Evidence map›Paper›PMID 10082528›Full record

ArticleMolecular and cellular biology1999

The Ets2 transcription factor inhibits apoptosis induced by colony-stimulating factor 1 deprivation of macrophages through a Bcl-xL-dependent mechanism.

L Sevilla, C Aperlo, V Dulic, J C Chambard, C Boutonnet, O Pasquier, P Pognonec, K E Boulukos

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.4field-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

34 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Bcl-xL: A Focus on Melanoma Pathobiology.International journal of molecular sciences · 2021
    Review
  5. Review
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  16. Activation of Ets-2 by oxidative stress induces Bcl-xL expression and accounts for glial survival in amyotrophic lateral sclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009
    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

8 authors at 2 institutions in 1 country.

L SevillaCentre de Biochimie, Université de Nice, Faculté des Sciences, 06108 Nice, France.
C Aperlo
V Dulic
J C Chambard
C Boutonnet
O Pasquier
P Pognonec
K E Boulukos
Université Côte d'Azur · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bcl-xL, a member of the Bcl-2 family, inhibits apoptosis, and its expression is regulated at the transcriptional level, yet nothing is known about the transcription factors specifically activating this promoter. The bcl-x promoter contains potential Ets binding sites, and we show that the transcription factor, Ets2, first identified by its sequence identity to v-ets of the E26 retrovirus, can transactivate the bcl-x promoter. Transient expression of Ets2 results in the upregulation of Bcl-xL but not of Bcl-xS, an alternatively spliced gene product which induces apoptosis. Ets2 is ubiquitously expressed at low levels in a variety of cell types and tissues but is specifically induced to abundant levels during macrophage differentiation. Since Bcl-xL is also upregulated during macrophage differentiation, we asked whether the bcl-x could be a direct downstream target gene of Ets2 in macrophages. BAC1.2F5 macrophages, which are dependent on macrophage colony-stimulating factor 1 (CSF-1) for their growth and survival, were used in these studies. We show that CSF-1 stimulation of BAC1.2F5 macrophages results in the upregulation of expression of ets2 and bcl-xL with similar kinetics of induction. In the absence of CSF-1, these macrophages undergo cell death by apoptosis, whereas constitutive expression of Ets2 rescues these cells from cell death, and bcl-xL is upregulated. These results strongly suggest a novel role of Ets2 in affecting apoptosis through its regulation of Bcl-xL transcription.

Indexed as

DNA-Binding ProteinsRepressor ProteinsTranscription FactorsAlternative SplicingApoptosisbcl-X ProteinCell DivisionMacrophage Colony-Stimulating FactorMacrophagesPhosphorylationProto-Oncogene Protein c-ets-2Proto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Retinoblastoma ProteinTrans-ActivatorsTranscriptional Activationbcl-X ProteinDNA-Binding ProteinsERF protein, humanMacrophage Colony-Stimulating FactorProto-Oncogene Protein c-ets-2Proto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Repressor ProteinsRetinoblastoma ProteinTrans-ActivatorsTranscription Factors

Identifiers

PMID10082528
PMCPMC84055
OpenAlexW1762333703

What OpenQuestion holds

Texttitle and abstract
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.