6dca - Revision history

OCA at 07:53, 17 October 2024

2024-10-17T07:53:20Z

← Older revision		Revision as of 07:53, 17 October 2024
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	<StructureSection load='6dca' size='340' side='right'caption='[[6dca]], [[Resolution\|resolution]] 2.60Å' scene=''>		<StructureSection load='6dca' size='340' side='right'caption='[[6dca]], [[Resolution\|resolution]] 2.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[6dca]] is a 12 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6DCA OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6DCA FirstGlance]. <br>		<table><tr><td colspan='2'>[[6dca]] is a 12 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=6DCA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6DCA FirstGlance]. <br>
	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat"~~><scene name~~=~~'pdbligand=PO4:PHOSPHATE+ION'>PO4</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]] 2.599Å</td></tr>
	<tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=NH2:AMINO+GROUP'>NH2</scene></td></tr>		<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NH2:AMINO+GROUP'>NH2</scene>, <scene name='pdbligand=PO4:PHOSPHATE+ION'>PO4</scene></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=6dca FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6dca OCA], [~~http~~://pdbe.org/6dca PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6dca RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6dca PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6dca 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=6dca FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6dca OCA], [https://pdbe.org/6dca PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6dca RCSB], [https://www.ebi.ac.uk/pdbsum/6dca PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6dca ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[~~[http~~://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:[~~http~~://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:[~~http~~://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:[~~http~~://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:[~~http~~://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>		[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 ==		== Function ==
	[~~[http~~://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>		[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 ==
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	</div>		</div>
	<div class="pdbe-citations 6dca" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 6dca" style="background-color:#fffaf0;"></div>

			==See Also==
			*[[Monoclonal Antibodies 3D structures\|Monoclonal Antibodies 3D structures]]
			*[[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: Mus musculus]]		[[Category: Mus musculus]]
	[[Category: Chukwu~~, J E~~]]		[[Category: Chukwu JE]]
	[[Category: Kong, X P]]		[[Category: Kong X-P]]
	~~[[Category: Fab]]~~
	~~[[Category: Immune system]]~~
	~~[[Category: Monoclonal antibody]]~~
	~~[[Category: Phosphorylation state-specific antibody]]~~
	~~[[Category: Tau~~]]

OCA at 07:47, 20 March 2019

2019-03-20T07:47:35Z

@@ Line 1: / Line 1: @@
-The entry 6dca is ON HOLD  until Paper Publication
+==Fab/epitope complex of mouse monoclonal antibody 6B2 targeting a non-phosphorylated tau epitope.==
-Authors: Chukwu, J.E., Kong, X.-P.
+Structural characterization of monoclonal antibodies targeting C-terminal Ser(404) region of phosphorylated tau protein.,Chukwu JE, Congdon EE, Sigurdsson EM, Kong XP MAbs. 2019 Feb 22:1-12. doi: 10.1080/19420862.2019.1574530. PMID:30794086<ref>PMID:30794086</ref>
-Description: Fab/epitope complex of mouse monoclonal antibody 6B2 targeting a non-phosphorylated tau epitope.
+From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
-[[Category: Unreleased Structures]]
+</div>
-[[Category: Kong, X.-P]]
+<div class="pdbe-citations 6dca" style="background-color:#fffaf0;"></div>
-[[Category: Chukwu, J.E]]
+== References ==

OCA at 04:37, 22 August 2018

2018-08-22T04:37:41Z

← Older revision		Revision as of 04:37, 22 August 2018
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	'''Unreleased structure'''		'''Unreleased structure'''

	The entry 6dca is ON HOLD		The entry 6dca is ON HOLD until Paper Publication

	Authors: Chukwu, J.E., Kong, X.-P.		Authors: Chukwu, J.E., Kong, X.-P.

OCA at 14:44, 15 August 2018

2018-08-15T14:44:33Z

← Older revision		Revision as of 14:44, 15 August 2018
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	'''Unreleased structure'''		'''Unreleased structure'''

	The entry 6dca is ON HOLD ~~until Paper Publication~~		The entry 6dca is ON HOLD

	Authors: Chukwu, J.E., Kong, X.-P.		Authors: Chukwu, J.E., Kong, X.-P.

OCA at 03:56, 27 June 2018

2018-06-27T03:56:38Z

← Older revision		Revision as of 03:56, 27 June 2018
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	'''Unreleased structure'''		'''Unreleased structure'''

	The entry 6dca is ON HOLD		The entry 6dca is ON HOLD until Paper Publication

	Authors: Chukwu, J.E., Kong, X.-P.		Authors: Chukwu, J.E., Kong, X.-P.

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

2018-05-16T04:05:15Z

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

← Older revision	Revision as of 04:05, 16 May 2018
(No difference)

OCA: New page: '''Unreleased structure''' The entry 6dca is ON HOLD Authors: Chukwu, J.E., Kong, X.-P. Description: Fab/epitope complex of mouse monoclonal antibody 6B2 targeting a non-phosphorylated...

2018-05-16T04:05:14Z

New page: '''Unreleased structure''' The entry 6dca is ON HOLD Authors: Chukwu, J.E., Kong, X.-P. Description: Fab/epitope complex of mouse monoclonal antibody 6B2 targeting a non-phosphorylated...

New page

'''Unreleased structure'''

The entry 6dca is ON HOLD

Authors: Chukwu, J.E., Kong, X.-P.

Description: Fab/epitope complex of mouse monoclonal antibody 6B2 targeting a non-phosphorylated tau epitope.
[[Category: Unreleased Structures]]
[[Category: Kong, X.-P]]
[[Category: Chukwu, J.E]]