Evidence map›Paper›PMID 28819043›Full record

ArticleDisease models & mechanisms2017

Increased acetylation of microtubules rescues human tau-induced microtubule defects and neuromuscular junction abnormalities in

Chuan-Xi Mao, Xue Wen, Shan Jin, Yong Q Zhang

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Tubulin Acetylation: A Critical Regulator of Microtubule Function.Results and problems in cell differentiation · 2025
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Chronic MAP4343 reverses escalated alcohol drinking in a mouse model of alcohol use disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Chuan-Xi MaoKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.ORCID 0000-0002-0220-4141
Xue WenCollege of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.
Shan JinCollege of Life Sciences, Hubei University, Wuhan, Hubei 430062, China yqzhang@genetics.ac.cn jinshan@hubu.edu.cn.ORCID 0000-0002-3392-3851
Yong Q ZhangKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China yqzhang@genetics.ac.cn jinshan@hubu.edu.cn.ORCID 0000-0003-0581-4882
Chinese Academy of Sciences · CNHubei University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tau normally associates with and stabilizes microtubules (MTs), but is hyperphosphorylated and aggregated into neurofibrillary tangles in Alzheimer's disease and related neurodegenerative diseases, which are collectively known as tauopathies. MTs are regulated by different forms of post-translational modification, including acetylation; acetylated MTs represent a more stable microtubule population. In our previous study, we showed that inhibition of histone deacetylase 6 (HDAC6), which deacetylates tubulin at lysine 40, rescues defects in MTs and in neuromuscular junction growth caused by tau overexpression. However, HDAC6 also acts on other proteins that are involved in distinct biological processes unrelated to tubulins. In order to examine directly the role of increased tubulin acetylation against tau toxicity, we generated a site-directed

Indexed as

AcetylationAnimalsAnimals, Genetically ModifiedDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsGenetic Predisposition to DiseaseHistone Deacetylase 6Histone Deacetylase InhibitorsHumansMicrotubulesMutationNeuromuscular JunctionPhenotypeTauopathiestau ProteinsDrosophila ProteinsHDAC6 protein, DrosophilaHistone Deacetylase 6Histone Deacetylase InhibitorsMAPT protein, humantau ProteinsAcetylationDrosophilaMicrotubuleTauopathy

Identifiers

PMID28819043
PMCPMC5665452
OpenAlexW2748286811

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.