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dc.contributor.author Chinopoulos, Christos
dc.date.accessioned 2021-05-28T08:19:34Z
dc.date.available 2021-05-28T08:19:34Z
dc.date.issued 2018
dc.identifier 85047184255
dc.identifier.citation journalVolume=27;journalIssueNumber=6;journalTitle=CELL METABOLISM;pagerange=1165-1167;journalAbbreviatedTitle=CELL METAB;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/6690
dc.identifier.uri doi:10.1016/j.cmet.2018.05.010
dc.description.abstract Mutations in mtDNA associated with OXPHOS defects preclude energy harnessing by OXPHOS. The work of Chen et al. (2018) is previewed, reporting flux pathways of glutamine catabolism in mtDNA mutant cells yielding high-energy phosphates through substrate-level phosphorylation and the influence exerted by the severity of OXPHOS impairment. Mutations in mtDNA associated with OXPHOS defects preclude energy harnessing by OXPHOS. The work of Chen et al. is previewed, reporting flux pathways of glutamine catabolism in mtDNA mutant cells yielding high-energy phosphates through substrate-level phosphorylation and the influence exerted by the severity of OXPHOS impairment. © 2018 Elsevier Inc.
dc.format.extent 1165-1167
dc.relation.ispartof urn:issn:1550-4131
dc.title OXPHOS Defects Due to mtDNA Mutations: Glutamine to the Rescue!
dc.type Journal Article
dc.date.updated 2019-01-28T14:08:18Z
dc.language.rfc3066 en
dc.rights.holder NULL
dc.identifier.mtmt 3382132
dc.identifier.wos 000434480000005
dc.identifier.wos WOS:000434480000005
dc.identifier.pubmed 29874564
dc.contributor.department SE/AOK/I/Orvosi Biokémiai Intézet
dc.contributor.institution Semmelweis Egyetem


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