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dc.contributor.author
Wang, Yuan
dc.contributor.author
Werz, Christian
dc.contributor.author
Xu, Dongbin
dc.contributor.author
Chen, Zhihong
dc.contributor.author
Li, Ying
dc.contributor.author
Hafen, Ernst
dc.contributor.author
Bergmann, Andreas
dc.date.accessioned
2018-08-09T13:53:58Z
dc.date.available
2017-06-08T21:08:07Z
dc.date.available
2018-08-09T13:53:58Z
dc.date.issued
2008-01-16
dc.identifier.issn
1932-6203
dc.identifier.other
10.1371/journal.pone.0001447
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/13727
dc.identifier.doi
10.3929/ethz-b-000013727
dc.description.abstract
Background Activation of cell surface receptors transduces extracellular signals into cellular responses such as proliferation, differentiation and survival. However, as important as the activation of these receptors is their appropriate spatial and temporal down-regulation for normal development and tissue homeostasis. The Cbl family of E3-ubiquitin ligases plays a major role for the ligand-dependent inactivation of receptor tyrosine kinases (RTKs), most notably the Epidermal Growth Factor Receptor (EGFR) through ubiquitin-mediated endocytosis and lysosomal degradation. Methodology/Principal Findings Here, we report the mutant phenotypes of Drosophila cbl (D-cbl) during eye development. D-cbl mutants display overgrowth, inhibition of apoptosis, differentiation defects and increased ommatidial spacing. Using genetic interaction and molecular markers, we show that most of these phenotypes are caused by increased activity of the Drosophila EGFR. Our genetic data also indicate a critical role of ubiquitination for D-cbl function, consistent with biochemical models. Conclusions/Significance These data may provide a mechanistic model for the understanding of the oncogenic activity of mammalian cbl genes.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Public Library of Science
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/3.0/
dc.title
Drosophila cbl is essential for control of cell death and cell differentiation during eye development
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 3.0 Unported
ethz.journal.title
PLoS ONE
ethz.journal.volume
3
en_US
ethz.journal.issue
1
en_US
ethz.journal.abbreviated
PLoS ONE
ethz.pages.start
e1447
en_US
ethz.pages.end
e1447
en_US
ethz.size
8 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.publication.place
Lawrence, Kan.
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02538 - Institut für Molekulare Systembiologie / Institute for Molecular Systems Biology::03710 - Hafen, Ernst (emeritus) / Hafen, Ernst (emeritus)
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02538 - Institut für Molekulare Systembiologie / Institute for Molecular Systems Biology::03710 - Hafen, Ernst (emeritus) / Hafen, Ernst (emeritus)
ethz.date.deposited
2017-06-08T21:08:27Z
ethz.source
ECIT
ethz.identifier.importid
imp59364c3084f6738012
ethz.ecitpid
pub:25210
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-18T18:39:39Z
ethz.rosetta.lastUpdated
2021-02-15T01:12:20Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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