Evidence map›Paper›PMID 23475424›Full record

ArticleMolecules and cells2013

p53 and PI3K/AKT signalings are up-regulated in flies with defects in the THO complex.

Sungjin Moon, Yun Doo Chung

Open access · greenAbstract read
In one paragraph

Article in Molecules and cells, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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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

2 authors at 1 institution in 1 country.

Sungjin MoonDepartment of Life Science, University of Seoul, Seoul 130-743, Korea.
Yun Doo Chung
University of Seoul · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The THO complex (THO) is an evolutionary conserved protein required for the formation of export-competent mRNP. The growing evidence indicates that the metazoan THO plays important roles in cell differentiation and cellular stress response. But the underlying mechanisms are poorly understood. Herein we examined the relevance of THO to cellular signaling pathways involved in cell differentiation and cellular stress response. When we examined the endogenous p53 level in the testis, it was sustained much longer during spermatogenesis in the THO mutant compared to that of wild-type. In flies with impaired THO, overexpression of p53 by eye-specific GAL4 not only enhanced p53-mediated retinal degeneration, but p53 level was also elevated compared to the control flies. Since the body size of the THO mutant flies was significantly larger than control flies, we also examined whether the PI3K/AKT signaling is enhanced in the mutant flies. The results showed that the endogenous level of phosphorylated AKT, which is the active form, was highly elevated in the THO mutants. Taken together our results suggested that both p53 and PI3K/AKT signalings are up-regulated in the flies with impaired THO.

Indexed as

AnimalsBody SizeCompound Eye, ArthropodDrosophila melanogasterDrosophila ProteinsEpistasis, GeneticGene ExpressionMaleMultiprotein ComplexesMutationNuclear ProteinsPhosphatidylinositol 3-KinasesPhosphorylationPigmentationProtein Processing, Post-TranslationalProtein SubunitsDrosophila ProteinsGAL4 protein, DrosophilaMultiprotein ComplexesNuclear ProteinsPhosphatidylinositol 3-KinasesProtein SubunitsProto-Oncogene Proteins c-aktTHOC5 protein, DrosophilaTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID23475424
PMCPMC3887910
OpenAlexW2018067705

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.