Evidence map›Paper›PMID 10523858›Full record

ArticleOncogene1999

Dissociation of the recombination control and the sequence-specific transactivation function of P53.

C Dudenhöffer, M Kurth, F Janus, W Deppert, L Wiesmüller

Abstract read
PubMed Publisher
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 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Chromosome instability and deregulated proliferation: an unavoidable duo.Cellular and molecular life sciences : CMLS · 2012
    Review
  13. Article
  14. Applications of the human p53 knock-in (Hupki) mouse model for human carcinogen testing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

C DudenhöfferHeinrich-Pette-Institut für Experimentelle Virologie und Immunologie an der Universität Hamburg, Martinistrasse 52, D-20251 Hamburg, Germany.
M Kurth
F Janus
W Deppert
L Wiesmüller
Universität Hamburg · DELeibniz Institute of Virology (LIV) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, we described a new biological function of p53 in inhibiting recombination processes when encountering mismatches in heteroduplexes (Dudenhöffer et al., 1998). Here, we characterized protein domains of p53 participating in this process by in vitro analysis of mutated p53 proteins, and by applying our SV40-based assay system on monkey cells, which express different p53 variants. We present evidence that both binding of artificial recombination intermediates and p53-dependent recombination control require an intact p53 core and the oligomerization domain, strongly suggesting that the recognition of DNA undergoing recombination represents an essential step of this genomic surveillance mechanism. Further analyses indicated a role of the C-terminus in negatively regulating recombination control, an effect which can be neutralized by concurrent mismatch recognition. p53 lacking the oligomerization domain totally lost its ability to suppress homologous recombination. The cancer-related mutant p53(273H) was also significantly defective in this function, although we observed only twofold reductions in the corresponding transactivation activities on p53-response elements in episomal constructs. HDM2, an inhibitor of p53's transcriptional and growth regulatory activities, interfered with the inhibition of DNA exchange processes by p53 only weakly. Thus, functions of p53 in recombination control can be structurally dissociated from p53-dependent transcriptional transactivation.

Indexed as

Nuclear ProteinsRecombination, GeneticAnimalsAnimals, Genetically ModifiedBlotting, WesternCell DivisionCells, CulturedKidneyMacaca mulattaNeoplasm ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Regulatory Sequences, Nucleic AcidTrans-ActivatorsTumor Suppressor Protein p53Zinc FingersNeoplasm ProteinsNuclear ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Trans-ActivatorsTumor Suppressor Protein p53

Identifiers

PMID10523858
OpenAlexW2317412573

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.