Evidence map›Paper›PMID 32415281›Full record

ArticleCell death and differentiation2020

Staufen 1 amplifies proapoptotic activation of the unfolded protein response.

Mandi Gandelman, Warunee Dansithong, Karla P Figueroa, Sharan Paul, Daniel R Scoles, Stefan M Pulst

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. A genome-wide association study identified 10 novel genomic loci associated with intrinsic capacity.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. RNA-binding protein signaling in adult neurogenesis.Frontiers in cell and developmental biology · 2022
    Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Mandi GandelmanDepartment of Neurology, University of Utah, 175 North Medical Drive East, 5th Floor, Salt Lake City, UT, 84132, USA.
Warunee DansithongDepartment of Neurology, University of Utah, 175 North Medical Drive East, 5th Floor, Salt Lake City, UT, 84132, USA.
Karla P FigueroaDepartment of Neurology, University of Utah, 175 North Medical Drive East, 5th Floor, Salt Lake City, UT, 84132, USA.
Sharan PaulDepartment of Neurology, University of Utah, 175 North Medical Drive East, 5th Floor, Salt Lake City, UT, 84132, USA.
Daniel R ScolesDepartment of Neurology, University of Utah, 175 North Medical Drive East, 5th Floor, Salt Lake City, UT, 84132, USA.
Stefan M PulstDepartment of Neurology, University of Utah, 175 North Medical Drive East, 5th Floor, Salt Lake City, UT, 84132, USA. Stefan.pulst@hsc.utah.edu.
University of Utah · US

Funding

Spinocerebellar Ataxia Type 2 Gene and Gene ProductR37NS033123 · NINDS · UNIVERSITY OF UTAH · PI PULST, STEFAN M. · 2014 to 2020
$3.6M
RNA Granules in Cerebellar NeurodegenerationR01NS097903 · NINDS · UNIVERSITY OF UTAH · PI SCOLES, DANIEL R · 2017 to 2021
$2.7M
Antisense Oligonucleotides for treating Spinocerebellar Ataxia Type 2U01NS103883 · NINDS · UNIVERSITY OF UTAH · PI PULST, STEFAN M., SCOLES, DANIEL R · 2018 to 2020
$1.9M
Characterization of ATXN2 as a target for ALS in SCA2 motor neuronsR21NS103009 · NINDS · UNIVERSITY OF UTAH · PI PULST, STEFAN M., SCOLES, DANIEL R · 2018 to 2019
$419k
Antisense oligonucleotides for the treatment of spinocerebellar ataxia type 2R21NS081182 · NINDS · UNIVERSITY OF UTAH · PI PULST, STEFAN M., SCOLES, DANIEL R · 2013 to 2014
$408k
NINDS NIH HHS R01 NS097903NINDS NIH HHS R21 NS081182NINDS NIH HHS R21 NS103009NINDS NIH HHS R37 NS033123NINDS NIH HHS U01 NS103883
6 · The paper itself

Abstract

Staufen-1 (STAU1) is an RNA-binding protein that becomes highly overabundant in numerous neurodegenerative disease models, including those carrying mutations in presenilin1 (PSEN1), microtubule-associated protein tau (MAPT), huntingtin (HTT), TAR DNA-binding protein-43 gene (TARDBP), or C9orf72. We previously reported that elevations in STAU1 determine autophagy defects and its knockdown is protective in models of several neurodegenerative diseases. Additional functional consequences of STAU1 overabundance, however, have not been investigated. We studied the role of STAU1 in the chronic activation of the unfolded protein response (UPR), a common feature among neurodegenerative diseases and often directly associated with neuronal death. Here we report that STAU1 is a novel modulator of the UPR, and is required for apoptosis induced by activation of the PERK-CHOP pathway. STAU1 levels increased in response to multiple endoplasmic reticulum (ER) stressors, and exogenous expression of STAU1 was sufficient to cause apoptosis through the PERK-CHOP pathway of the UPR. Cortical neurons and skin fibroblasts derived from Stau1

Indexed as

Endoplasmic Reticulum StressAnimalsAutophagyFibroblastsHEK293 CellsHumansMiceMice, Inbred C57BLMice, KnockoutNeurodegenerative DiseasesNeuronsRNA-Binding ProteinsUnfolded Protein ResponseRNA-Binding ProteinsStau1 protein, mouse

Identifiers

PMID32415281
PMCPMC7492261
OpenAlexW3025263237

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.