Evidence map›Paper›PMID 23074225›Full record

ArticleThe Journal of biological chemistry2012

The p53-induced gene Ei24 is an essential component of the basal autophagy pathway.

Yan G Zhao, Hongyu Zhao, Lin Miao, Li Wang, Fei Sun, Hong Zhang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  9. Mitochondria-ER Tethering in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Role ofAutophagy · 2020
    Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  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 3 institutions in 1 country.

Yan G ZhaoState Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101 Beijing, P.R. China.
Hongyu Zhao
Lin Miao
Li Wang
Fei Sun
Hong Zhang
National Institute of Biological Sciences, Beijing · CNChinese Academy of Sciences · CNInstitute of Biophysics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ei24 is a DNA damage response gene involved in growth suppression and apoptosis. The physiological function of Ei24, however, is poorly understood. Here we generated conditional knock-out mice of Ei24 and demonstrated that EI24 is an essential component of the basal autophagy pathway. Mice with neural-specific Ei24 deficiency develop age-dependent neurological abnormalities caused by massive axon degeneration and extensive neuron loss in brain and spinal cord. Notably, ablation of Ei24 leads to vacuolated oligodendroglial cells and demyelination of axons. Liver-specific depletion of Ei24 causes severe hepatomegaly with hepatocyte hypertrophy. Ei24 deficiency impairs autophagic flux, leading to accumulation of LC3, p62 aggregates, and ubiquitin-positive inclusions. Our study indicates that Ei24 is an essential autophagy gene and plays an important role in clearance of aggregate-prone proteins in neurons and hepatocytes.

Indexed as

AnimalsApoptosis Regulatory ProteinsAutophagyAxonsHepatocytesHeredodegenerative Disorders, Nervous SystemMiceMice, TransgenicMicrotubule-Associated ProteinsNuclear ProteinsOligodendrogliaOrgan SpecificityTranscription FactorsTranscription Factor TFIIHApoptosis Regulatory ProteinsEI24 protein, mouseGtf2h1 protein, mouseMap1lc3b protein, mouseMicrotubule-Associated ProteinsNuclear ProteinsTranscription FactorsTranscription Factor TFIIH

Identifiers

PMID23074225
PMCPMC3516751
OpenAlexW2034130805

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.