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dc.contributor.authorYan, Yan
dc.contributor.authorOllila, Saara
dc.contributor.authorWong, Iris P. L.
dc.contributor.authorVallenius, Tea
dc.contributor.authorPalvimo, Jorma J.
dc.contributor.authorVaahtomeri, Kari
dc.contributor.authorMäkelä, Tomi P.
dc.date.accessioned2016-06-08T05:48:27Z
dc.date.available2016-06-08T05:48:27Z
dc.date.issued2015-10-23
dc.identifier10.1038/ncomms9979
dc.identifier.citationYan Yan, Saara Ollila, Iris P. L. Wong, Tea Vallenius, Jorma J. Palvimo, Kari Vaahtomeri & Tomi P. Mäkelä 2015. Nature Communications 6, Article number: 8979fi_FI
dc.identifier.issn2041-1723
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/46
dc.descriptionArticle
dc.description.abstractAMP-activated protein kinase (AMPK) inhibits several anabolic pathways such as fatty acid and protein synthesis, and identification of AMPK substrate specificity would be useful to understand its role in particular cellular processes and develop strategies to modulate AMPK activity in a substrate-specific manner. Here we show that SUMOylation of AMPKα1 attenuates AMPK activation specifically towards mTORC1 signalling. SUMOylation is also important for rapid inactivation of AMPK, to allow prompt restoration of mTORC1 signalling. PIAS4 and its SUMO E3 ligase activity are specifically required for the AMPKα1 SUMOylation and the inhibition of AMPKα1 activity towards mTORC1 signalling. The activity of a SUMOylation-deficient AMPKα1 mutant is higher than the wild type towards mTORC1 signalling when reconstituted in AMPKα-deficient cells. PIAS4 depletion reduced growth of breast cancer cells, specifically when combined with direct AMPK activator A769662, suggesting that inhibiting AMPKα1 SUMOylation can be explored to modulate AMPK activation and thereby suppress cancer cell growth.fi_FI
dc.language.isoENfi_FI
dc.publisherNature Publishing Groupfi_FI
dc.relation.ispartofseriesNature Communications
dc.relation.urihttp://dx.doi.org/10.1038/ncomms9979
dc.rightsCC BY 4.0 https://creativecommons.org/licenses/by/4.0/
dc.subjectBiological sciencesfi_FI
dc.subjectCell biologyfi_FI
dc.titleSUMOylation of AMPKα1 by PIAS4 specifically regulates mTORC1 signallingfi_FI
dc.typehttp://purl.org/eprint/type/JournalArticle
dc.description.versionPublisher's pdf
dc.contributor.departmentFaculty of Health Sciences
uef.solecris.id36517013
eprint.statushttp://purl.org/eprint/status/PeerReviewed
dc.type.publicationinfo:eu-repo/semantics/article
dc.rights.accessrights© Clearance Center, Inc
dc.relation.doi10.1038/ncomms9979
dc.description.reviewstatushttp://purl.org/eprint/status/PeerReviewed
dc.relation.issn2041-1723
dc.relation.issue8979
dc.relation.volume6
dc.rights.accesslevelopenAccess


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