Evidence map›Paper›PMID 19357962›Full record

ArticleJournal of neuro-oncology2009

Simultaneous phosphorylation of p53 at serine 15 and 20 induces apoptosis in human glioma cells by increasing expression of pro-apoptotic genes.

Toshiyuki Amano, Akira Nakamizo, Sandip K Mishra, Joy Gumin, Naoki Shinojima, Raymond Sawaya, Frederick F Lang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

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  16. Transformation of somatic cells into stem cell-like cells under a stromal niche.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
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  18. ASPP1/2 regulate p53-dependent death of retinal ganglion cells through PUMA and Fas/CD95 activation in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
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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

7 authors at 1 institution in 2 countries.

Toshiyuki AmanoDepartment of Neurosurgery, Unit 442, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030-4009, USA.
Akira Nakamizo
Sandip K Mishra
Joy Gumin
Naoki Shinojima
Raymond Sawaya
Frederick F Lang
The University of Texas MD Anderson Cancer Center · US

Funding

Regulation of p53-mediated apoptosis in gliomasR01CA098716 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LANG, FREDERICK F · 2003 to 2007
$1.3M
NCI NIH HHS CA098716
6 · The paper itself

Abstract

Understanding the mechanism underlying p53's ability to induce cell cycle arrest versus apoptosis is critical to treating human gliomas, 70% of which contain wild-type p53. Although N-terminal phosphorylation results in activation of p53, the role of N-terminal phosphorylation, particularly at serines 15 and 20, in p53's ability to induce cell cycle arrest versus apoptosis remains controversial. Here we test the hypothesis that phosphorylation of serine 15 and/or 20 is causally related to p53-mediated apoptosis in human gliomas. Introduction of p53 plasmids containing alanine mutations at serine 15 or/and serine 20 (which block phosphorylation) or aspartate mutations (which mimic phosphorylation) at the same sites, implicated simultaneous phosphorylation of both sites in the induction of apoptosis. When a double phosphorylation-mimicking adenoviral p53 vector (Ad-p53-15D20D) was compared with an unphosphorylated p53 vector (Ad-p53), treatment with Ad-p53 resulted in G1-arrest, whereas Ad-p53-15D20D induced apoptosis. These effects occurred independent of phosphorylation of other N-terminal serine (i.e., serines 6, 9, 33, 37, 46) indicating that phosphorylation of S15 and S20 is sufficient for inducing apoptosis. Mechanistically, Ad-p53 was capable only of increasing the expression of p21/CIP, whereas Ad-p53-15D20D increased the binding to and expression of the pro-apoptotic genes Fas, Puma and PIG3. However, Ad-p53-15D20D did not alter the expression of Noxa, Bid, IGFBP3, PERP and Killer/DR5, suggesting that phosphorylation of S15 and S20 resulted in the expression of specific pro-apoptotic gene. In conclusion, simultaneous phosphorylation of S15 and S20 is causally associated with apoptosis, resulting in increased expression of specific p53-responsive pro-apoptotic genes.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBlotting, WesternBrain NeoplasmsCell CycleCell Line, TumorFlow CytometryGene ExpressionGliomaHumansImmunoprecipitationMutationPhosphorylationSerineTumor Suppressor Protein p53SerineTumor Suppressor Protein p53

Identifiers

PMID19357962
OpenAlexW2092409426

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.