Evidence map›Paper›PMID 15366372›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2004

Wa5 is a novel ENU-induced antimorphic allele of the epidermal growth factor receptor.

Daekee Lee, Sally H Cross, Karen E Strunk, Joanne E Morgan, Candice L Bailey, Ian J Jackson, David W Threadgill

Abstract read
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In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 31% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Activating EGFR Signaling Attenuates Osteoarthritis Development Following Loading Injury in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
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  5. EGFR Signaling Is Required for Maintaining Adult Cartilage Homeostasis and Attenuating Osteoarthritis Progression.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
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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

7 authors at 2 institutions in 2 countries.

Daekee LeeDepartment of Genetics, University of North Carolina School of Medicine, CB#7264, Chapel Hill, North Carolina, 27599, USA.
Sally H Cross
Karen E Strunk
Joanne E Morgan
Candice L Bailey
Ian J Jackson
David W Threadgill
University of North Carolina at Chapel Hill · USWestern General Hospital · GB

Funding

Prevention &Metastasis: Final Frontiers in Colon CancerU01CA084239 · NCI · VANDERBILT UNIVERSITY · PI COFFEY, ROBERT J. · 1999 to 2009
$8.0M
ERBB receptors in normal and cancerous colon biologyR01CA092479 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI THREADGILL, DAVID W. · 2001 to 2012
$2.8M
Functional Genomics of Egfr in Placental DevelopmentR01HD039896 · NICHD · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI THREADGILL, DAVID W. · 2001 to 2005
$1.6M
NCI NIH HHS CA084239NCI NIH HHS CA092479NICHD NIH HHS HD039896
6 · The paper itself

Abstract

Mice heterozygous for the N-ethyl-N-nitrosourea-induced Waved-5 (Wa5) mutation, isolated in a screen for dominant, visible mutations, exhibit a wavy coat similar to mice homozygous for the recessive Tgfa wa1 or Egfr wa2 alleles. In this study, we show that Wa5 is a new allele of Egfr (Egfr Wa5) containing a missense mutation within the coding region for the highly conserved DFG motif of the tyrosine kinase domain. In vivo analysis of placental development, modification of Apc Min tumorigenesis, and levels of EGF-dependent EGFR phosphorylation demonstrates that Egfr Wa5 functions as an antimorphic allele, recapitulating many abnormalities associated with reduced EGFR activity. Furthermore, Egfr wa5 enhances Egfr Wa2 compound or Tgfa tm1Dcl double mutants exposing additional EGFR-dependent phenotypes. In vitro characterization shows that the antimorphic property of Egfr Wa5 is caused by a kinase-dead receptor acting as a dominant negative.

Indexed as

AllelesAlkylating AgentsAmino Acid MotifsAmino Acid SequenceAnimalsBase SequenceCricetinaeDNA Mutational AnalysisErbB ReceptorsEthylnitrosoureaGenes, DominantGenetic Complementation TestGenotypeHeterozygoteHomozygoteHumansAlkylating AgentsErbB ReceptorsEthylnitrosoureaMutagensProtein-Tyrosine Kinases

Identifiers

PMID15366372
OpenAlexW1992160099

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.