Evidence map›Paper›PMID 34435379›Full record

ArticleThe EMBO journal2021

NDST3 deacetylates α-tubulin and suppresses V-ATPase assembly and lysosomal acidification.

Qing Tang, Mingming Liu, Yang Liu, Ran-Der Hwang, Tao Zhang, Jiou Wang

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Defective Lamtor5 Leads to Autoimmunity by Deregulating v-ATPase and Lysosomal Acidification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Tubulin deacetylase NDST3 modulates lysosomal acidification: Implications in neurological diseases.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022
    Article
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Qing TangDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.ORCID 0000-0002-0946-7171
Mingming LiuDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Yang LiuDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Ran-Der HwangDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Tao ZhangDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Jiou WangDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.ORCID 0000-0001-9115-8708
Johns Hopkins University · US

Funding

Neurodegeneration and Proteotoxicity Dissected in C. elegans and MammalsR01NS074324 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WANG, JIOU · 2011 to 2025
$6.2M
Investigating the role of C9orf72 in autophagic and metabolic dysregulation in ALS/FTDR01NS089616 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Jiou Wang · 2015 to 2026
$6.0M
Mechanisms of RNA and Protein Dysregulations in ALS/FTD Associated with FUS and Ubiquilin 2R01NS110098 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Jiou Wang · 2019 to 2026
$5.0M
VA Biorepository Brain BankI01BX002466 · VA · VA BOSTON HEALTH CARE SYSTEM · PI Ann C. McKee, Haining Zhu · 2014 to 2026
–
BLRD VA I01 BX002466NINDS NIH HHS R01 NS074324NINDS NIH HHS R01 NS089616NINDS NIH HHS R01 NS110098
6 · The paper itself

Abstract

Lysosomes are key organelles maintaining cellular homeostasis in health and disease. Here, we report the identification of N-deacetylase and N-sulfotransferase 3 (NDST3) as a potent regulator of lysosomal functions through an unbiased genetic screen. NDST3 constitutes a new member of the histone deacetylase (HDAC) family and catalyzes the deacetylation of α-tubulin. Loss of NDST3 promotes assembly of the V-ATPase holoenzyme on the lysosomal membrane and thereby increases the acidification of the organelle. NDST3 is downregulated in tissues and cells from patients carrying the C9orf72 hexanucleotide repeat expansion linked to the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Deficiency in C9orf72 decreases the level of NDST3, and downregulation of NDST3 exacerbates the proteotoxicity of poly-dipeptides generated from the C9orf72 hexanucleotide repeats. These results demonstrate a previously unknown regulatory mechanism through which microtubule acetylation regulates lysosomal activities and suggest that NDST3 could be targeted to modulate microtubule and lysosomal functions in relevant diseases.

Indexed as

AcetylationAmyotrophic Lateral SclerosisAnimalsC9orf72 ProteinCell LineCRISPR-Cas SystemsFluorescent Antibody TechniqueGene ExpressionGene Knockdown TechniquesGene LibraryGenes, ReporterHumansHydrogen-Ion ConcentrationLysosomesMacrolidesMiceC9orf72 Proteinheparitin sulfotransferaseMacrolidesSulfotransferasesTubulinVacuolar Proton-Translocating ATPasesamyotrophic lateral sclerosislysosomal acidificationmicrotubule acetylationN-deacetylase and N-sulfotransferase 3V-ATPase assembly

Identifiers

PMID34435379
PMCPMC8488563
OpenAlexW3195198619

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.