMID:10802785</ref> <ref>PMID:11071507</ref> <ref>PMID:11585254</ref> <ref>PMID:11278002</ref> <ref>PMID:12473774</ref> <ref>PMID:11921059</ref> <ref>PMID:11906000</ref> <ref>PMID:11889249</ref> <ref>PMID:12509859</ref> <ref>PMID:16240366</ref> <ref>PMID:15883319</ref> Defects in MAPT are a cause of Pick disease of the brain (PIDB) [MIM:[https://omim.org/entry/172700 172700]. It is a rare form of dementia pathologically defined by severe atrophy, neuronal loss and gliosis. It is characterized by the occurrence of tau-positive inclusions, swollen neurons (Pick cells) and argentophilic neuronal inclusions known as Pick bodies that disproportionally affect the frontal and temporal cortical regions. Clinical features include aphasia, apraxia, confusion, anomia, memory loss and personality deterioration.<ref>PMID:19451179</ref> <ref>PMID:2484340</ref> <ref>PMID:14517953</ref> <ref>PMID:10604746</ref> <ref>PMID:11117542</ref> <ref>PMID:11089577</ref> <ref>PMID:11601501</ref> <ref>PMID:11891833</ref> Note=Defects in MAPT are a cause of corticobasal degeneration (CBD). It is marked by extrapyramidal signs and apraxia and can be associated with memory loss. Neuropathologic features may overlap Alzheimer disease, progressive supranuclear palsy, and Parkinson disease.<ref>PMID:19451179</ref> <ref>PMID:2484340</ref> <ref>PMID:14517953</ref> Defects in MAPT are a cause of progressive supranuclear palsy type 1 (PSNP1) [MIM:[https://omim.org/entry/601104 601104]; also abbreviated as PSP and also known as Steele-Richardson-Olszewski syndrome. PSNP1 is characterized by akinetic-rigid syndrome, supranuclear gaze palsy, pyramidal tract dysfunction, pseudobulbar signs and cognitive capacities deterioration. Neurofibrillary tangles and gliosis but no amyloid plaques are found in diseased brains. Most cases appear to be sporadic, with a significant association with a common haplotype including the MAPT gene and the flanking regions. Familial cases show an autosomal dominant pattern of transmission with incomplete penetrance; genetic analysis of a few cases showed the occurrence of tau mutations, including a deletion of Asn-613.<ref>PMID:19451179</ref> <ref>PMID:2484340</ref> <ref>PMID:14517953</ref> <ref>PMID:10534245</ref> <ref>PMID:11220749</ref> <ref>PMID:12325083</ref> <ref>PMID:14991829</ref> <ref>PMID:14991828</ref> <ref>PMID:16157753</ref> Defects in MAPT are a cause of Parkinson-dementia syndrome (PARDE) [MIM:[https://omim.org/entry/260540 260540]. A syndrome characterized by parkinsonism tremor, rigidity, dementia, ophthalmoparesis and pyramidal signs. Neurofibrillary degeneration occurs in the hippocampus, basal ganglia and brainstem nuclei.<ref>PMID:19451179</ref> <ref>PMID:2484340</ref> <ref>PMID:14517953</ref>
		+	== Function ==
		+	[https://www.uniprot.org/uniprot/TAU_HUMAN TAU_HUMAN] Promotes microtubule assembly and stability, and might be involved in the establishment and maintenance of neuronal polarity. The C-terminus binds axonal microtubules while the N-terminus binds neural plasma membrane components, suggesting that tau functions as a linker protein between both. Axonal polarity is predetermined by TAU/MAPT localization (in the neuronal cell) in the domain of the cell body defined by the centrosome. The short isoforms allow plasticity of the cytoskeleton whereas the longer isoforms may preferentially play a role in its stabilization.<ref>PMID:21985311</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 19:		Line 23:

	==See Also==		==See Also==
-	*[[Tau protein\|Tau protein]]	+	*[[Tau protein 3D structures\|Tau protein 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: ~~Lk3 transgenic mice~~]]	+	[[Category: Mus musculus]]
-	[[Category: Malia, T]]	+	[[Category: Malia T]]
-	[[Category: Teplyakov, A]]	+	[[Category: Teplyakov A]]
-	~~[[Category: Immune system~~]]	+

OCA at 06:41, 22 April 2020

OCA — Wed, 22 Apr 2020 06:41:41 GMT

←Older revision		Revision as of 06:41, 22 April 2020
Line 1:		Line 1:

	==Anti-TAU AT8 FAB with triply phosphorylated TAU peptide==		==Anti-TAU AT8 FAB with triply phosphorylated TAU peptide==
-	<StructureSection load='5e2w' size='340' side='right' caption='[[5e2w]], [[Resolution\|resolution]] 1.50Å' scene=''>	+	<StructureSection load='5e2w' size='340' side='right'caption='[[5e2w]], [[Resolution\|resolution]] 1.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5e2w]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E2W OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5E2W FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5e2w]] is a 3 chain structure with sequence from [http://en.wikipedia.org/wiki/Lk3_transgenic_mice Lk3 transgenic mice]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E2W OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=5E2W FirstGlance]. <br>
	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene>, <scene name='pdbligand=TPO:PHOSPHOTHREONINE'>TPO</scene></td></tr>		</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene>, <scene name='pdbligand=TPO:PHOSPHOTHREONINE'>TPO</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5e2v\|5e2v]], [[5e2u\|5e2u]], [[5e2t\|5e2t]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5e2v\|5e2v]], [[5e2u\|5e2u]], [[5e2t\|5e2t]]</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=5e2w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e2w OCA], [http://pdbe.org/5e2w PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5e2w RCSB], [http://www.ebi.ac.uk/pdbsum/5e2w PDBsum]</span></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=5e2w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e2w OCA], [http://pdbe.org/5e2w PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5e2w RCSB], [http://www.ebi.ac.uk/pdbsum/5e2w PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5e2w ProSAT]</span></td></tr>
	</table>		</table>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 17:		Line 17:
	</div>		</div>
	<div class="pdbe-citations 5e2w" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5e2w" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Tau protein\|Tau protein]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Lk3 transgenic mice]]
	[[Category: Malia, T]]		[[Category: Malia, T]]
	[[Category: Teplyakov, A]]		[[Category: Teplyakov, A]]
	[[Category: Immune system]]		[[Category: Immune system]]

OCA at 18:08, 26 February 2016

OCA — Fri, 26 Feb 2016 18:08:46 GMT

←Older revision		Revision as of 18:08, 26 February 2016
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 5e2w is ~~ON HOLD until Paper~~ Publication	+	==Anti-TAU AT8 FAB with triply phosphorylated TAU peptide==
		+	<StructureSection load='5e2w' size='340' side='right' caption='[[5e2w]], [[Resolution\|resolution]] 1.50Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[5e2w]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E2W OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5E2W FirstGlance]. <br>
		+	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene>, <scene name='pdbligand=TPO:PHOSPHOTHREONINE'>TPO</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5e2v\|5e2v]], [[5e2u\|5e2u]], [[5e2t\|5e2t]]</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=5e2w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e2w OCA], [http://pdbe.org/5e2w PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5e2w RCSB], [http://www.ebi.ac.uk/pdbsum/5e2w PDBsum]</span></td></tr>
		+	</table>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Microtubule-associated protein tau becomes abnormally phosphorylated in Alzheimer's disease and other tauopathies and forms aggregates of paired helical filaments (PHF-tau). AT8 is a PHF-tau specific monoclonal antibody that is a commonly used marker of neuropathology because of its recognition of abnormally phosphorylated tau. Previous reports described the AT8 epitope to include pS202/pT205. Our studies support and extend previous findings by also identifying pS208 as part of the binding epitope. We characterized the phosphoepitope of AT8 through both peptide binding studies and co-structures with phosphopeptides. From the co-crystal structure of AT8 Fab with the di-phosphorylated (pS202/pT205) peptide it appeared that an additional phosphorylation at S208 would also be accommodated by AT8. Phosphopeptide binding studies showed that AT8 bound to the triply phosphorylated tau peptide (pS202/pT205/pS208) 30-fold stronger than to the pS202/pT205 peptide, supporting the role of pS208 in AT8 recognition. We also show that the binding kinetics of the triply phosphorylated peptide pS202/pT205/pS208 was remarkably similar to that of PHF-tau. The co-structure of AT8 Fab with a pS202/pT205/pS208 peptide shows that the interaction interface involves all six CDRs and tau residues 202-209. All three phosphorylation sites are recognized by AT8, with pT205 acting as the anchor. Crystallization of the Fab/peptide complex under acidic conditions shows that CDR-L2 is prone to unfolding and precludes peptide binding, and may suggest a general instability in the antibody. This article is protected by copyright. All rights reserved.

-	~~Authors: Malia, T~~., ~~Teplyakov~~, A.	+	Epitope mapping and structural basis for the recognition of phosphorylated tau by the anti-tau antibody AT8.,Malia TJ, Teplyakov A, Ernst R, Wu SJ, Lacy ER, Liu X, Vandermeeren M, Mercken M, Luo J, Sweet RW, Gilliland GL Proteins. 2016 Jan 21. doi: 10.1002/prot.24988. PMID:26800003<ref>PMID:26800003</ref>

-	~~Description: Anti-TAU AT8 FAB with triply phosphorylated TAU peptide~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[Category~~: ~~Unreleased Structures]]~~	+	</div>
		+	<div class="pdbe-citations 5e2w" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Malia, T]]		[[Category: Malia, T]]
	[[Category: Teplyakov, A]]		[[Category: Teplyakov, A]]
		+	[[Category: Immune system]]

OCA at 04:18, 22 October 2015

OCA — Thu, 22 Oct 2015 04:18:25 GMT

←Older revision		Revision as of 04:18, 22 October 2015
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5e2w is ON HOLD	+	The entry 5e2w is ON HOLD until Paper Publication

	Authors: Malia, T., Teplyakov, A.		Authors: Malia, T., Teplyakov, A.

-	Description: ~~ANTI~~-TAU AT8 FAB ~~WITH TRIPLY PHOSPHORYLATED~~ TAU ~~PEPTIDE~~	+	Description: Anti-TAU AT8 FAB with triply phosphorylated TAU peptide
	[[Category: Unreleased Structures]]		[[Category: Unreleased Structures]]
	[[Category: Malia, T]]		[[Category: Malia, T]]
	[[Category: Teplyakov, A]]		[[Category: Teplyakov, A]]

OCA: Protected "5e2w" [edit=sysop:move=sysop]

OCA — Wed, 07 Oct 2015 12:53:50 GMT

Protected "5e2w" [edit=sysop:move=sysop]

←Older revision

Revision as of 12:53, 7 October 2015

OCA: New page: '''Unreleased structure''' The entry 5e2w is ON HOLD Authors: Malia, T., Teplyakov, A. Description: ANTI-TAU AT8 FAB WITH TRIPLY PHOSPHORYLATED TAU PEPTIDE [[Category: Unreleased Struc...

OCA — Wed, 07 Oct 2015 12:53:49 GMT

New page: '''Unreleased structure''' The entry 5e2w is ON HOLD Authors: Malia, T., Teplyakov, A. Description: ANTI-TAU AT8 FAB WITH TRIPLY PHOSPHORYLATED TAU PEPTIDE [[Category: Unreleased Struc...

New page

'''Unreleased structure'''

The entry 5e2w is ON HOLD

Authors: Malia, T., Teplyakov, A.

Description: ANTI-TAU AT8 FAB WITH TRIPLY PHOSPHORYLATED TAU PEPTIDE
[[Category: Unreleased Structures]]
[[Category: Malia, T]]
[[Category: Teplyakov, A]]