Evidence map›Paper›PMID 10490623›Full record

ArticleMolecular and cellular biology1999

Controlled dimerization of ErbB receptors provides evidence for differential signaling by homo- and heterodimers.

S K Muthuswamy, M Gilman, J S Brugge

Open access · bronzeAbstract 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 158 papers.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

158 citing papers in PubMed, 367 citations in OpenAlex.

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  20. Review

98 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

S K MuthuswamyDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
M Gilman
J S Brugge
Harvard University · USAridis Pharmaceuticals (United States) · US

Funding

SIGNAL TRANSDUCTION EVENTS REGULATED BY INTEGRINSR01CA078773 · NCI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BRUGGE, JOAN SIEFERT · 1998 to 2003
$1.7M
NCI NIH HHS CA78773NCI NIH HHS R01 CA078773
6 · The paper itself

Abstract

The four members of the ErbB family of receptor tyrosine kinases are involved in a complex array of combinatorial interactions involving homo- and heterodimers. Since most cell types express more than one member of the ErbB family, it is difficult to distinguish the biological activities of different homo- and heterodimers. Here we describe a method for inducing homo- or heterodimerization of ErbB receptors by using synthetic ligands without interference from the endogenous receptors. ErbB receptor chimeras containing synthetic ligand binding domains (FK506-binding protein [FKBP] or FKBP-rapamycin-binding domain [FRB]) were homodimerized with the bivalent FKBP ligand AP1510 and heterodimerized with the bifunctional FKBP-FRB ligand rapamycin. AP1510 treatment induced tyrosine phosphorylation of ErbB1 and ErbB2 homodimers and recruitment of Src homology 2 domain-containing proteins (Shc and Grb2). In addition, ErbB1 and ErbB2 homodimers activated downstream signaling pathways leading to Erk2 and Akt phosphorylation. However, only ErbB1 homodimers were internalized upon AP1510 stimulation, and only ErbB1 homodimers were able to associate with and induce phosphorylation of c-Cbl. Cells expressing AP1510-induced ErbB1 homodimers were able to associate with and induce phosphorylation of c-Cbl. Cells expressing AP1510-induced ErbB1 homodimers were able to form foci; however, cells expressing ErbB2 homodimers displayed a five- to sevenfold higher focus-forming ability. Using rapamycin-inducible heterodimerization we show that c-Cbl is unable to associate with ErbB1 in a ErbB1-ErbB2 heterodimer most likely because ErbB2 is unable to phosphorylate the c-Cbl binding site on ErbB1. Thus, we demonstrate that ErbB1 and ErbB2 homodimers differ in their abilities to transform fibroblasts and provide evidence for differential signaling by ErbB homodimers and heterodimers. These observations also validate the use of synthetic ligands to study the signaling and biological specificity of selected ErbB dimers in any cell type.

Indexed as

Ubiquitin-Protein LigasesAnimalsCell CycleCell Transformation, NeoplasticDimerizationDose-Response Relationship, DrugEndocytosisEpidermal Growth FactorErb-b2 Receptor Tyrosine KinasesErbB ReceptorsLigandsPhosphorylationProto-Oncogene ProteinsProto-Oncogene Proteins c-cblRatsRecombinant Fusion ProteinsAP 1510Epidermal Growth FactorErb-b2 Receptor Tyrosine KinasesErbB ReceptorsLigandsProto-Oncogene ProteinsProto-Oncogene Proteins c-cblRecombinant Fusion ProteinsTacrolimusUbiquitin-Protein Ligases

Identifiers

PMID10490623
PMCPMC84681
OpenAlexW2111004422

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.