Evidence map›Paper›PMID 33184261›Full record

ArticleNature communications2020

Akt1 and dCIZ1 promote cell survival from apoptotic caspase activation during regeneration and oncogenic overgrowth.

Gongping Sun, Xun Austin Ding, Yewubdar Argaw, Xiaoran Guo, Denise J Montell

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. 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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 64 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Gongping SunThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Anatomy and Histoembryology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China. sgp@sdu.edu.cn.
Xun Austin DingMolecular, Cellular, and Developmental Biology Department, University of California, Santa Barbara, CA, 93106, USA.
Yewubdar ArgawMolecular, Cellular, and Developmental Biology Department, University of California, Santa Barbara, CA, 93106, USA.
Xiaoran GuoMolecular, Cellular, and Developmental Biology Department, University of California, Santa Barbara, CA, 93106, USA.ORCID 0000-0002-3011-4514
Denise J MontellMolecular, Cellular, and Developmental Biology Department, University of California, Santa Barbara, CA, 93106, USA. dmontell@ucsb.edu.ORCID 0000-0001-8924-5925
University of California, Santa Barbara · USShandong University · CN

Funding

Anastasis, a new mechanism driving cell survival and evolutionDP1CA195760 · NCI · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI MONTELL, DENISE J. · 2014 to 2018
$3.8M
NCI NIH HHS DP1 CA195760
6 · The paper itself

Abstract

Apoptosis is an ancient and evolutionarily conserved cell suicide program. During apoptosis, executioner caspase enzyme activation has been considered a point of no return. However, emerging evidence suggests that some cells can survive caspase activation following exposure to apoptosis-inducing stresses, raising questions as to the physiological significance and underlying molecular mechanisms of this unexpected phenomenon. Here, we show that, following severe tissue injury, Drosophila wing disc cells that survive executioner caspase activation contribute to tissue regeneration. Through RNAi screening, we identify akt1 and a previously uncharacterized Drosophila gene CG8108, which is homologous to the human gene CIZ1, as essential for survival from the executioner caspase activation. We also show that cells expressing activated oncogenes experience apoptotic caspase activation, and that Akt1 and dCIZ1 are required for their survival and overgrowth. Thus, survival following executioner caspase activation is a normal tissue repair mechanism usurped to promote oncogene-driven overgrowth.

Indexed as

Cell SurvivalAnimalsApoptosisCarcinogenesisCaspasesCell DeathDrosophilaDrosophila ProteinsHumansNuclear ProteinsOncogenesProto-Oncogene Proteins c-aktRNA InterferenceTranscription FactorsWings, AnimalZinc FingersAkt1 protein, DrosophilaAKT1 protein, humanCaspasesCiz1 protein, humanDrosophila ProteinsGAL4 protein, DrosophilaNuclear ProteinsProto-Oncogene Proteins c-aktTranscription Factors

Identifiers

PMID33184261
PMCPMC7664998
OpenAlexW3098198823

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.