OCA at 06:27, 22 April 2026

2026-04-22T06:27:39Z

← Older revision		Revision as of 06:27, 22 April 2026
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	~~'''Unreleased structure'''~~

	~~The entry~~ 9o7c is ~~ON HOLD~~		==Recombinant AD THF incubated with DMSO (Flat Backbone E342)==
			<StructureSection load='9o7c' size='340' side='right'caption='[[9o7c]], [[Resolution\|resolution]] 2.31Å' scene=''>
	~~Authors~~: ~~Kunach~~, P., ~~Diamond~~, M.I.		== Structural highlights ==
			<table><tr><td colspan='2'>[[9o7c]] is a 15 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=9O7C OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9O7C FirstGlance]. <br>
	~~Description~~: ~~Recombinant~~ AD ~~THF incubated~~ with ~~DMSO~~ (~~Flat Backbone E342~~)		</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution\|Resolution]] 2.31Å</td></tr>
	[[Category: ~~Unreleased~~ Structures]]		<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=9o7c FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9o7c OCA], [https://pdbe.org/9o7c PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9o7c RCSB], [https://www.ebi.ac.uk/pdbsum/9o7c PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9o7c ProSAT]</span></td></tr>
	[[Category: Diamond~~, M.I~~]]		</table>
	[[Category: Kunach, P]]		== 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>
			== References ==
			<references/>
			__TOC__
			</StructureSection>
			[[Category: Homo sapiens]]
			[[Category: Large Structures]]
			[[Category: Diamond MI]]
			[[Category: Kunach P]]

OCA: Protected "9o7c" [edit=sysop:move=sysop]

2025-04-23T04:05:10Z

Protected "9o7c" [edit=sysop:move=sysop]

← Older revision	Revision as of 04:05, 23 April 2025
(No difference)

OCA: New page: '''Unreleased structure''' The entry 9o7c is ON HOLD Authors: Kunach, P., Diamond, M.I. Description: Recombinant AD THF incubated with DMSO (Flat Backbone E342) [[Category: Unreleased ...

2025-04-23T04:05:09Z

New page: '''Unreleased structure''' The entry 9o7c is ON HOLD Authors: Kunach, P., Diamond, M.I. Description: Recombinant AD THF incubated with DMSO (Flat Backbone E342) [[Category: Unreleased ...

New page

'''Unreleased structure'''

The entry 9o7c is ON HOLD

Authors: Kunach, P., Diamond, M.I.

Description: Recombinant AD THF incubated with DMSO (Flat Backbone E342)
[[Category: Unreleased Structures]]
[[Category: Diamond, M.I]]
[[Category: Kunach, P]]

9o7c - Revision history

OCA at 06:27, 22 April 2026

OCA: Protected "9o7c" [edit=sysop:move=sysop]

OCA: New page: '''Unreleased structure''' The entry 9o7c is ON HOLD Authors: Kunach, P., Diamond, M.I. Description: Recombinant AD THF incubated with DMSO (Flat Backbone E342) [[Category: Unreleased ...