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dc.date.accessioned2018-06-08T11:19:31Z
dc.date.issued2015-06
dc.identifier6
dc.identifier.citationPLOS ONE, 2015, 10 pp. 19 - 19
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1761
dc.description.abstractSignalling through the Hippo (Hpo) pathway involves a kinase cascade, which leads to the phosphorylation and inactivation of the pro-growth transcriptional co-activator Yorkie (Yki). Despite the identification of a large number of pathway members and modulators, our understanding of the molecular events that lead to activation of Hpo and the downstream kinase Warts (Wts) remain incomplete. Recently, targeted degradation of several Hpo pathway components has been demonstrated as a means of regulating pathway activity. In particular, the stability of scaffold protein Salvador (Sav), which is believed to promote Hpo/Wts association, is crucially dependent on its binding partner Hpo. In a cell-based RNAi screen for ubiquitin regulators involved in Sav stability, we identify the HECT domain protein Herc4 (HECT and RLD domain containing E3 ligase) as a Sav E3 ligase. Herc4 expression promotes Sav ubiquitylation and degradation, while Herc4 depletion stabilises Sav. Interestingly, Hpo reduces Sav/Herc4 interaction in a kinase-dependent manner. This suggests the existence of a positive feedback loop, where Hpo stabilises its own positive regulator by antagonising Herc4-mediated degradation of Sav.
dc.format.extent19 - 19
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleHippo Stabilises Its Adaptor Salvador by Antagonising the HECT Ubiquitin Ligase Herc4
dc.typeJournal Article
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2015-06
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfPLOS ONE
pubs.notesISI Document Delivery No.: CN1BR Times Cited: 0 Cited Reference Count: 61 Aerne, Birgit L. Gailite, Ieva Sims, David Tapon, Nicolas Cancer Research UK [17064] This work was funded by Cancer Research UK (number 17064). 0 PUBLIC LIBRARY SCIENCE SAN FRANCISCO PLOS ONE keywords: TUMOR-SUPPRESSOR PROTEIN CELL-CYCLE EXIT PROMOTES APOPTOSIS SIZE-CONTROL PROLIFERATION ARREST DROSOPHILA HOMOLOG SIGNALING PATHWAY BANTAM MICRORNA GROWTH-CONTROL TISSUE-GROWTH
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR
pubs.volume10
pubs.embargo.termsNot known
dc.contributor.icrauthorSims, Daviden


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