Evidence map›Paper›PMID 16170378›Full record

ArticleOncogene2005

Disruption of B-myb in DT40 cells reveals novel function for B-Myb in the response to DNA-damage.

Dörthe Ahlbory, Hartmut Appl, Detlef Lang, Karl-Heinz Klempnauer

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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  6. CommonClinical cancer research : an official journal of the American Association for Cancer Research · 2017
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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

4 authors at 1 institution in 1 country.

Dörthe AhlboryInstitute for Biochemistry, Westfälische-Wilhelms-Universität Münster, Wilhelm-Klemm-Str. 2, Münster D-48149, Germany.
Hartmut Appl
Detlef Lang
Karl-Heinz Klempnauer
University of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B-Myb is a highly conserved vertebrate member of the Myb transcription factor family, which is expressed in virtually all proliferating cells. A large body of evidence suggests that B-Myb plays an important role in cell cycle regulation; however, the exact nature of its function has not yet been clarified. We have used gene targeting in chicken DT40 cells, a cell line exhibiting very high rates of homologous recombination, to create cells expressing endogenous B-myb in a doxycyclin-dependent manner. We find that the cells proliferate well in the absence of B-Myb, suggesting that B-Myb is not essential for cell proliferation per se. However, cells lacking B-Myb are more sensitive to DNA-damage induced by UV-irradiation and alkylation. Our work provides the first direct evidence for a novel function of B-Myb in the response to DNA-damage. The cells described here should be a useful model to characterize this function in more detail.

Indexed as

DNA DamageGenes, mybAnimalsApoptosisCell CycleCell LineCell ProliferationCell SurvivalChickensClone CellsDoxycyclineGene Expression RegulationGene TargetingGenetic EngineeringMicroarray AnalysisPromoter Regions, GeneticDoxycyclineProto-Oncogene Proteins c-mybRNA, MessengerTranscription Factors

Identifiers

PMID16170378
OpenAlexW2071571150

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.