Evidence map›Paper›PMID 10359526›Full record

ArticleOncogene1999

Mutations in serines 15 and 20 of human p53 impair its apoptotic activity.

T Unger, R V Sionov, E Moallem, C L Yee, P M Howley, M Oren, Y Haupt

Abstract read
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In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 191 citations in OpenAlex.

  1. Article
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  4. Translational Control inInternational journal of molecular sciences · 2019
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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
    Article
  19. Article
  20. Article

12 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

T UngerDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
R V Sionov
E Moallem
C L Yee
P M Howley
M Oren
Y Haupt
Weizmann Institute of Science · ILHarvard University · USNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphorylation of the p53 tumor suppressor protein is likely to play an important role in regulating its activity. To study the regulatory role of potential phosphorylation sites within the N-terminal transactivation domain of human p53 (hp53), a series of p53 serine mutants were evaluated for transcriptional transactivation and sequence specific DNA binding. The role of these mutations in regulating p53-mediated growth suppression and programmed cell death was examined. This mutational analysis comprised serine residues located at positions 6, 9, 15, 20, 33 and 37 of human p53. Substitution of serine for alanine, either at individual residues or at all six residues together, did not affect the suppression of cell growth and cell transformation, or the ability to bind DNA specifically and to transactivate different promoters, nor did it alter p53 expression. However, the ability of p53 to induce apoptosis was impaired by specific serine substitutions. Mutations in all six N-terminal serines together reduced the apoptotic activity of p53 in H1299 cells by 50%. Analysis of individual mutants revealed that mutations in serine 15 and 20 are primarily responsible for this impairment. Our results suggest that these serines play a role in the regulation of p53-mediated apoptosis.

Indexed as

ApoptosisMutagenesis, Site-DirectedAlanineAnimalsBinding SitesCell Transformation, NeoplasticDNAGene ExpressionHumansMiceSerineTranscriptional ActivationTranscription, GeneticTumor Suppressor Protein p53AlanineDNASerineTumor Suppressor Protein p53

Identifiers

PMID10359526
OpenAlexW2314811539

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.