Evidence map›Paper›PMID 25956028›Full record

ReviewThe American journal of pathology2015

Multiple Mechanisms of Unfolded Protein Response-Induced Cell Death.

Nobuhiko Hiramatsu, Wei-Chieh Chiang, Timothy D Kurt, Christina J Sigurdson, Jonathan H Lin

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 183 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Comprehensive analysis of the potential role of Ferroptosis-related genes in glioblastoma multiforme.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  5. Ambiguous Role of p53 in Transcription-Dependent Tumor Cell Death.International journal of molecular sciences · 2026
    Review
  6. Developmentally-regulated post-apocrine cell death ofFrontiers in cell and developmental biology · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Comparative Multi-Omics Analysis and Antitumor Activity ofJournal of microbiology and biotechnology · 2025
    Article
  11. Sigma-1 Receptor Activation by Fluvoxamine Ameliorates ER Stress, Synaptic Dysfunction and Behavioral Deficits in a Ketamine Model of Schizophrenia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  12. Article
  13. Article
  14. Unraveling the Connection: Pain and Endoplasmic Reticulum Stress.International journal of molecular sciences · 2024
    Review
  15. Review
  16. Article
  17. Review
  18. Immunomodulatory and Antioxidant Drugs in Glaucoma Treatment.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  19. Review
  20. Article

55 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Nobuhiko HiramatsuDepartment of Pathology, University of California-San Diego, La Jolla, California.
Wei-Chieh ChiangDepartment of Pathology, University of California-San Diego, La Jolla, California.
Timothy D KurtDepartment of Pathology, University of California-San Diego, La Jolla, California.
Christina J SigurdsonDepartment of Pathology, University of California-San Diego, La Jolla, California.
Jonathan H LinDepartment of Pathology, University of California-San Diego, La Jolla, California. Electronic address: jlin@ucsd.edu.
University of California, San Diego · US

Funding

Mechanisms of Prion Aggregation and Species BarriersR01NS069566 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ESKO, JEFFREY D, RAVITS, JOHN · 2011 to 2025
$5.7M
Mechanisms of Prion SpreadR01NS076896 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SIGURDSON, CHRISTINA · 2012 to 2021
$3.4M
Protein Homeostasis and Proteotoxicity MechanismsR01NS088485 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIN, JONATHAN · 2015 to 2024
$3.0M
UCSD Research Training Program for VeterinariansT32OD017863 · OD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ERNST, PETER B., SIGURDSON, CHRISTINA · 2014 to 2023
$2.0M
Endoplasmic Reticulum Stress in Retinal DegenerationR01EY020846 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIN, JONATHAN · 2010 to 2014
$1.9M
Investigating molecular mechanisms of cross-species prion transmissionK01OD019919 · OD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KURT, TIMOTHY DANIEL · 2015 to 2016
$176k
Cellular and Molecular Mechanisms of Age-Related Retinal DegenerationI01BX002284 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI LIN, JONATHAN · 2014 to 2023
–
BLRD VA I01 BX002284NEI NIH HHS R01 EY020846NEI NIH HHS R01EY020846NIH HHS K01 OD019919NIH HHS T32 OD017863NINDS NIH HHS R01 NS069566NINDS NIH HHS R01NS069566NINDS NIH HHS R01 NS076896NINDS NIH HHS R01NS076896NINDS NIH HHS R01 NS088485NINDS NIH HHS R01NS088485
6 · The paper itself

Abstract

Eukaryotic cells fold and assemble membrane and secreted proteins in the endoplasmic reticulum (ER), before delivery to other cellular compartments or the extracellular environment. Correctly folded proteins are released from the ER, and poorly folded proteins are retained until they achieve stable conformations; irreparably misfolded proteins are targeted for degradation. Diverse pathological insults, such as amino acid mutations, hypoxia, or infection, can overwhelm ER protein quality control, leading to misfolded protein buildup, causing ER stress. To cope with ER stress, eukaryotic cells activate the unfolded protein response (UPR) by increasing levels of ER protein-folding enzymes and chaperones, enhancing the degradation of misfolded proteins, and reducing protein translation. In mammalian cells, three ER transmembrane proteins, inositol-requiring enzyme-1 (IRE1; official name ERN1), PKR-like ER kinase (PERK; official name EIF2AK3), and activating transcription factor-6, control the UPR. The UPR signaling triggers a set of prodeath programs when the cells fail to successfully adapt to ER stress or restore homeostasis. ER stress and UPR signaling are implicated in the pathogenesis of diverse diseases, including neurodegeneration, cancer, diabetes, and inflammation. This review discusses the current understanding in both adaptive and apoptotic responses as well as the molecular mechanisms instigating apoptosis via IRE1 and PERK signaling. We also examine how IRE1 and PERK signaling may be differentially used during neurodegeneration arising in retinitis pigmentosa and prion infection.

Indexed as

ApoptosisSignal TransductionUnfolded Protein ResponseAnimalsAwards and PrizeseIF-2 KinaseEndoplasmic ReticulumEndoplasmic Reticulum StressEndoribonucleasesEukaryotic CellsHumansMammalsModels, BiologicalMolecular ChaperonesPathologyProtein BiosynthesiseIF-2 KinaseEndoribonucleasesERN1 protein, humanMolecular ChaperonesProtein Serine-Threonine Kinases

Identifiers

PMID25956028
PMCPMC4484218
OpenAlexW1651776210

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.