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- PDB-8otf: Ab typeII filament from Guam ALS/PDC -

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Entry
Database: PDB / ID: 8otf
TitleAb typeII filament from Guam ALS/PDC
ComponentsAmyloid-beta precursor protein
KeywordsPROTEIN FIBRIL / Ab typeII filaments / Guam ALS/PDC
Function / homology
Function and homology information


amyloid-beta complex / growth cone lamellipodium / cellular response to norepinephrine stimulus / collateral sprouting in absence of injury / growth cone filopodium / microglia development / Formyl peptide receptors bind formyl peptides and many other ligands / axo-dendritic transport / regulation of Wnt signaling pathway / axon midline choice point recognition ...amyloid-beta complex / growth cone lamellipodium / cellular response to norepinephrine stimulus / collateral sprouting in absence of injury / growth cone filopodium / microglia development / Formyl peptide receptors bind formyl peptides and many other ligands / axo-dendritic transport / regulation of Wnt signaling pathway / axon midline choice point recognition / regulation of synapse structure or activity / hippocampal neuron apoptotic process / astrocyte activation involved in immune response / NMDA selective glutamate receptor signaling pathway / regulation of spontaneous synaptic transmission / mating behavior / growth factor receptor binding / peptidase activator activity / Insertion of tail-anchored proteins into the endoplasmic reticulum membrane / PTB domain binding / positive regulation of amyloid fibril formation / Golgi-associated vesicle / astrocyte projection / Lysosome Vesicle Biogenesis / neuron remodeling / Deregulated CDK5 triggers multiple neurodegenerative pathways in Alzheimer's disease models / nuclear envelope lumen / dendrite development / TRAF6 mediated NF-kB activation / positive regulation of protein metabolic process / signaling receptor activator activity / negative regulation of long-term synaptic potentiation / Advanced glycosylation endproduct receptor signaling / transition metal ion binding / The NLRP3 inflammasome / main axon / regulation of multicellular organism growth / modulation of excitatory postsynaptic potential / intracellular copper ion homeostasis / ECM proteoglycans / response to insulin-like growth factor stimulus / regulation of presynapse assembly / positive regulation of T cell migration / neuronal dense core vesicle / Purinergic signaling in leishmaniasis infection / cellular response to manganese ion / positive regulation of chemokine production / Notch signaling pathway / swimming behavior / neuron projection maintenance / extracellular matrix organization / clathrin-coated pit / astrocyte activation / positive regulation of mitotic cell cycle / axonogenesis / Mitochondrial protein degradation / positive regulation of calcium-mediated signaling / ionotropic glutamate receptor signaling pathway / platelet alpha granule lumen / response to interleukin-1 / regulation of neuron apoptotic process / cellular response to copper ion / cellular response to cAMP / positive regulation of glycolytic process / endosome lumen / positive regulation of long-term synaptic potentiation / trans-Golgi network membrane / central nervous system development / dendritic shaft / positive regulation of interleukin-1 beta production / protein serine/threonine kinase binding / learning / adult locomotory behavior / Post-translational protein phosphorylation / serine-type endopeptidase inhibitor activity / locomotory behavior / microglial cell activation / cellular response to nerve growth factor stimulus / TAK1-dependent IKK and NF-kappa-B activation / positive regulation of non-canonical NF-kappaB signal transduction / synapse organization / visual learning / regulation of long-term neuronal synaptic plasticity / positive regulation of interleukin-6 production / recycling endosome / Golgi lumen / positive regulation of JNK cascade / response to lead ion / cognition / Regulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs) / cellular response to amyloid-beta / endocytosis / positive regulation of tumor necrosis factor production / neuron projection development / positive regulation of inflammatory response / calcium ion transport / Platelet degranulation / regulation of translation / heparin binding / regulation of gene expression
Similarity search - Function
Amyloidogenic glycoprotein, copper-binding / Amyloidogenic glycoprotein, copper-binding domain conserved site / Amyloidogenic glycoprotein, copper-binding domain superfamily / Copper-binding of amyloid precursor, CuBD / Amyloid precursor protein (APP) copper-binding (CuBD) domain signature. / Amyloidogenic glycoprotein, heparin-binding / Amyloid A4 N-terminal heparin-binding / Amyloidogenic glycoprotein, amyloid-beta peptide superfamily / Beta-amyloid peptide (beta-APP) / Amyloidogenic glycoprotein, amyloid-beta peptide ...Amyloidogenic glycoprotein, copper-binding / Amyloidogenic glycoprotein, copper-binding domain conserved site / Amyloidogenic glycoprotein, copper-binding domain superfamily / Copper-binding of amyloid precursor, CuBD / Amyloid precursor protein (APP) copper-binding (CuBD) domain signature. / Amyloidogenic glycoprotein, heparin-binding / Amyloid A4 N-terminal heparin-binding / Amyloidogenic glycoprotein, amyloid-beta peptide superfamily / Beta-amyloid peptide (beta-APP) / Amyloidogenic glycoprotein, amyloid-beta peptide / Beta-amyloid precursor protein C-terminal / Amyloidogenic glycoprotein, intracellular domain, conserved site / Beta-amyloid precursor protein C-terminus / Amyloid precursor protein (APP) intracellular domain signature. / Amyloidogenic glycoprotein, extracellular / Amyloidogenic glycoprotein, E2 domain / E2 domain superfamily / Amyloidogenic glycoprotein, heparin-binding domain superfamily / E2 domain of amyloid precursor protein / Amyloid precursor protein (APP) E1 domain profile. / Amyloid precursor protein (APP) E2 domain profile. / amyloid A4 / Amyloidogenic glycoprotein / Proteinase inhibitor I2, Kunitz, conserved site / Pancreatic trypsin inhibitor (Kunitz) family signature. / BPTI/Kunitz family of serine protease inhibitors. / Pancreatic trypsin inhibitor Kunitz domain / Kunitz/Bovine pancreatic trypsin inhibitor domain / Pancreatic trypsin inhibitor (Kunitz) family profile. / Pancreatic trypsin inhibitor Kunitz domain superfamily / PH-like domain superfamily
Similarity search - Domain/homology
Amyloid-beta precursor protein
Similarity search - Component
Biological speciesHomo sapiens (human)
MethodELECTRON MICROSCOPY / helical reconstruction / cryo EM / Resolution: 3.3 Å
AuthorsQi, C. / Yang, S. / Scheres, S.H.W. / Goedert, M.
Funding support United Kingdom, 2items
OrganizationGrant numberCountry
Medical Research Council (MRC, United Kingdom)MC_UP_A025_1013 United Kingdom
Medical Research Council (MRC, United Kingdom)MC_U105184291 United Kingdom
CitationJournal: Proc Natl Acad Sci U S A / Year: 2023
Title: Tau filaments from amyotrophic lateral sclerosis/parkinsonism-dementia complex adopt the CTE fold.
Authors: Chao Qi / Bert M Verheijen / Yasumasa Kokubo / Yang Shi / Stephan Tetter / Alexey G Murzin / Asa Nakahara / Satoru Morimoto / Marc Vermulst / Ryogen Sasaki / Eleonora Aronica / Yoshifumi ...Authors: Chao Qi / Bert M Verheijen / Yasumasa Kokubo / Yang Shi / Stephan Tetter / Alexey G Murzin / Asa Nakahara / Satoru Morimoto / Marc Vermulst / Ryogen Sasaki / Eleonora Aronica / Yoshifumi Hirokawa / Kiyomitsu Oyanagi / Akiyoshi Kakita / Benjamin Ryskeldi-Falcon / Mari Yoshida / Masato Hasegawa / Sjors H W Scheres / Michel Goedert /
Abstract: The amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) of the island of Guam and the Kii peninsula of Japan is a fatal neurodegenerative disease of unknown cause that is ...The amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) of the island of Guam and the Kii peninsula of Japan is a fatal neurodegenerative disease of unknown cause that is characterized by the presence of abundant filamentous tau inclusions in brains and spinal cords. Here, we used electron cryo-microscopy to determine the structures of tau filaments from the cerebral cortex of three cases of ALS/PDC from Guam and eight cases from Kii, as well as from the spinal cord of two of the Guam cases. Tau filaments had the chronic traumatic encephalopathy (CTE) fold, with variable amounts of Type I and Type II filaments. Paired helical tau filaments were also found in three Kii cases and tau filaments with the corticobasal degeneration fold in one Kii case. We identified a new Type III CTE tau filament, where protofilaments pack against each other in an antiparallel fashion. ALS/PDC is the third known tauopathy with CTE-type filaments and abundant tau inclusions in cortical layers II/III, the others being CTE and subacute sclerosing panencephalitis. Because these tauopathies are believed to have environmental causes, our findings support the hypothesis that ALS/PDC is caused by exogenous factors.
History
DepositionApr 20, 2023Deposition site: PDBE / Processing site: PDBE
Revision 1.0Mar 27, 2024Provider: repository / Type: Initial release

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Structure visualization

Structure viewerMolecule:
MolmilJmol/JSmol

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Assembly

Deposited unit
A: Amyloid-beta precursor protein
B: Amyloid-beta precursor protein
C: Amyloid-beta precursor protein
D: Amyloid-beta precursor protein
E: Amyloid-beta precursor protein
F: Amyloid-beta precursor protein


Theoretical massNumber of molelcules
Total (without water)522,2776
Polymers522,2776
Non-polymers00
Water00
1


  • Idetical with deposited unit
  • defined by author
  • Evidence: electron microscopy
TypeNameSymmetry operationNumber
identity operation1_5551

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Components

#1: Protein
Amyloid-beta precursor protein / APP / ABPP / APPI / Alzheimer disease amyloid A4 protein homolog / Alzheimer disease amyloid ...APP / ABPP / APPI / Alzheimer disease amyloid A4 protein homolog / Alzheimer disease amyloid protein / Amyloid precursor protein / Amyloid-beta (A4) precursor protein / Amyloid-beta A4 protein / Cerebral vascular amyloid peptide / CVAP / PreA4 / Protease nexin-II / PN-II


Mass: 87046.219 Da / Num. of mol.: 6 / Source method: isolated from a natural source / Source: (natural) Homo sapiens (human) / References: UniProt: P05067

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Experimental details

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Experiment

ExperimentMethod: ELECTRON MICROSCOPY
EM experimentAggregation state: FILAMENT / 3D reconstruction method: helical reconstruction

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Sample preparation

ComponentName: Ab typeII filaments from Guam ALS/PDC / Type: COMPLEX / Entity ID: all / Source: NATURAL
Source (natural)Organism: Homo sapiens (human)
Buffer solutionpH: 7.4
SpecimenEmbedding applied: NO / Shadowing applied: NO / Staining applied: NO / Vitrification applied: YES
VitrificationCryogen name: ETHANE

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Electron microscopy imaging

Experimental equipment
Model: Titan Krios / Image courtesy: FEI Company
MicroscopyModel: FEI TITAN KRIOS
Electron gunElectron source: FIELD EMISSION GUN / Accelerating voltage: 300 kV / Illumination mode: FLOOD BEAM
Electron lensMode: BRIGHT FIELD / Nominal defocus max: 2000 nm / Nominal defocus min: 1000 nm
Image recordingElectron dose: 40 e/Å2 / Film or detector model: GATAN K3 (6k x 4k)

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Processing

Image processingDetails: Ab typeII filament from Guam ALS/PDC
CTF correctionType: NONE
Helical symmertyAngular rotation/subunit: -2.99 ° / Axial rise/subunit: 4.79 Å / Axial symmetry: C2
3D reconstructionResolution: 3.3 Å / Resolution method: FSC 0.143 CUT-OFF / Num. of particles: 20363 / Symmetry type: HELICAL

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