Evidence map›Paper›PMID 12787468›Full record

ArticleBMC genetics2003

Involvement of an SCFSlmb complex in timely elimination of E2F upon initiation of DNA replication in Drosophila.

Jean-Karim Hériché, Dan Ang, Ethan Bier, Patrick H O'Farrell

Open access · diamondAbstract read
In one paragraph

Article in BMC genetics, 2003. 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
1.8field-weighted citation impact, top 16% 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, 36 citations in OpenAlex.

  1. Embedded CRISPRi Enhances Gene-Silencing Efficiency in Drosophila.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  4. MEK inhibitor effective against proliferation in breast cancer cell.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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  9. Pharmacological and genetic reversal of age-dependent cognitive deficits attributable to decreased presenilin function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
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  14. dDP is needed for normal cell proliferation.Molecular and cellular biology · 2005
    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

4 authors at 2 institutions in 1 country.

Jean-Karim HérichéDepartment of Biochemistry and Biophysics, University of California, San Francisco, 513 Parnassus Street, San Francisco, CA 94143-0448, USA. heriche@cgl.ucsf.edu
Dan Ang
Ethan Bier
Patrick H O'Farrell
University of California, San Diego · USUniversity of California, San Francisco · US

Funding

MOLECULAR DETERMINANTS OF DEVELOPMENTAL FATER01GM037193 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI O'FARRELL, PATRICK H · 1986 to 2009
$4.4M
NIGMS NIH HHS R01 GM037193
6 · The paper itself

Abstract

backgroundCul1 is a core component of the evolutionarily conserved SCF-type ubiquitin ligases that target specific proteins for destruction. SCF action contributes to cell cycle progression but few of the key targets of its action have been identified.

resultsWe found that expression of the mouse Cul1 (mCul1) in the larval wing disc has a dominant negative effect. It reduces, but does not eliminate, the function of SCF complexes, promotes accumulation of Cubitus interruptus (a target of SCF action), triggers apoptosis, and causes a small wing phenotype. A screen for mutations that dominantly modify this phenotype showed effective suppression upon reduction of E2F function, suggesting that compromised downregulation of E2F contributes to the phenotype. Partial inactivation of Cul1 delayed the abrupt loss of E2F immunofluorescence beyond its normal point of downregulation at the onset of S phase. Additional screens showed that mild reduction in function of the F-box encoding gene slimb enhanced the mCul1 overexpression phenotype. Cell cycle modulation of E2F levels is virtually absent in slimb mutant cells in which slimb function is severely reduced. This implicates Slimb, a known targeting subunit of SCF, in E2F downregulation. In addition, Slimb and E2F interacted in vitro in a phosphorylation-dependent manner.

conclusionWe have used genetic and physical interactions to identify the G1/S transcription factor E2F as an SCFSlmb target in Drosophila. These results argue that the SCFSlmb ubiquitin ligase directs E2F destruction in S phase.

Indexed as

DNA ReplicationAnimalsAnimals, Genetically ModifiedApoptosisCell Cycle ProteinsCullin ProteinsDNA-Binding ProteinsDown-RegulationDrosophila melanogasterDrosophila ProteinsE2F Transcription FactorsFemaleGene Expression Regulation, DevelopmentalMaleMiceMutationCell Cycle ProteinsCullin 1Cullin ProteinsDNA-Binding ProteinsDrosophila ProteinsE2F Transcription FactorsSKP Cullin F-Box Protein Ligasesslmb protein, DrosophilaTranscription FactorsUbiquitin-Protein Ligases

Identifiers

PMID12787468
PMCPMC161817
OpenAlexW1531957421

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.