Evidence map›Paper›PMID 22096569›Full record

ArticlePloS one2011

Ku70 alleviates neurodegeneration in Drosophila models of Huntington's disease.

Takuya Tamura, Masaki Sone, Takeshi Iwatsubo, Kazuhiko Tagawa, Erich E Wanker, Hitoshi Okazawa

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 34 citations in OpenAlex.

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  20. The role of RecQ helicases in non-homologous end-joining.Critical reviews in biochemistry and molecular biology
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Takuya TamuraDepartment of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Masaki Sone
Takeshi Iwatsubo
Kazuhiko Tagawa
Erich E Wanker
Hitoshi Okazawa
Tokyo Medical and Dental University · JPJapan Science and Technology Agency · JPMax Delbrück Center · DEThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage accumulates in genome DNA during the long life of neurons, thus DNA damage repair is indispensable to keep normal functions of neurons. We previously reported that Ku70, a critical molecule for DNA double strand break (DSB) repair, is involved in the pathology of Huntington's disease (HD). Mutant huntingtin (Htt) impaired Ku70 function via direct interaction, and Ku70 supplementation recovered phenotypes of a mouse HD model. In this study, we generate multiple Drosophila HD models that express mutant huntingtin (Htt) in eye or motor neuron by different drivers and show various phenotypes. In such fly models, Ku70 co-expression recovers lifespan, locomotive activity and eye degeneration. In contrast, Ku70 reduction by heterozygous null mutation or siRNA-mediated knock down accelerates lifespan shortening and locomotion disability. These results collectively support that Ku70 is a critical mediator of the HD pathology and a candidate therapeutic target in HD.

Indexed as

AnimalsAntigens, NuclearDisease Models, AnimalDNA-Binding ProteinsDNA DamageDrosophilaDrosophila ProteinsHuntingtin ProteinHuntington DiseaseKu AutoantigenLocomotionMicrotubule-Associated ProteinsMutationNeuronsRNA, Small InterferingAntigens, NuclearDNA-Binding ProteinsDrosophila ProteinsHtt protein, DrosophilaHuntingtin ProteinKu AutoantigenMicrotubule-Associated ProteinsRNA, Small InterferingXrcc6 protein, mouse

Identifiers

PMID22096569
PMCPMC3210167
OpenAlexW2013341319

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.