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

zu Verbundenen Objekten

Standort: Deutsche Nationalbibliothek Frankfurt am Main

Umfang: 1 Online-Ressource.

Sprache: Englisch

Erschienen in: 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

Urheber: 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

Beteiligte Personen und Organisationen: SpringerLink (Online service)

DOI: 10.1186/s13024-024-00735-7

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

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

Letzte Aktualisierung: 15.08.2025, 07:27 MESZ

Datenpartner

Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.

Original beim Datenpartner anzeigen

Beteiligte

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)

Ähnliche Objekte (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

Informationen zur Registrierung von Kultur- und Wissenseinrichtungen finden Sie hier.

Felder mit * müssen ausgefüllt werden.

Benutzername*

Bitte geben Sie Ihren Benutzernamen ein

E-Mail*

Bitte geben Sie Ihre E-Mail ein

Bitte füllen Sie dieses Feld nicht aus

Vorname

Nachname

Passwort*

Bitte geben Sie Ihr Passwort ein

Passwort bestätigen*

Bitte geben Sie das gleiche Passwort ein

Ich habe die Nutzungsbedingungen und die Datenschutzerklärung zur Erhebung persönlicher Daten gelesen und stimme ihnen zu. *

Dieses Feld ist ein Pflichtfeld.

Ich möchte den Newsletter der Deutschen Digitalen Bibliothek abonnieren. Siehe Informationen zum Newsletter-Abonnement.

Benutzerkonto angelegt

Ihr „Meine DDB“-Konto wurde erfolgreich angelegt. Bevor Sie sich in Ihrem Konto anmelden können, müssen Sie auf den Bestätigungslink in der Nachricht klicken, die wir gerade an die von Ihnen angegebene E-Mail-Adresse geschickt haben

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

Angaben zum Objekt

Verweise und Beziehungen

Beteiligte, Orts- und Zeitangaben

Weitere Informationen

Datenpartner

Beteiligte

Ähnliche Objekte (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

Verbundene Objekte

Passwort zurücksetzen