Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits

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Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: 1 Online-Ressource.

Language: Englisch

Bibliographic citation: Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits ; volume:19 ; number:1 ; day:20 ; month:6 ; year:2024 ; pages:1-23 ; date:12.2024
Molecular neurodegeneration ; 19, Heft 1 (20.6.2024), 1-23, 12.2024

Creator: Hu, Yiying
Hruscha, Alexander
Pan, Chenchen
Schifferer, Martina
Schmidt, Michael K.
Nuscher, Brigitte
Giera, Martin
Kostidis, Sarantos
Burhan, Özge
Bebber, Frauke van
Edbauer, Dieter
Arzberger, Thomas
Haass, Christian
Schmid, Bettina

Contributor: SpringerLink (Online service)

DOI: 10.1186/s13024-024-00735-7

URN: urn:nbn:de:101:1-2409160927428.577906760720

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:27 AM CEST

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Associated

Hu, Yiying
Hruscha, Alexander
Pan, Chenchen
Schifferer, Martina
Schmidt, Michael K.
Nuscher, Brigitte
Giera, Martin
Kostidis, Sarantos
Burhan, Özge
Bebber, Frauke van
Edbauer, Dieter
Arzberger, Thomas
Haass, Christian
Schmid, Bettina
SpringerLink (Online service)

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Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits

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Importance of the Q/N-rich segment for protein stability of endogenous mouse TDP-43

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Antibody against TDP-43 phosphorylated at serine 375 suggests conformational differences of TDP-43 aggregates among FTLD–TDP subtypes

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Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits

Endogenous TDP-43, but not FUS, contributes to stress granule assembly via G3BP

Accelerated long-term forgetting reveals everyday memory deficits in early-stage multiple sclerosis

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Importance of the Q/N-rich segment for protein stability of endogenous mouse TDP-43

Author Correction: TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Evidence of cerebellar TDP-43 loss of function in FTLD-TDP

Disease‐linked TDP‐43 hyperphosphorylation suppresses TDP‐43 condensation and aggregation

Antibody against TDP-43 phosphorylated at serine 375 suggests conformational differences of TDP-43 aggregates among FTLD–TDP subtypes

The effect of TDP-43 antibodies on TDP-43 aggregation and toxicity

Mice with endogenous TDP ‐43 mutations exhibit gain of splicing function and characteristics of amyotrophic lateral sclerosis

Heteromeric amyloid filaments of ANXA11 and TDP-43 in FTLD-TDP type C

Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits

Endogenous TDP-43, but not FUS, contributes to stress granule assembly via G3BP

Accelerated long-term forgetting reveals everyday memory deficits in early-stage multiple sclerosis

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Importance of the Q/N-rich segment for protein stability of endogenous mouse TDP-43

Author Correction: TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Evidence of cerebellar TDP-43 loss of function in FTLD-TDP

Disease‐linked TDP‐43 hyperphosphorylation suppresses TDP‐43 condensation and aggregation

Antibody against TDP-43 phosphorylated at serine 375 suggests conformational differences of TDP-43 aggregates among FTLD–TDP subtypes

The effect of TDP-43 antibodies on TDP-43 aggregation and toxicity

Mice with endogenous TDP ‐43 mutations exhibit gain of splicing function and characteristics of amyotrophic lateral sclerosis

Heteromeric amyloid filaments of ANXA11 and TDP-43 in FTLD-TDP type C

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Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits

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Other Objects (12)

Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits

Endogenous TDP-43, but not FUS, contributes to stress granule assembly via G3BP

Accelerated long-term forgetting reveals everyday memory deficits in early-stage multiple sclerosis

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Importance of the Q/N-rich segment for protein stability of endogenous mouse TDP-43

Author Correction: TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Evidence of cerebellar TDP-43 loss of function in FTLD-TDP

Disease‐linked TDP‐43 hyperphosphorylation suppresses TDP‐43 condensation and aggregation

Antibody against TDP-43 phosphorylated at serine 375 suggests conformational differences of TDP-43 aggregates among FTLD–TDP subtypes

The effect of TDP-43 antibodies on TDP-43 aggregation and toxicity

Mice with endogenous TDP ‐43 mutations exhibit gain of splicing function and characteristics of amyotrophic lateral sclerosis

Heteromeric amyloid filaments of ANXA11 and TDP-43 in FTLD-TDP type C

Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits

Endogenous TDP-43, but not FUS, contributes to stress granule assembly via G3BP

Accelerated long-term forgetting reveals everyday memory deficits in early-stage multiple sclerosis

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Importance of the Q/N-rich segment for protein stability of endogenous mouse TDP-43

Author Correction: TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Evidence of cerebellar TDP-43 loss of function in FTLD-TDP

Disease‐linked TDP‐43 hyperphosphorylation suppresses TDP‐43 condensation and aggregation

Antibody against TDP-43 phosphorylated at serine 375 suggests conformational differences of TDP-43 aggregates among FTLD–TDP subtypes

The effect of TDP-43 antibodies on TDP-43 aggregation and toxicity

Mice with endogenous TDP ‐43 mutations exhibit gain of splicing function and characteristics of amyotrophic lateral sclerosis

Heteromeric amyloid filaments of ANXA11 and TDP-43 in FTLD-TDP type C

Mis-localization of endogenous TDP-43 leads to ALS-like early-stage metabolic dysfunction and progressive motor deficits

Endogenous TDP-43, but not FUS, contributes to stress granule assembly via G3BP

Accelerated long-term forgetting reveals everyday memory deficits in early-stage multiple sclerosis

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Importance of the Q/N-rich segment for protein stability of endogenous mouse TDP-43

Author Correction: TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Evidence of cerebellar TDP-43 loss of function in FTLD-TDP

Disease‐linked TDP‐43 hyperphosphorylation suppresses TDP‐43 condensation and aggregation

Antibody against TDP-43 phosphorylated at serine 375 suggests conformational differences of TDP-43 aggregates among FTLD–TDP subtypes

The effect of TDP-43 antibodies on TDP-43 aggregation and toxicity

Mice with endogenous TDP ‐43 mutations exhibit gain of splicing function and characteristics of amyotrophic lateral sclerosis

Heteromeric amyloid filaments of ANXA11 and TDP-43 in FTLD-TDP type C

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