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dc.contributor.authorD'Souza, aaron
dc.contributor.authorMinczuk, M
dc.date.accessioned2018-10-04T09:38:45Z
dc.date.available2018-10-04T09:38:45Z
dc.date.issued2018-07-20
dc.identifier.issn0071-1365
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/283188
dc.description.abstractMitochondria are the major source of ATP in the cell. Five multi-subunit complexes in the inner membrane of the organelle are involved in the oxidative phosphorylation required for ATP production. Thirteen subunits of these complexes are encoded by the mitochondrial genome often referred to as mtDNA. For this reason, the expression of mtDNA is vital for the assembly and functioning of the oxidative phosphorylation complexes. Defects of the mechanisms regulating mtDNA gene expression have been associated with deficiencies in assembly of these complexes, resulting in mitochondrial diseases. Recently, numerous factors involved in these processes have been identified and characterised leading to a deeper understanding of the mechanisms that underlie mitochondrial diseases.
dc.languageeng
dc.publisherPortland Press, Ltd.
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleMitochondrial Transcription and Translation: Overview
dc.typeArticle
prism.endingPage320
prism.publicationNameEssays in Biochemistry
prism.startingPage309
prism.volume62
dc.identifier.doi10.17863/CAM.30551
dcterms.dateAccepted2018-05-14
rioxxterms.versionofrecord10.1042/EBC20170102
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/
rioxxterms.licenseref.startdate2018-05-14
dc.contributor.orcidMinczuk, Michal [0000-0001-8242-1420]
dc.identifier.eissn1744-1358
dc.publisher.urlhttp://essays.biochemistry.org/content/62/3/309.full-text.pdf
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMedical Research Council (MC_U105697135)
pubs.funder-project-idMedical Research Council (MC_UU_00015/4)
cam.issuedOnline2018-07-20
rioxxterms.freetoread.startdate2100-01-01


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International