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dc.contributor.authorAbdelwahab, E. M. M.
dc.contributor.authorPal, S.
dc.contributor.authorKvell, K.
dc.contributor.authorSarosi, V.
dc.contributor.authorBai, P.
dc.contributor.authorRue, R.
dc.contributor.authorKrymskaya, V.
dc.contributor.authorMcPhail, D.
dc.contributor.authorPorter, A.
dc.contributor.authorPongracz, J. E.
dc.date.accessioned2019-01-17T09:40:06Z
dc.date.available2019-01-17T09:40:06Z
dc.date.issued2019
dc.identifier.citationAbdelwahab , E M M , Pal , S , Kvell , K , Sarosi , V , Bai , P , Rue , R , Krymskaya , V , McPhail , D , Porter , A & Pongracz , J E 2019 , ' Mitochondrial dysfunction is a key determinant of the rare disease lymphangioleiomyomatosis and provides a novel therapeutic target ' , Oncogene , vol. 38 , pp. 3093-3101 . https://doi.org/10.1038/s41388-018-0625-1en
dc.identifier.issn1476-5594
dc.identifier.otherPURE: 141706801
dc.identifier.otherPURE UUID: 6f9d8d96-fbaa-4027-b5bd-c967caf267e9
dc.identifier.otherRIS: urn:4DD4F61B3ED263D6AB099AEA3231E6DD
dc.identifier.otherRIS: Abdelwahab2018
dc.identifier.otherScopus: 85058854414
dc.identifier.otherMendeley: 36e6dfde-b7b9-3d37-854b-7497f4cc948b
dc.identifier.otherWOS: 000465167600015
dc.identifier.urihttp://hdl.handle.net/2164/11805
dc.descriptionAcknowledgements The authors are grateful to Prof. Dr. Laszlo Seress, Professor Emeritus, Central Electron Microscope Laboratory, University of Pecs, Pecs, Hungary for his invaluable assistance with electron microscopic studies using the Jeol 1200 TEM and Jeol 1400 TEM electron microscopes. Jeol TEM was funded by the GINOP-2.3.3-15-2016-0002 (New generation electron microscope: 3D ultrastructure). We would also like to thank Dr. Veronika Csongei, PhD, Senior Lecturer, Department of Pharmaceutical Biotechnology and Janos Szentagothai Research Centre, University of Pecs, Pecs, Hungary for assistance with statistical analysis. Funding JEP was supported by the European Union and the State of Hungary, co-financed by the European Social Fund in the framework of TÁMOP-4.2.4.A/2-11/1-2012-0001 “National Excellence Program”.en
dc.format.extent9
dc.language.isoeng
dc.relation.ispartofOncogeneen
dc.rightsOpen Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.en
dc.subjectSDG 3 - Good Health and Well-beingen
dc.subjectBIOGENESISen
dc.subjectCELLen
dc.subjectCHAINen
dc.subjectCYTOCHROME-Cen
dc.subjectESTROGENen
dc.subjectFEATURESen
dc.subjectGENEen
dc.subjectPHOSPHORYLATIONen
dc.subjectTSC2en
dc.subjectQH301 Biologyen
dc.subjectGeneticsen
dc.subjectMolecular Biologyen
dc.subjectCancer Researchen
dc.subjectSupplementary Dataen
dc.subject.lccQH301en
dc.titleMitochondrial dysfunction is a key determinant of the rare disease lymphangioleiomyomatosis and provides a novel therapeutic targeten
dc.typeJournal articleen
dc.contributor.institutionUniversity of Aberdeen.Institute of Medical Sciencesen
dc.contributor.institutionUniversity of Aberdeen.Medical Sciencesen
dc.description.statusPeer revieweden
dc.description.versionPublisher PDFen
dc.identifier.doihttps://doi.org/10.1038/s41388-018-0625-1
dc.identifier.urlhttp://www.scopus.com/inward/record.url?scp=85058854414&partnerID=8YFLogxKen
dc.identifier.urlhttp://www.mendeley.com/research/mitochondrial-dysfunction-key-determinant-rare-disease-lymphangioleiomyomatosis-provides-novel-theraen
dc.identifier.vol38en


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