Evidence map›Paper›PMID 21293491›Full record

ArticleCell death and differentiation2011

Control of AIF-mediated cell death by antagonistic functions of CHIP ubiquitin E3 ligase and USP2 deubiquitinating enzyme.

K H Oh, S W Yang, J M Park, J H Seol, S Iemura, T Natsume, S Murata, K Tanaka, Y J Jeon, C H Chung

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. USP2-Related Cellular Signaling and Consequent Pathophysiological Outcomes.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Diverse roles of C-terminal Hsp70-interacting protein (CHIP) in tumorigenesis.Journal of cancer research and clinical oncology · 2014
    Review
  19. Article
  20. USP47 and C terminus of Hsp70-interacting protein (CHIP) antagonistically regulate katanin-p60-mediated axonal growth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    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

10 authors at 5 institutions in 2 countries.

K H OhSchool of Biological Sciences, Seoul National University, Seoul, Korea.
S W Yang
J M Park
J H Seol
S Iemura
T Natsume
S Murata
K Tanaka
Y J Jeon
C H Chung
Seoul National University · KRAdvanced Institute of Industrial Technology · JPNational Institute of Advanced Industrial Science and Technology · JPThe University of Tokyo · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis inducing factor (AIF) is a mitochondrial oxidoreductase that scavenges reactive oxygen species under normal conditions. Under certain stresses, such as exposure to N-methyl-N'-nitro-N'-nitrosoguanidine (MNNG), AIF is truncated and released from the mitochondria and translocated into the nucleus, where the truncated AIF (tAIF) induces caspase-independent cell death. However, it is unknown how cells decide to kill themselves or operate ways to survive when they encounter stresses that induce the release of tAIF. Here, we demonstrated that USP2 and CHIP contribute to the control of tAIF stability. USP2 deubiquitinated and stabilized tAIF, thus promoting AIF-mediated cell death. In contrast, CHIP ubiquitinated and destabilized tAIF, thus preventing the cell death. Consistently, CHIP-deficient cells showed an increased sensitivity to MNNG. On the other hand, knockdown of USP2 attenuated MNNG-induced cell death. Moreover, exposure to MNNG caused a dramatic decrease in CHIP level, but not that of USP2, concurrent with cell shrinkage and chromatin condensation. These findings indicate that CHIP and USP2 show antagonistic functions in the control of AIF-mediated cell death, and implicate the role of the enzymes as a switch for cells to live or die under stresses that cause tAIF release.

Indexed as

AnimalsApoptosis Inducing FactorCell DeathChromatinEndopeptidasesHEK293 CellsHeLa CellsHumansMiceProtein StabilityReactive Oxygen SpeciesUbiquitinationUbiquitin-Protein LigasesUbiquitin ThiolesteraseApoptosis Inducing FactorChromatinEndopeptidasesReactive Oxygen SpeciesSTUB1 protein, humanUbiquitin-Protein LigasesUbiquitin ThiolesteraseUSP2 protein, human

Identifiers

PMID21293491
PMCPMC3172096
OpenAlexW2058020340

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.