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dc.contributor.authorRuiz L.M.
dc.contributor.authorJensen E.L.
dc.contributor.authorRossel Y.
dc.contributor.authorPuas G.I.
dc.contributor.authorGonzalez-Ibanez A.M.
dc.contributor.authorBustos R.I.
dc.contributor.authorFerrick D.A.
dc.contributor.authorElorza A.A.
dc.date.accessioned2020-09-02T22:27:32Z
dc.date.available2020-09-02T22:27:32Z
dc.date.issued2016
dc.identifier10.1016/j.mito.2016.04.005
dc.identifier.citation29, , 18-30
dc.identifier.issn15677249
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6112
dc.descriptionCopper is integral to the mitochondrial respiratory complex IV and contributes to proliferation and differentiation, metabolic reprogramming and mitochondrial function. The K562 cell line was exposed to a non-cytotoxic copper overload to evaluate mitochondrial dynamics, function and cell fate. This induced higher rates of mitochondrial turnover given by an increase in mitochondrial fusion and fission events and in the autophagic flux. The appearance of smaller and condensed mitochondria was also observed. Bioenergetics activity included more respiratory complexes, higher oxygen consumption rate, superoxide production and ATP synthesis, with no decrease in membrane potential. Increased cell proliferation and inhibited differentiation also occurred. Non-cytotoxic copper levels can modify mitochondrial metabolism and cell fate, which could be used in cancer biology and regenerative medicine. © 2016 Elsevier B.V. and Mitochondria Research Society.
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectAutophagy
dc.subjectBioenergetics
dc.subjectCopper
dc.subjectErythropoiesis
dc.subjectMitochondria
dc.subjectMitochondrial dynamics
dc.subjectadenosine triphosphate
dc.subjectcopper
dc.subjectreactive oxygen metabolite
dc.subjectcopper
dc.subjectaerobic metabolism
dc.subjectArticle
dc.subjectautophagy
dc.subjectbioenergy
dc.subjectcell differentiation
dc.subjectcell fate
dc.subjectcell function
dc.subjectcell proliferation
dc.subjectcell structure
dc.subjectcontrolled study
dc.subjectcopper overload
dc.subjectenergy metabolism
dc.subjectenzyme synthesis
dc.subjecterythroleukemia cell
dc.subjecthuman
dc.subjecthuman cell
dc.subjectmitochondrial dynamics
dc.subjectmitochondrial membrane potential
dc.subjectmitochondrial respiration
dc.subjectnutritional disorder
dc.subjectoxygen consumption
dc.subjectpriority journal
dc.subjectupregulation
dc.subjectdrug effects
dc.subjectenergy metabolism
dc.subjectK-562 cell line
dc.subjectmetabolism
dc.subjectmitochondrion
dc.subjectCell Differentiation
dc.subjectCell Proliferation
dc.subjectCopper
dc.subjectEnergy Metabolism
dc.subjectHumans
dc.subjectK562 Cells
dc.subjectMitochondria
dc.titleNon-cytotoxic copper overload boosts mitochondrial energy metabolism to modulate cell proliferation and differentiation in the human erythroleukemic cell line K562
dc.typeArticle


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