Evidence map›Paper›PMID 36271102›Full record

ArticleScientific reports2022

Transcriptional targets of senataxin and E2 promoter binding factors are associated with neuro-degenerative pathways during increased autophagic flux.

Aaron E Casey, Wenjun Liu, Leanne K Hein, Timothy J Sargeant, Stephen M Pederson, Ville-Petteri Mäkinen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Role of Senataxin in Amyotrophic Lateral Sclerosis.Journal of molecular neuroscience : MN · 2023
    Review
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 2 countries.

Aaron E Casey *Computational and Systems Biology Program, Precision Medicine Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, SA, 5000, Australia. aaron.casey@sahmri.com.
Wenjun Liu *Dame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Leanne K HeinLysosomal Health in Ageing, Hopwood Centre for Neurobiology, Lifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, Australia.
Timothy J SargeantLysosomal Health in Ageing, Hopwood Centre for Neurobiology, Lifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, Australia.
Stephen M PedersonDame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Ville-Petteri MäkinenComputational and Systems Biology Program, Precision Medicine Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, SA, 5000, Australia.
South Australian Health and Medical Research Institute · AUUniversity of Adelaide · AUUniversity of Oulu · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an intracellular recycling process that degrades harmful molecules and enables survival during starvation, with implications for diseases including dementia, cancer and atherosclerosis. Previous studies demonstrate how a limited number of transcription factors (TFs) can increase autophagy. However, this knowledge has not resulted in translation into therapy, thus, to gain understanding of more suitable targets, we utilized a systems biology approach. We induced autophagy by amino acid starvation and mTOR inhibition in HeLa, HEK 293 and SH-SY5Y cells and measured temporal gene expression using RNA-seq. We observed 456 differentially expressed genes due to starvation and 285 genes due to mTOR inhibition (P

Indexed as

DNA HelicasesMultifunctional EnzymesRNA HelicasesAmino AcidsAutophagyCell Line, TumorHEK293 CellsHumansTOR Serine-Threonine KinasesTranscription FactorsAmino AcidsDNA HelicasesMultifunctional EnzymesRNA HelicasesSETX protein, humanTOR Serine-Threonine KinasesTranscription Factors

Identifiers

PMID36271102
PMCPMC9587291
OpenAlexW4306989167

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.