Evidence map›Paper›PMID 18706412›Full record

ReviewExperimental cell research2009

Mechanisms of ErbB receptor negative regulation and relevance in cancer.

William H D Fry, Lakmal Kotelawala, Colleen Sweeney, Kermit L Carraway

Open access · greenAbstract readReview
In one paragraph

Review in Experimental cell research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  19. Transformation of polarized epithelial cells by apical mistrafficking of epiregulin.Proceedings of the National Academy of Sciences of the United States of America · 2013
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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

4 authors at 2 institutions in 1 country.

William H D FryUC Davis Cancer Center, Research Building III, Rm 1100B, 4645 2nd Avenue, Sacramento, California 95817, USA.
Lakmal Kotelawala
Colleen Sweeney
Kermit L Carraway
UC Davis Comprehensive Cancer CenterUniversity of California Davis Medical Center · US

Funding

NRDP1 PROTEIN DEGRADATION PATHWAY IN MAMMARY TUMOR PROGRESSIONR01CA123541 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARRAWAY, KERMIT L · 2006 to 2016
$2.5M
Mechanisms of Receptor Tyrosine Kinase InhibitionR01CA118384 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SWEENEY, COLLEEN ANN · 2006 to 2016
$2.4M
Modulation of ErbB Receptor Tyrosine Kinase SignalingR01GM068994 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI CARRAWAY, KERMIT L · 2003 to 2011
$2.4M
NCI NIH HHS CA118384NCI NIH HHS CA123541NCI NIH HHS R01 CA118384NCI NIH HHS R01 CA123541NIGMS NIH HHS GM068994NIGMS NIH HHS R01 GM068994
6 · The paper itself

Abstract

The ErbB family of receptor tyrosine kinases engages a wide variety of signaling pathways that collectively direct transcriptional programs controlling organogenesis during development and tissue maintenance in the adult. These receptors are also frequently found overexpressed or aberrantly activated in various cancers, suggesting that ErbB receptor signaling activity must be very tightly regulated. Sufficient levels of ErbB signaling are necessary to mediate tissue homeostasis, for example, but over-signaling can trigger cellular processes that contribute to cancer initiation or progression. Efforts over the last quarter century have led to a thorough understanding of the signaling pathways that are activated by these receptors and the mechanisms by which ErbB receptors engage these pathways. However, the compensatory negative regulatory mechanisms responsible for attenuating receptor activation have only more recently begun to be explored. Here we review the different known mechanisms of ErbB negative regulation, with particular emphasis on those proteins that exhibit some specificity for the ErbB family. We also describe how loss or suppression of ErbB negative regulators may contribute to tumor development, and discuss how restoration or augmentation of these pathways may represent a novel avenue for the development of ErbB-targeted therapies.

Indexed as

Down-RegulationAnimalsErb-b2 Receptor Tyrosine KinasesHumansModels, MolecularNeoplasmsSignal TransductionErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID18706412
PMCPMC2667444
OpenAlexW1963811231

What OpenQuestion holds

Textmetadata
LicenceTDM
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.