000131393 001__ 131393
000131393 005__ 20240208155436.0
000131393 0247_ $$2doi$$a10.1038/s41598-017-12662-3
000131393 0248_ $$2sideral$$a136812
000131393 037__ $$aART-2017-136812
000131393 041__ $$aeng
000131393 100__ $$aFakouri, Nima Borhan
000131393 245__ $$aRev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1a axis
000131393 260__ $$c2017
000131393 5060_ $$aAccess copy available to the general public$$fUnrestricted
000131393 5203_ $$aNucleic acids, which constitute the genetic material of all organisms, are continuously exposed to endogenous and exogenous damaging agents, representing a significant challenge to genome stability and genome integrity over the life of a cell or organism. Unrepaired DNA lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-stranded gaps can block progression of the DNA replication fork, causing replicative stress and/or cell cycle arrest. However, translesion synthesis (TLS) DNA polymerases, such as Rev1, have the ability to bypass some DNA lesions, which can circumvent the process leading to replication fork arrest and minimize replicative stress. Here, we show that Rev1-deficiency in mouse embryo fibroblasts or mouse liver tissue is associated with replicative stress and mitochondrial dysfunction. In addition, Rev1-deficiency is associated with high poly(ADP) ribose polymerase 1 (PARP1) activity, low endogenous NAD+, low expression of SIRT1 and PGC1α and low adenosine monophosphate (AMP)-activated kinase (AMPK) activity. We conclude that replication stress via Rev1-deficiency contributes to metabolic stress caused by compromized mitochondrial function via the PARP-NAD+-SIRT1-PGC1α axis.
000131393 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000131393 590__ $$a4.122$$b2017
000131393 591__ $$aMULTIDISCIPLINARY SCIENCES$$b12 / 64 = 0.188$$c2017$$dQ1$$eT1
000131393 592__ $$a1.533$$b2017
000131393 593__ $$aMultidisciplinary$$c2017$$dQ1
000131393 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000131393 700__ $$aDurhuus, Jon Ambæk
000131393 700__ $$aRegnell, Christine Elisabeth
000131393 700__ $$aAngleys, Maria
000131393 700__ $$aDesler, Claus
000131393 700__ $$aHasan-Olive, Md Mahdi
000131393 700__ $$aMartín-Pardillos, Ana
000131393 700__ $$aTsaalbi-Shtylik, Anastasia
000131393 700__ $$aThomsen, Kirsten
000131393 700__ $$aLauritzen, Martin
000131393 700__ $$aBohr, Vilhelm A.
000131393 700__ $$ade Wind, Niels
000131393 700__ $$aBergersen, Linda Hildegard
000131393 700__ $$aRasmussen, Lene Juel
000131393 773__ $$g7, 1 (2017), [28 pp.]$$pSci. rep. (Nat. Publ. Group)$$tScientific reports (Nature Publishing Group)$$x2045-2322
000131393 8564_ $$s16490745$$uhttps://zaguan.unizar.es/record/131393/files/texto_completo.pdf$$yVersión publicada
000131393 8564_ $$s2657337$$uhttps://zaguan.unizar.es/record/131393/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000131393 909CO $$ooai:zaguan.unizar.es:131393$$particulos$$pdriver
000131393 951__ $$a2024-02-08-14:38:18
000131393 980__ $$aARTICLE