Evidence map›Paper›PMID 16091742›Full record

ArticleOncogene2005

c-Abl regulates early growth response protein (EGR1) in response to oxidative stress.

Jeremy R Stuart, Hidehiko Kawai, Kelvin K C Tsai, Eric Y Chuang, Zhi-Min Yuan

Abstract read
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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Environmental Epigenetics of Diesel Particulate Matter Toxicogenomics.International journal of environmental research and public health · 2020
    Article
  7. Article
  8. Involvement of c-Abl Kinase in Microglial Activation of NLRP3 Inflammasome and Impairment in Autolysosomal System.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017
    Article
  9. Article
  10. Article
  11. A phosphotyrosine switch determines the antitumor activity of ERβ.The Journal of clinical investigation · 2014
    Article
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  13. Review
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  15. Article
  16. 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

5 authors at 2 institutions in 1 country.

Jeremy R StuartDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Hidehiko Kawai
Kelvin K C Tsai
Eric Y Chuang
Zhi-Min Yuan
Harvard University · USNational Cancer Institute · US

Funding

MOLECULAR BASIS OF P53 INDUCTION TO DNA DAMAGER01CA085679 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI YUAN, ZHI-MIN · 2001 to 2015
$3.4M
NCI NIH HHS R29 CA85679
6 · The paper itself

Abstract

c-Abl is a tyrosine kinase that can act as a regulator of cell growth and apoptosis in response to stress. Using cell lines expressing c-Abl in an inducible manner, we identified genes whose expression was regulated by c-Abl kinase activity. Microarray analysis indicated that Early Growth Response-1 (EGR1) gene expression is induced by c-Abl kinase activity, which was confirmed at the message and protein levels. Promoter mapping experiments revealed that c-Abl utilizes three distal serum response elements (SREs) in the EGR1 promoter, which are transactivated by mitogen/extracellular receptor kinase (MEK/ERK) signaling. PD 95089, a specific inhibitor of MEK/ERK signaling, attenuated c-Abl-mediated upregulation of EGR1 expression in a dose-dependent manner. Similar results were obtained by using a dominant-negative mutant of mitogen/extracellular kinase. Significantly, hydrogen peroxide-induced EGR1 expression appears to be mediated by c-Abl, as cells expressing dominant negative c-Abl, and c-Abl-/- murine embryonic fibroblasts, are completely defective in hydrogen peroxide-induced EGR1 expression. In addition, c-Abl-induced apoptosis is partially mitigated by EGR1 activity, as cells devoid of EGR1 expression undergo reduced rates of c-Abl-induced apoptosis. Together, these results indicate that c-Abl promotes the induction of EGR1 through the MEK/ERK pathway in regulating apoptotic response to oxidative stress.

Indexed as

AnimalsApoptosisCell LineEarly Growth Response Protein 1FibroblastsGene Expression RegulationGenes, ReporterHumansHydrogen PeroxideMAP Kinase Signaling SystemMiceOligonucleotide Array Sequence AnalysisOxidative StressPromoter Regions, GeneticProto-Oncogene Proteins c-ablReverse Transcriptase Polymerase Chain ReactionEarly Growth Response Protein 1EGR1 protein, humanEgr1 protein, mouseHydrogen PeroxideProto-Oncogene Proteins c-abl

Identifiers

PMID16091742
OpenAlexW2103536763

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.