Evidence map›Paper›PMID 23736031›Full record

ArticleBritish journal of cancer2013

p28, a first in class peptide inhibitor of cop1 binding to p53.

T Yamada, K Christov, A Shilkaitis, L Bratescu, A Green, S Santini, A R Bizzarri, S Cannistraro, T K D Gupta, C W Beattie

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.2field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Efficient Cytotoxicity of Recombinant Azurin inBioengineering (Basel, Switzerland) · 2023
    Article
  11. Review
  12. Review
  13. Review
  14. A Method of Tumor In Vivo Imaging with a New Peptide-Based Fluorescent Probe.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  15. Article
  16. Review
  17. 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

10 authors at 3 institutions in 2 countries.

T YamadaDepartment of Surgery, Division of Surgical Oncology, University of Illinois at Chicago College of Medicine, Chicago, IL, USA.
K Christov
A Shilkaitis
L Bratescu
A Green
S Santini
A R Bizzarri
S Cannistraro
T K D Gupta
C W Beattie
University of Illinois Chicago · USNational Interuniversity Consortium for the Physical Sciences of Matter · ITUniversità degli Studi della Tuscia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA 28 amino-acid (aa) cell-penetrating peptide (p28) derived from azurin, a redox protein secreted from the opportunistic pathogen Pseudomonas aeruginosa, produces a post-translational increase in p53 in cancer cells by inhibiting its ubiquitination.

methodsIn silico computational simulations were used to predict motifs within the p53 DNA-binding domain (DBD) as potential sites for p28 binding. In vitro direct and competitive pull-down studies as well as western blot and RT-PCR analyses were used to validate predictions.

resultsThe L1 loop (aa 112-124), a region within the S7-S8 loop (aa 214-236) and T140, P142, Q144, W146, R282 and L289 of the p53DBD were identified as potential sites for p28 binding. p28 decreased the level of the E3 ligase COP1 >80%, in p53wt and p53mut cells with no decrease in COP1 in p53dom/neg or p53null cells. Brief increases in the expression of the E3 ligases, TOPORS, Pirh2 and HDM2 (human double minute 2) in p53wt and p53mut cells were in response to sustained increases in p53.

conclusionThese data identify the specific motifs within the DBD of p53 that bind p28 and suggest that p28 inhibition of COP1 binding results in the sustained, post-translational increase in p53 levels and subsequent inhibition of cancer cell growth independent of an HDM2 pathway.

Indexed as

Amino Acid SequenceAnimalsAzurinCell Line, TumorDown-RegulationEnzyme InhibitorsFemaleHumansMaleMiceMice, NudeModels, MolecularMolecular Dynamics SimulationMolecular Sequence DataPeptide FragmentsProtein BindingAzurinazurin (50-77)COP1 protein, humanEnzyme InhibitorsPeptide FragmentsTP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID23736031
PMCPMC3694247
OpenAlexW2028374237

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.