Evidence map›Paper›PMID 24008732›Full record

ArticleCell death & disease2013

ING1 induces apoptosis through direct effects at the mitochondria.

P Bose, S Thakur, S Thalappilly, B Y Ahn, S Satpathy, X Feng, K Suzuki, S W Kim, K Riabowol

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. 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
2.4field-weighted citation impact, top 11% 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, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
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  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Senescence and Apoptosis: Architects of Mammalian Development.Frontiers in cell and developmental biology · 2020
    Review
  17. Review
  18. INGs are potential drug targets for cancer.Journal of cancer research and clinical oncology · 2017
    Review
  19. Article
  20. Histone modifications as regulators of life and death inMicrobial cell (Graz, Austria) · 2015
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

P BoseDepartment of Biochemistry and Molecular Biology, Southern Alberta Cancer Research Institute, University of Calgary, Calgary, Alberta, Canada.
S Thakur
S Thalappilly
B Y Ahn
S Satpathy
X Feng
K Suzuki
S W Kim
K Riabowol
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ING family of tumor suppressors acts as readers and writers of the histone epigenetic code, affecting DNA repair, chromatin remodeling, cellular senescence, cell cycle regulation and apoptosis. The best characterized member of the ING family, ING1,interacts with the proliferating cell nuclear antigen (PCNA) in a UV-inducible manner. ING1 also interacts with members of the14-3-3 family leading to its cytoplasmic relocalization. Overexpression of ING1 enhances expression of the Bax gene and was reported to alter mitochondrial membrane potential in a p53-dependent manner. Here we show that ING1 translocates to the mitochondria of primary fibroblasts and established epithelial cell lines in response to apoptosis inducing stimuli, independent of the cellular p53 status. The ability of ING1 to induce apoptosis in various breast cancer cell lines correlates well with its degree of translocation to the mitochondria after UV treatment. Endogenous ING1 protein specifically interacts with the pro-apoptotic BCL2 family member BAX, and colocalizes with BAX in a UV-inducible manner. Ectopic expression of a mitochondria-targeted ING1 construct is more proficient in inducing apoptosis than the wild type ING1 protein. Bioinformatic analysis of the yeast interactome indicates that yeast ING proteins interact with 64 mitochondrial proteins. Also, sequence analysis of ING1 reveals the presence of a BH3-like domain. These data suggest a model in which stress-induced cytoplasmic relocalization of ING1 by14-3-3 induces ING1-BAX interaction to promote mitochondrial membrane permeability and represent a paradigm shift in our understanding of ING1 function in the cytoplasm and its contribution to apoptosis [corrected].

Indexed as

Apoptosisbcl-2-Associated X ProteinHEK293 CellsHumansInhibitor of Growth Protein 1Intracellular Signaling Peptides and ProteinsMitochondriaMitochondrial ProteinsNuclear ProteinsProtein BindingProtein TransportSaccharomyces cerevisiae ProteinsStress, PhysiologicalTumor Suppressor Protein p53Tumor Suppressor ProteinsUltraviolet Raysbcl-2-Associated X ProteinING1 protein, humanInhibitor of Growth Protein 1Intracellular Signaling Peptides and ProteinsMitochondrial ProteinsNuclear ProteinsSaccharomyces cerevisiae ProteinsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID24008732
PMCPMC3789179
OpenAlexW1987978369

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.