Evidence map›Paper›PMID 19718045›Full record

ArticleOncogene2009

The prolyl cis/trans isomerase cyclophilin 18 interacts with the tumor suppressor p53 and modifies its functions in cell cycle regulation and apoptosis.

N Baum, C Schiene-Fischer, M Frost, M Schumann, K Sabapathy, O Ohlenschläger, F Grosse, B Schlott

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Translation factors that keep the ribosome Pro-active.Microbiology and molecular biology reviews : MMBR · 2026
    Review
  2. Review
  3. Article
  4. AssessingPharmaceutics · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Non-Immunosuppressive Cyclophilin Inhibitors.Angewandte Chemie (International ed. in English) · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Selective targeting p53Oncogene · 2017
    Article
  13. Article
  14. Article
  15. p53 suppresses CCL2-induced subcutaneous tumor xenograft.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

8 authors at 4 institutions in 2 countries.

N BaumDepartment of Biochemistry, Leibniz-Institute for Age Research (Fritz Lipmann Institute), Jena, Germany.
C Schiene-Fischer
M Frost
M Schumann
K Sabapathy
O Ohlenschläger
F Grosse
B Schlott
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEMax Planck Research Unit for Enzymology of Protein Folding · DELeibniz Association · DENational Cancer Centre Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The functional diversity of the tumor suppressor protein p53 is mainly regulated by protein interactions. In this study, we describe a new interaction with the peptidyl-prolyl cis/trans isomerase cyclophilin 18 (Cyp18). The interaction reduced the sequence-specific DNA binding of p53 in vitro, whereas the inhibition of the interaction increased p53-reporter gene activity in vivo. The active site of the folding helper enzyme Cyp18 was directly involved in binding. The proline-rich region (amino acids 64-91) of p53 was most likely responsible for the observed binding because a synthetic peptide comprising amino acids 68-81 of p53 inhibited this interaction, and a p53 variant containing a proline residue at position 72 (p53(P72)) interacted with Cyp18 more effectively than the corresponding p53(R72) variant. Impairment of the Cyp18-p53 interaction induced an accumulation of cells in the G2/M phase of the cell cycle, which was more pronounced when p53(P72) was expressed compared with p53(R72) in an otherwise isogenic cellular background. Moreover, p53-dependent apoptosis was elevated in Cyp18 knockout cells, suggesting an antiapoptotic potential of Cyp18-p53 complexes. Functional in vivo data hint to a possible clinical relevance of the p53-Cyp18 interaction observed.

Indexed as

Protein FoldingAmino Acid SubstitutionApoptosisBinding SitesCell DivisionCell Line, TumorCyclophilinsG2 PhaseHumansMutation, MissenseProtein BindingTumor Suppressor Protein p53CyclophilinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID19718045
OpenAlexW2082194694

What OpenQuestion holds

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Registered trials

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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.