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image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao ZENODOarrow_drop_down
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
ZENODO
Dataset . 2024
License: CC BY
Data sources: ZENODO
ZENODO
Dataset . 2024
License: CC BY
Data sources: Datacite
ZENODO
Dataset . 2024
License: CC BY
Data sources: Datacite
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HDAC6 and TDP-43 promote autophagy impairment in Amyotrophic Lateral Sclerosis

Authors: Bordoni, Matteo; Scarian, Eveljn; Jacchetti, Emanuela; Viola, Camilla; Diamanti, Luca; Dragoni, Francesca; Di Gerlando, Rosalinda; +4 Authors

HDAC6 and TDP-43 promote autophagy impairment in Amyotrophic Lateral Sclerosis

Abstract

The database includes the raw data of the article “HDAC6 and TDP-43 promote autophagy impairment in Amyotrophic Lateral Sclerosis”. Aim of this work was to investigate how TDP-43 and HDAC6 interacts, leading to the impairment of the autophagy pathway. The work was performed in both PBMCs and in transfected SH-SY5Y cells. The database contains the data obtained by the following evaluations: a) western blot (WB) analysis in healthy control and sporadic ALS patients PBMCs b) western blot analysis of protein involved in autophagy pathway after transfection with TDP-43 WT plasmid c) western blot analysis of protein involved in autophagy pathway after silencing of HDAC6. This work provides solid evidence supporting the hypothesis that dysregulation of HDAC6 is a key factor in the disruption of the autophagy pathway previously detected in sALS PBMCs. To the best of our knowledge, we demonstrated for the first time that both excessive reduction in acetylated α-tubulin levels, due to HDAC6 overexpression, and excessive increase in acetylated α-tubulin levels, resulting from HDAC6 downregulation, lead to impairments in autophagy. These findings could be exploited as possible therapeutic target.

Keywords

neuroblastoma, TDP-43, ALS, HDAC6, peripheral blood mononuclear cells

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
Average
Average
Average