Evidence map›Paper›PMID 30143980›Full record

ArticleNeuroscience bulletin2018

Loss of VAPB Regulates Autophagy in a Beclin 1-Dependent Manner.

Dan Wu, Zongbing Hao, Haigang Ren, Guanghui Wang

Open access · bronzeAbstract read
In one paragraph

Article in Neuroscience bulletin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. ALS-Linked VapB P56S Mutation Alters Neuronal Mitochondrial Turnover at the Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  4. Article
  5. Review
  6. Effect of moxibustion on autophagy and the inflammatory response of synovial cells in rheumatoid arthritis model rat.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022
    Article
  7. Sequestosome 1 Is Part of the Interaction Network of VAPB.International journal of molecular sciences · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. 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 1 institution in 1 country.

Dan WuLaboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, 215021, China.ORCID http://orcid.org/0000-0001-5313-4510
Zongbing HaoLaboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, 215021, China.
Haigang RenLaboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, 215021, China. rhg@suda.edu.cn.ORCID http://orcid.org/0000-0001-8844-4754
Guanghui WangLaboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, 215021, China. wanggh@suda.edu.cn.ORCID http://orcid.org/0000-0001-8551-6468
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an evolutionarily-conserved self-degradative process that maintains cellular homeostasis by eliminating protein aggregates and damaged organelles. Recently, vesicle-associated membrane protein-associated protein B (VAPB), which is associated with the familial form of amyotrophic lateral sclerosis, has been shown to regulate autophagy. In the present study, we demonstrated that knockdown of VAPB induced the up-regulation of beclin 1 expression, which promoted LC3 (microtubule-associated protein light chain 3) conversion and the formation of LC3 puncta, whereas overexpression of VAPB inhibited these processes. The regulation of beclin 1 by VAPB was at the transcriptional level. Moreover, knockdown of VAPB increased autophagic flux, which promoted the degradation of the autophagy substrate p62 and neurodegenerative disease proteins. Our study provides evidence that the regulation of autophagy by VAPB is associated with the autophagy-initiating factor beclin 1.

Indexed as

AutophagyBeclin-1Cell Line, TransformedGene Expression RegulationGreen Fluorescent ProteinsHumansMicrotubule-Associated ProteinsRNA-Binding ProteinsRNA, MessengerRNA, Small InterferingR-SNARE ProteinsTransfectionBeclin-1BECN1 protein, humanGreen Fluorescent ProteinsMAP1LC3B protein, humanMicrotubule-Associated ProteinsP62 protein, humanRNA-Binding ProteinsRNA, MessengerRNA, Small InterferingR-SNARE ProteinsALSAutophagic fluxAutophagyBeclin 1LC3VAPB

Identifiers

PMID30143980
PMCPMC6246830
OpenAlexW2888591933

What OpenQuestion holds

Textmetadata
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.