Evidence map›Paper›PMID 21959934›Full record

ArticleCell death and differentiation2012

Loss of programmed cell death 4 induces apoptosis by promoting the translation of procaspase-3 mRNA.

K Eto, S Goto, W Nakashima, Y Ura, S-I Abe

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  14. Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions.International journal of molecular sciences · 2019
    Review
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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.

K EtoDepartment of Biological Sciences, Graduate School of Science and Technology, Kumamoto University, Japan. etoko@gpo.kumamoto-u.ac.jp
S Goto
W Nakashima
Y Ura
S-I Abe
Kumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The programmed cell death 4 (Pdcd4), a translation inhibitor, plays an essential role in tumor suppression, but its role in apoptosis remains unclear. Here we show that Pdcd4 is a critical suppressor of apoptosis by inhibiting the translation of procaspase-3 mRNA. Pdcd4 protein decreased more rapidly through microRNA-mediated translational repression following apoptotic stimuli than did the activation of procaspase-3, cleavage of poly(ADP)ribose polymerase (PARP) by active caspase-3, and nuclear fragmentation. Strikingly, the loss of Pdcd4 by the specific RNA interference increased procaspase-3 expression, leading to its activation and PARP cleavage even without apoptotic stimuli, and sensitized the cells to apoptosis. Thus, our findings provide insight into a novel mechanism for Pdcd4 as a regulator of apoptosis.

Indexed as

ApoptosisApoptosis Regulatory ProteinsCaspase 3Gene Expression Regulation, EnzymologicHeLa CellsHumansProtein BiosynthesisRNA-Binding ProteinsRNA, MessengerApoptosis Regulatory ProteinsCaspase 3PDCD4 protein, humanRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID21959934
PMCPMC3307972
OpenAlexW1967600311

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.