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the experimental conditionscreatinglow [ ATP
the disruption of Tim21(passive) caused bya low amount of ATP
mitochondrial disruption(passive) caused bya low amount of ATP
mitochondrial dysfunction(passive) caused bylow ATP levels
the CCCP and succinate(passive) caused bylow ATP conditions
a variety of reasons(passive) can be caused byLow ATP
CBScan causelow ATP production
Low CoQ10leadsto low ATP
DNA damage(passive) can be caused bylow ATP energy
peroxynitrite that results in low uric acid(passive) caused bythe low ATP
bacteria ... ableto causelow ATP enery
the presence of amygdalin in the kernels(passive) caused bylow ATP levels
a unique , pleomorphic bacteria which gets inside cells and blocks the production of ATP energy(passive) is caused byLow ATP energy
the presence of amygdalin in apricot kernels(passive) caused bylow ATP levels
antimycin(passive) caused bya low amount of ATP
cells to be sick and decrease their ability to heal , regenerate or function properlycausescells to be sick and decrease their ability to heal , regenerate or function properly
our cells to be sick and decreases their ability to heal , regenerate , or function properlycauseour cells to be sick and decreases their ability to heal , regenerate , or function properly
our cells to be sick and decreases their ability to recover , regenerate , and/or function properlycauseour cells to be sick and decreases their ability to recover , regenerate , and/or function properly
a decline in cognitive function – the “ brain fog ” so commonly reported , in which victims find themselves struggling through a dark haze , unable to concentrate and often forgetting simple thoughts and tasksmay causea decline in cognitive function – the “ brain fog ” so commonly reported , in which victims find themselves struggling through a dark haze , unable to concentrate and often forgetting simple thoughts and tasks
in a lack of uncoupling ... thus making the product ineffectiveresultedin a lack of uncoupling ... thus making the product ineffective
phosphorylation of FPR1 and thus preserves the unphosphorylated FPR1 C - terminuspreventsphosphorylation of FPR1 and thus preserves the unphosphorylated FPR1 C - terminus
a reduction in mTOR signalling and thus protein synthesis[76,90causesa reduction in mTOR signalling and thus protein synthesis[76,90
to the activation of AMPK , the master cell energy sensor that shifts cellular metabolism to a more efficient pathway relying on mitochondrial ATP production ( i.e. , OXPHOS ) andleadsto the activation of AMPK , the master cell energy sensor that shifts cellular metabolism to a more efficient pathway relying on mitochondrial ATP production ( i.e. , OXPHOS ) and
to reduced calcium ATPase activity and thus a failure to repair any injury caused by reactive metabolites , such as an increase in intracellular calciumcould leadto reduced calcium ATPase activity and thus a failure to repair any injury caused by reactive metabolites , such as an increase in intracellular calcium
the resting KATP channel tone in DA neurons(passive) was caused bythe resting KATP channel tone in DA neurons
a lack of energy and endurancecausesa lack of energy and endurance
to fatigue and weak musclesleadto fatigue and weak muscles
an absence of vitality and continuancecausean absence of vitality and continuance
a metabolic disease(passive) caused bya metabolic disease
in less strengthresultin less strength
to lower PARG / TRMP2 in the endleadto lower PARG / TRMP2 in the end
to a low ratio of ATP/[ADP+AMPleadingto a low ratio of ATP/[ADP+AMP
to low Glutathione level in the bodyleadsto low Glutathione level in the body
activation of Ira2 activity to reduce GTP - Ras1 levelscausesactivation of Ira2 activity to reduce GTP - Ras1 levels
to AMPK activationleadsto AMPK activation
in increased concentrations of AMPresultin increased concentrations of AMP
mitochondria disruptioncausemitochondria disruption
cell dysfunctioncan causecell dysfunction
to fatigue and feelings of sluggishnessleadto fatigue and feelings of sluggishness
acceptor - side limitation(passive) caused byacceptor - side limitation
in toleranceresultin tolerance
preferential binding of AdpA and high ATP levels causing dissociation of AdpA and association of DnaA.causingpreferential binding of AdpA and high ATP levels causing dissociation of AdpA and association of DnaA.
in low energy levelswill resultin low energy levels
to AMPK stimulation ( 1 ) and presumably autophagy inductionleadsto AMPK stimulation ( 1 ) and presumably autophagy induction
mitochondrial disruption , which results in either apoptosis or necrosis depending on the level of ATP left in the cell ( 4 , 19–21 , 31causemitochondrial disruption , which results in either apoptosis or necrosis depending on the level of ATP left in the cell ( 4 , 19–21 , 31
the cells to " revert to fermentationcausesthe cells to " revert to fermentation
to the induction of AMPK , which in turn activates PGC-1 alpha in WAT of SSAT miceleadto the induction of AMPK , which in turn activates PGC-1 alpha in WAT of SSAT mice
to 3 things protein + hemeleadsto 3 things protein + heme
apoptosome formation and caspase activation ... shifting the CD execution toward necrosis ( Nicotera et al . , 1998preventapoptosome formation and caspase activation ... shifting the CD execution toward necrosis ( Nicotera et al . , 1998
to the induction of AMPK , which in turn activates PGC-1α in WAT of SSAT miceleadto the induction of AMPK , which in turn activates PGC-1α in WAT of SSAT mice
vascular relaxationwill causevascular relaxation
a significant negative shift in the Ih activation curve ( Carbone et al . , 2017 ... suggesting that Ih dysfunction may be linked to the mechanisms that trigger PD , such as mitochondrial failure and ATP depletion , and that Ih dysfunction may act in concert with SNc - specific synaptic connectivity to promote selective vulnerability ( Masi et al . , 2015causeda significant negative shift in the Ih activation curve ( Carbone et al . , 2017 ... suggesting that Ih dysfunction may be linked to the mechanisms that trigger PD , such as mitochondrial failure and ATP depletion , and that Ih dysfunction may act in concert with SNc - specific synaptic connectivity to promote selective vulnerability ( Masi et al . , 2015
numerous bodily dysfunctions ... because organs do n't have the energy they need to work rightcan causenumerous bodily dysfunctions ... because organs do n't have the energy they need to work right
in increased and accelerated illness , metabolic diseases , and easier weight gaincan resultin increased and accelerated illness , metabolic diseases , and easier weight gain
opening of ATP - sensitive K+ ( K+ATP ) channels , which would counteract the depolarization ... ultimately reducing the time for Ca2 + influxmay ... triggeropening of ATP - sensitive K+ ( K+ATP ) channels , which would counteract the depolarization ... ultimately reducing the time for Ca2 + influx