Evidence map›Paper›PMID 37721642›Full record

ReviewJournal of cell communication and signaling2023

Dual RNase activity of IRE1 as a target for anticancer therapies.

Sylwia Bartoszewska, Jakub Sławski, James F Collawn, Rafał Bartoszewski

Abstract readReview
In one paragraph

Review in Journal of cell communication and signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Review
  3. The "cutting edge" of non-canonical RNA splicing.Frontiers in molecular biosciences · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Old drugs, new challenges: reassigning drugs for cancer therapies.Cellular & molecular biology letters · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. 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.

Sylwia BartoszewskaDepartment of Inorganic Chemistry, Medical University of Gdansk, Gdansk, Poland.
Jakub SławskiDepartment of Biophysics, Faculty of Biotechnology, University of Wrocław, F. Joliot-Curie 14a Street, 50-383, Wrocław, Poland.
James F CollawnDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, 35233, USA.
Rafał BartoszewskiDepartment of Biophysics, Faculty of Biotechnology, University of Wrocław, F. Joliot-Curie 14a Street, 50-383, Wrocław, Poland. rafal.bartoszewski@uwr.edu.pl.ORCID http://orcid.org/0000-0002-2864-6757

Funding

Narodowym Centrum Nauki UMO-2020/37/B/NZ3/00861
6 · The paper itself

Abstract

The unfolded protein response (UPR) is a cellular mechanism that protects cells during stress conditions in which there is an accumulation of misfolded proteins in the endoplasmic reticulum (ER). UPR activates three signaling pathways that function to alleviate stress conditions and promote cellular homeostasis and cell survival. During unmitigated stress conditions, however, UPR activation signaling changes to promote cell death through apoptosis. Interestingly, cancer cells take advantage of this pathway to facilitate survival and avoid apoptosis even during prolonged cell stress conditions. Here, we discuss different signaling pathways associated with UPR and focus specifically on one of the ER signaling pathways activated during UPR, inositol-requiring enzyme 1α (IRE1). The rationale is that the IRE1 pathway is associated with cell fate decisions and recognized as a promising target for cancer therapeutics. Here we discuss IRE1 inhibitors and how they might prove to be an effective cancer therapeutic.

Indexed as

Basal RIDDER-stressIRE1αRIDDUPRXBP1

Identifiers

PMID37721642
PMCPMC10713974

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.