Evidence map›Paper›PMID 23059819›Full record

ArticleCell death & disease2012

p53 is a major component of the transcriptional and apoptotic program regulated by PI 3-kinase/Akt/GSK3 signaling.

G Nayak, G M Cooper

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Activation of Galanin Receptor 1 with M617 Attenuates Neuronal Apoptosis via ERK/GSK-3β/TIP60 Pathway After Subarachnoid Hemorrhage in Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  4. 1,25(OH)International journal of molecular sciences · 2020
    Article
  5. TGF-β1-p53 cooperativity regulates a profibrotic genomic program in the kidney: molecular mechanisms and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. p53: key conductor of all anti-acne therapies.Journal of translational medicine · 2017
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. TAp73 promotes anabolism.Oncotarget · 2014
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Molecular dynamics of the full-length p53 monomer.Cell cycle (Georgetown, Tex.) · 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

2 authors at 1 institution in 1 country.

G NayakDepartment of Biology, Boston University, Boston, MA 02215, USA.
G M Cooper
Boston University · US

Funding

Regulation of apoptosis by PI 3-kinase/Akt signalingR01CA018689 · NCI · DANA-FARBER CANCER INSTITUTE · PI COOPER, GEOFFREY M · 1985 to 2012
$6.2M
NCI NIH HHS R01 CA018689
6 · The paper itself

Abstract

The phosphatidylinositol (PI) 3-kinase/Akt signaling pathway has a prominent role in cell survival and proliferation, in part, by regulating gene expression at the transcriptional level. Previous work using global expression profiling identified FOXOs and the E-box-binding transcription factors MITF and USF1 as key targets of PI 3-kinase signaling that lead to the induction of proapoptotic and cell cycle arrest genes in response to inhibition of PI 3-kinase. In this study, we investigated the role of p53 downstream of PI 3-kinase signaling by analyzing the effects of inhibition of PI 3-kinase in Rat-1 cells, which have wild-type p53, compared with Rat-1 cells expressing a dominant-negative p53 mutant. Expression of dominant-negative p53 conferred partial resistance to apoptosis induced by inhibition of PI 3-kinase. Global gene expression profiling combined with computational and experimental analysis of transcription factor binding sites demonstrated that p53, along with FOXO, MITF and USF1, contributed to gene induction in response to PI 3-kinase inhibition. Activation of p53 was mediated by phosphorylation of the histone acetyltransferase Tip60 by glycogen synthase kinase (GSK) 3, leading to activation of p53 by acetylation. Many of the genes targeted by p53 were also targeted by FOXO and E-box-binding transcription factors, indicating that p53 functions coordinately with these factors to regulate gene expression downstream of PI 3-kinase/Akt/GSK3 signaling.

Indexed as

Signal TransductionAnimalsApoptosisCell LineForkhead Box Protein O1Forkhead Box Protein O3Forkhead Transcription FactorsGlycogen Synthase Kinase 3Histone AcetyltransferasesMicrophthalmia-Associated Transcription FactorNerve Tissue ProteinsPhosphatidylinositol 3-KinasePhosphorylationProtein BindingProto-Oncogene Proteins c-aktRatsForkhead Box Protein O1Forkhead Box Protein O3Forkhead Transcription FactorsFoxo1 protein, ratFOXO3 protein, ratGlycogen Synthase Kinase 3Histone AcetyltransferasesMicrophthalmia-Associated Transcription FactorNerve Tissue ProteinsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktTumor Suppressor Protein p53Upstream Stimulatory FactorsUsf1 protein, rat

Identifiers

PMID23059819
PMCPMC3481126
OpenAlexW2043012035

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.