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Article: Mule Regulates the Intestinal Stem Cell Niche via the Wnt Pathway and Targets EphB3 for Proteasomal and Lysosomal Degradation

TitleMule Regulates the Intestinal Stem Cell Niche via the Wnt Pathway and Targets EphB3 for Proteasomal and Lysosomal Degradation
Authors
Dominguez-Brauer, CarmenHao, ZhenyueElia, Andrew J.Fortin, Jérôme M.Nechanitzky, RobertBrauer, Patrick M.Sheng, YiMana, Miyeko D.Chio, Iok In ChristineHaight, JillianPollett, AaronCairns, RobertTworzyanski, LeanneInoue, SatoshiReardon, ColinMarques, AnaSilvester, JenniferCox, Maureen A.Wakeham, AndrewYilmaz, Omer H.Sabatini, David M.van Es, Johan H.Clevers, HansSato, ToshiroMak, Tak W.
Issue Date2016
Citation
Cell Stem Cell, 2016, v. 19, n. 2, p. 205-216 How to Cite?
DOI: http://dx.doi.org/10.1016/j.stem.2016.04.002
Abstract© 2016 Elsevier Inc. The E3 ubiquitin ligase Mule is often overexpressed in human colorectal cancers, but its role in gut tumorigenesis is unknown. Here, we show in vivo that Mule controls murine intestinal stem and progenitor cell proliferation by modulating Wnt signaling via c-Myc. Mule also regulates protein levels of the receptor tyrosine kinase EphB3 by targeting it for proteasomal and lysosomal degradation. In the intestine, EphB/ephrinB interactions position cells along the crypt-villus axis and compartmentalize incipient colorectal tumors. Our study thus unveils an important new avenue by which Mule acts as an intestinal tumor suppressor by regulation of the intestinal stem cell niche.
Persistent Identifierhttp://hdl.handle.net/10722/292941
ISSN
1934-5909
2021 Impact Factor: 25.269
2020 SCImago Journal Rankings: 8.860
PubMed Central ID
PMC5193118
ISI Accession Number ID
WOS:000381622000014

 

DC FieldValueLanguage
dc.contributor.authorDominguez-Brauer, Carmen-
dc.contributor.authorHao, Zhenyue-
dc.contributor.authorElia, Andrew J.-
dc.contributor.authorFortin, Jérôme M.-
dc.contributor.authorNechanitzky, Robert-
dc.contributor.authorBrauer, Patrick M.-
dc.contributor.authorSheng, Yi-
dc.contributor.authorMana, Miyeko D.-
dc.contributor.authorChio, Iok In Christine-
dc.contributor.authorHaight, Jillian-
dc.contributor.authorPollett, Aaron-
dc.contributor.authorCairns, Robert-
dc.contributor.authorTworzyanski, Leanne-
dc.contributor.authorInoue, Satoshi-
dc.contributor.authorReardon, Colin-
dc.contributor.authorMarques, Ana-
dc.contributor.authorSilvester, Jennifer-
dc.contributor.authorCox, Maureen A.-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorYilmaz, Omer H.-
dc.contributor.authorSabatini, David M.-
dc.contributor.authorvan Es, Johan H.-
dc.contributor.authorClevers, Hans-
dc.contributor.authorSato, Toshiro-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:57:32Z-
dc.date.available2020-11-17T14:57:32Z-
dc.date.issued2016-
dc.identifier.citationCell Stem Cell, 2016, v. 19, n. 2, p. 205-216-
dc.identifier.issn1934-5909-
dc.identifier.urihttp://hdl.handle.net/10722/292941-
dc.description.abstract© 2016 Elsevier Inc. The E3 ubiquitin ligase Mule is often overexpressed in human colorectal cancers, but its role in gut tumorigenesis is unknown. Here, we show in vivo that Mule controls murine intestinal stem and progenitor cell proliferation by modulating Wnt signaling via c-Myc. Mule also regulates protein levels of the receptor tyrosine kinase EphB3 by targeting it for proteasomal and lysosomal degradation. In the intestine, EphB/ephrinB interactions position cells along the crypt-villus axis and compartmentalize incipient colorectal tumors. Our study thus unveils an important new avenue by which Mule acts as an intestinal tumor suppressor by regulation of the intestinal stem cell niche.-
dc.languageeng-
dc.relation.ispartofCell Stem Cell-
dc.titleMule Regulates the Intestinal Stem Cell Niche via the Wnt Pathway and Targets EphB3 for Proteasomal and Lysosomal Degradation-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.stem.2016.04.002-
dc.identifier.pmid27184401-
dc.identifier.pmcidPMC5193118-
dc.identifier.scopuseid_2-s2.0-84966668081-
dc.identifier.volume19-
dc.identifier.issue2-
dc.identifier.spage205-
dc.identifier.epage216-
dc.identifier.eissn1875-9777-
dc.identifier.isiWOS:000381622000014-
dc.identifier.issnl1875-9777-

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