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a mutationcausesone mitochondria
illness or genetic mutationcan causemitochondria myopathy
by the flavonoid(passive) caused byintracellular mitochondria
In addition , while initially SCNT - ESCs were considered a panacea for patients with mitochondrial disorders , recent studies have shown that mitochondrial - mismatched stem cells when reintroduced into the cells from which the donor nuclei were obtainedcan causemitochondria - related antigenicity
that upon Bcl - xL phosphorylation , the interaction of Bax and Bcl - xL was impairedresultingin Bax translocating to the mitochondria
in the bases(passive) was contributed22,000 mitochondria
of proteins encoded by the nuclear and mitochondrial genomes(passive) are composedMitochondria
by defects of mitochondrial fission(passive) caused bymitochondria
by increased permeability of their inner membrane(passive) caused bymitochondria
Bcl-2 family proteins ... apoptotic thresholdsetup the mitochondria
The role of Bcl-2 family proteinssetup the mitochondria
of outer membrane , intermembrane space , inner membrane , and mitochondrial matrix(passive) are composedMitochondria
Egg cellscontributemitochondria
only egg cellscontributemitochondria
Mutations in one of these genesleadmitochondria
the proteins / genesoriginatingfrom the mitochondria
of proteins and enzymes(passive) is composedmitochondria
resveratrol - induced apoptosisoriginatesin the mitochondria
Mitochondria depolarizationcausedmitochondria
The proapoptotic gene Bax from the BCL familycan causemitochondria
of outer membrane and inner membrane(passive) are composedMitochondria
the cellsresultingin the mitochondria
the egg cellcontributesmitochondria
by Ca2 + release from the ER(passive) to be influenced bymitochondria
by oxidative stress or ischemia(passive) caused bymitochondria
the damage these drugscauseto the mitochondria
of two membranes , an inner and outer membrane(passive) are also composedMitochondria
overexpression of Drp1can influencemitochondria
by ROS(passive) caused bymitochondria
ROSlargely originatingin the mitochondria
ROSoriginatingin mitochondria
the ROSoriginatein mitochondria
by proteins and lipids(passive) are ... composed byMitochondria
by proteins and lipids(passive) are ... composedMitochondria
mutationsdiscoveredin mitochondria
a mild increase in reactive oxygen species generationoriginatingfrom the mitochondria
oxidative stressoriginatingin the mitochondria
oxidative stressoriginatingfrom the mitochondria
by exposure to reactive oxygen species(passive) can be caused bymitochondria
by free radicals(passive) caused bymitochondria
cytochrome c release and caspase activationcausescytochrome c release and caspase activation
to an increase in mitochondrial oxygen consumption and ATP formation that enhanced cell growth [ 41,42ledto an increase in mitochondrial oxygen consumption and ATP formation that enhanced cell growth [ 41,42
a green shift in cells indicating they are apoptoticwill causea green shift in cells indicating they are apoptotic
from the inner cell mass where oxygen is low13 and glycolysisoriginatefrom the inner cell mass where oxygen is low13 and glycolysis
alsomay ... leadalso
mitochondrial stress(passive) caused bymitochondrial stress
NLRP3 inflammasome activationcausedNLRP3 inflammasome activation
in cell deathresultingin cell death
neutrophil recruitmentcauseneutrophil recruitment
to an equilibration of activated and nonactivated mitochondrialeadingto an equilibration of activated and nonactivated mitochondria
in decreased citrate oxidaseresultingin decreased citrate oxidase
to decreased ATP production and increased ROS formationleadingto decreased ATP production and increased ROS formation
to increased ROS production , oxidative stress and cellular dysfunctionleadingto increased ROS production , oxidative stress and cellular dysfunction
in cytochrome c release ... leading to caspase activation and cell deathresultsin cytochrome c release ... leading to caspase activation and cell death
to increased ROS production , oxidative stress and cellular dysfunction [ 33leadingto increased ROS production , oxidative stress and cellular dysfunction [ 33
in increased adenosine triphosphate ( ATP ) production and increase in intracellular reactive oxygen speciesresultingin increased adenosine triphosphate ( ATP ) production and increase in intracellular reactive oxygen species
to longevity determinationcontributesto longevity determination
in the release of cytochrome C , apoptosome formation , and the activation of caspase-9 , which then activates caspase-3 triggering the subsequent apoptotic eventsresultingin the release of cytochrome C , apoptosome formation , and the activation of caspase-9 , which then activates caspase-3 triggering the subsequent apoptotic events
to mitochondrial membrane potential m changes and cytochrome C release from the mitochondrialeadingto mitochondrial membrane potential m changes and cytochrome C release from the mitochondria
to increased ROS production , oxidative stress and cellular dysfunction ( Saben et al . , 2014leadingto increased ROS production , oxidative stress and cellular dysfunction ( Saben et al . , 2014
to effects that may confoundleadingto effects that may confound
the activation of a cascade of caspases ... pro - apoptosis proteinscausesthe activation of a cascade of caspases ... pro - apoptosis proteins
to a reduction of cellular and mitochondrial damage andleadingto a reduction of cellular and mitochondrial damage and
to a reduction of cellular and mitochondrial damageleadingto a reduction of cellular and mitochondrial damage
release of more ROS and depletion of ATPcausesrelease of more ROS and depletion of ATP
to excessive mitochondrial potential and expression of uncoupling protein and collapse of ATP levels with the mitochondrial potentialleadingto excessive mitochondrial potential and expression of uncoupling protein and collapse of ATP levels with the mitochondrial potential
in formation of ATP through oxidative phosphorylationresultin formation of ATP through oxidative phosphorylation
to the increased release of cytochrome c and the activation of caspase-3 and may enter the nucleus to affect genetic regulation of some genes and finally to deathleadsto the increased release of cytochrome c and the activation of caspase-3 and may enter the nucleus to affect genetic regulation of some genes and finally to death
during a shift in per- meability of the outer mitochondrial membrane and the release of molecules from mitochondria ... and in especially cytochrome c ( cyt cis causedduring a shift in per- meability of the outer mitochondrial membrane and the release of molecules from mitochondria ... and in especially cytochrome c ( cyt c
in the loss of mitochondrial membrane potential , ROS generationresultedin the loss of mitochondrial membrane potential , ROS generation
to activation of caspase-9 , which activates effector caspases that degrade cellular proteinsleadsto activation of caspase-9 , which activates effector caspases that degrade cellular proteins
release of cytochrome c and apoptosiscausingrelease of cytochrome c and apoptosis
to the maintenance of cellular integrity through various mechanisms , including oxidative adenosine triphosphate production and calcium homeostasis regulationstrongly contributeto the maintenance of cellular integrity through various mechanisms , including oxidative adenosine triphosphate production and calcium homeostasis regulation
to the dynamics of cellular metabolism and reactive oxygen species ( ROS ) productioncontributeto the dynamics of cellular metabolism and reactive oxygen species ( ROS ) production
to decreased ATP production andleadingto decreased ATP production and
to decreased ATP productionleadingto decreased ATP production
to the reduction of mitochondrial oxidative phosphorylationmay leadto the reduction of mitochondrial oxidative phosphorylation
to synaptic dysfunction and apoptotic cell deathleadingto synaptic dysfunction and apoptotic cell death
free - radical production and mitochondrial depolarizationcausesfree - radical production and mitochondrial depolarization
to free radical production and mitochondrial depolarizationleadsto free radical production and mitochondrial depolarization