Evidence map›Paper›PMID 25697356›Full record

ArticleThe Journal of biological chemistry2015

Proapoptotic activities of protein disulfide isomerase (PDI) and PDIA3 protein, a role of the Bcl-2 protein Bak.

Guoping Zhao, Huayi Lu, Chi Li

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Frontiers in cellular and infection microbiology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Antioxidants (Basel, Switzerland) · 2022
    Review
  11. ERp57/PDIA3: new insight.Cellular & molecular biology letters · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  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

3 authors at 2 institutions in 2 countries.

Guoping ZhaoFrom the Molecular Targets Program, Departments of Medicine, Pharmacology, and Toxicology, University of Louisville, Louisville, Kentucky 40202 and.
Huayi Luthe Second Hospital, Jilin University, Changchun, Jilin Province, China 130041.
Chi LiFrom the Molecular Targets Program, Departments of Medicine, Pharmacology, and Toxicology, University of Louisville, Louisville, Kentucky 40202 and chi.li@louisville.edu.
University of Louisville · USSecond Affiliated Hospital of Jilin University · CN

Funding

PROJ 12: STEM CELL-BASED VACCINE FOR CANCER PROPHYLAXISP20RR018733 · NCRR · UNIVERSITY OF LOUISVILLE · PI YADDANAPUDI, KAVITHA · 2003 to 2011
$18.9M
Activating Bax as a therapeutic strategy for lung cancerR01CA175003 · NCI · UNIVERSITY OF LOUISVILLE · PI LI, CHI · 2013 to 2017
$1.5M
Regulation of apoptosis by Bcl-XL, Bak and BaxK01CA106599 · NCI · UNIVERSITY OF PENNSYLVANIA · PI LI, CHI · 2005 to 2009
$787k
NCI NIH HHS CA106599NCI NIH HHS CA175003NCI NIH HHS K01 CA106599NCI NIH HHS R01 CA175003NCRR NIH HHS P20 RR018733NCRR NIH HHS RR018733
6 · The paper itself

Abstract

Protein disulfide isomerase (PDI) family proteins are classified as enzymatic chaperones for reconstructing misfolded proteins. Previous studies have shown that several PDI members possess potential proapoptotic functions. However, the detailed molecular mechanisms of PDI-mediated apoptosis are not completely known. In this study, we investigated how two members of PDI family, PDI and PDIA3, modulate apoptotic signaling. Inhibiting PDI and PDIA3 activities pharmacologically alleviates apoptosis induced by various apoptotic stimuli. Although a decrease of PDIA3 expression alleviates apoptotic responses, overexpression of PDIA3 exacerbates apoptotic signaling. Importantly, Bak, but not Bax, is essential for PDIA3-induced proapoptotic signaling. Furthermore, both purified PDI and PDIA3 proteins induce Bak-dependent, but not Bax-dependent, mitochondrial outer membrane permeabilization in vitro, probably through triggering Bak oligomerization on mitochondria. Our results suggest that both of PDI and PDIA3 possess Bak-dependent proapoptotic function through inducing mitochondrial outer membrane permeabilization, which provides a new mechanism linking ER chaperone proteins and apoptotic signaling.

Indexed as

ApoptosisAnimalsbcl-2 Homologous Antagonist-Killer ProteinBiocatalysisFluorescent Antibody TechniqueMiceProtein Disulfide-IsomerasesBak1 protein, mousebcl-2 Homologous Antagonist-Killer ProteinPdia3 protein, mouseProtein Disulfide-IsomerasesApoptosisBakBaxB Cell Lymphoma 2 (Bcl-2)Endoplasmic Reticulum (ER)Mitochondrial Outer Membrane PermeabilizationProtein Disulfide Isomerase

Identifiers

PMID25697356
PMCPMC4423685
OpenAlexW2323395911

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.