Evidence map›Paper›PMID 19144825›Full record

ArticleMolecular biology of the cell2009

Association of v-ErbA with Smad4 disrupts TGF-beta signaling.

Richard A Erickson, Xuedong Liu

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Recruitment of the oncoprotein v-ErbA to aggresomes.Molecular and cellular endocrinology · 2011
    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 1 institution in 1 country.

Richard A EricksonDepartment of Chemistry and Biochemistry, University of Colorado-Boulder, Boulder, CO 80309, USA.
Xuedong Liu
University of Colorado Boulder · US

Funding

MECHANISMS OF CARDIOVASCULAR DISEASE AND GENE THERAPYT32HL007851 · NHLBI · UNIVERSITY OF COLORADO AT BOULDER · PI LEINWAND, LESLIE ANNE · 1996 to 2005
$1.1M
Quantitative Analysis of TGF-b/Smad Signaling DynamicsR01GM083172 · NIGMS · UNIVERSITY OF COLORADO · PI LIU, XUEDONG · 2008 to 2011
$1.0M
NHLBI NIH HHS 5T32HL07851NHLBI NIH HHS T32 HL007851NIGMS NIH HHS GM083172NIGMS NIH HHS R01 GM083172
6 · The paper itself

Abstract

Disruption of the transforming growth factor-beta (TGF-beta) pathway is observed in the majority of cancers. To further understand TGF-beta pathway inactivation in cancer, we stably expressed the v-ErbA oncoprotein in TGF-beta responsive cells. v-ErbA participates in erythroleukemic transformation of cells induced by the avian erythroblastosis virus (AEV). Here we demonstrate that expression of v-ErbA was sufficient to antagonize TGF-beta-induced cell growth inhibition and that dysregulation of TGF-beta signaling required that v-ErbA associate with the Smad4 which sequesters Smad4 in the cytoplasm. We also show that AEV-transformed erythroleukemia cells were resistant to TGF-beta-induced growth inhibition and that TGF-beta sensitivity could be recovered by reducing v-ErbA expression. Our results reveal a novel mechanism for oncogenic disruption of TGF-beta signaling and provide a mechanistic explanation of v-ErbA activity in AEV-induced erythroleukemia.

Indexed as

Binding SitesCell LineCell NucleusCell ProliferationErythroblastsHumansMutationOncogene Proteins v-erbASignal TransductionSmad4 ProteinTransforming Growth Factor betaOncogene Proteins v-erbASmad4 ProteinSMAD4 protein, humanTransforming Growth Factor beta

Identifiers

PMID19144825
PMCPMC2649266
OpenAlexW2093004745

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.