Evidence map›Paper›PMID 21776408›Full record

ArticleSmall GTPases2011

Characterization of ATF2 in Rel/NFκB oncogenesis reveals its role in the regulation of Ras signaling.

Andrew S Liss, Henry R Bose

Open access · hybridAbstract read
In one paragraph

Article in Small GTPases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 41% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. 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

2 authors at 2 institutions in 2 countries.

Andrew S LissSection of Molecular Genetics and Microbiology and the Institute of Cellular and Molecular Biology; University of Texas at Austin; Austin, TX USA.
Henry R Bose
Institute of Molecular Genetics · RUThe University of Texas at Austin · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The v-Rel oncoprotein is the acutely transforming member of the Rel/NFκB family of transcription factors. v-Rel transforms cells through the inappropriate activation and suppression of genes normally regulated by cellular Rel/NFκB family members. We have recently demonstrated that activation of Ha-Ras by v-Rel contributes to transformation. Characterization of AP-1 family members in v-Rel-mediated transformation revealed ectopic expression of ATF2 inhibited transformation by blocking Ha-Ras activity. This lack of Ha-Ras activity prevented downstream activation of the Raf-MEK-ERK pathway, a critical pathway for v-Rel-mediated transformation. Microarray analysis of cells treated with an inhibitor to the ERK pathway revealed a relatively small number of genes that are specifically regulated by ERK activity in cells expressing v-Rel. These studies suggest the main contribution of ERK activity is to temper the expression of genes in v-Rel transformed cells. The mechanism by which ATF2 regulates Ras-Raf-MEK-ERK signaling appears to be a context dependent event. The ectopic expression of ATF2 in cells that are not expressing v-Rel results in the activation of Ha-Ras. However, activation of downstream Raf-MEK-ERK signaling pathway is blocked, likely through the recruitment of inhibitory 14-3-3 proteins to c-Raf. These results suggest a diverse role for ATF2 in the regulation of the Ras-Raf-MEK-ERK pathway.

Identifiers

PMID21776408
PMCPMC3136910
OpenAlexW2033152952

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.