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a reduction in Ca2 + flux into the mitochondrialedto lower ATP content in neuronal cells
that a reduction in Ca2 + flux into the mitochondrialedto lower ATP content in neuronal cells
the opening of the pores in the Mitochondrialeadingto a decrease of ATP which leads to apoptosis of cells
Impaired oxidative phosphorylationleadingto a decrease in cellular energy ( ATP ) production
This inhibitionleadsto a decline of adenosine triphosphate ( ATP ) in cells directly
This defectleadsto decreased cellular energy ( ATP ) production
ischemialeadsdecreased adenosine triphosphate ( ATP ) production , increased cell Ca2
Compounds that interfere with the synthesis of either mitochondrial DNA or mtDNA - encoded proteins reduce the levels of 13 proteins essential for oxidative phosphorylationleadingto a decrease in mitochondrial adenosine triphosphate ( ATP ) production
I activityresultedin decreased ATP levels in cultured cells
Ischemiaresultsin decreased cellular oxidative phosphorylation leading into decreased ATP
The metabolic poisoningresultedin a marked decrease in cellular ATP content
The metabolic poisoningresultedin a marked decrease in cellular ATP content by
Research indicatescan resultfrom a lack of ATP to power the cells
The lattermay resultfrom decreased ATP release from red blood cells [ 71
This inhibitionleadsto a decline of adenosine triphosphate ( ATP ) in cells
Acute hypoxialeadsto a decrease in cellular ATP levels
Enhanced expression of MYCcausesa decrease in cellular ATP levels
A progressive decline in levels of CBFeventually resultsin decreased ATP ( energy ) production within a neuron
11/01/1990 - " Acute hypoxialeadsto a decrease in cellular ATP levels
cerebral ischemialedto a decrease in intracellular ATP levels
These results ... in whichresultedin decreased intracellular ATP levels
that chronic alcohol consumption increases the sensitivity of liver cells to oxygen deficitsresultingin decreased ATP concentrations in the cells
disrupts the mitochondrial membraneleadingto a decrease in intracellular ATP levels
a factcausesATP release from glial cells
cisplatin - induced mitochondrial dysfunction ... the respiratory chainresultsin decreased intracellular levels of ATP
the oxidative phosphorylationleadsto the decreases of ATP levels in cell
Rho - kinase ... mechanismsinfluenceATP release from cells
blood glucoseleadingto depletion of Adenosine Triphosphate ( ATP ) in cells
This serotonin release then provides negative feedback onto the Type II cellsresultingin decreased release of ATP
Rotenone , an inhibitor of the electron transport chaincauseda significant decrease in cellular ATP levels
This defectleadsto decreased production of cellular energy ( ATP
It was suggested that the mitochondrial respiratory - chain is the site for metformin action in humancausesreduction in cellular ATP
This reduction in mitochondrial respirationleadsto a reduced ability to produce cellular adenosine triphosphate ( ATP
The nuclear changes ... oxidative phosphorylationleadsto decrease in cellular ATP
1 ) metformincausesa reduction in cellular ATP
The post - treatmentresultedin a decrease in the cellular ATP
environmental stressescauseATP depletion in cells
inhibits both respiration and glycolysisleadingto a decrease in cellular ATP
both respiration and glycolysisleadingto a decrease in cellular ATP
the presence of extracellular Ca2 +causesa decrease in intracellular ATP
from damage by free radicals in the aging processmight resultfrom damage by free radicals in the aging process
tissue acidosis in these areascan causetissue acidosis in these areas
in low cellular energy productionresultsin low cellular energy production
to cell deathleadsto cell death
due to this glucose uptakewould resultdue to this glucose uptake
to malignancymay leadto malignancy
in a huge increase in antibiotic toleranceresultedin a huge increase in antibiotic tolerance
howeverwould ... leadhowever
in an increase in the ratio of AMP / ATPresultingin an increase in the ratio of AMP / ATP
to cellular degenerationleadingto cellular degeneration
in a similar transcriptional signature as Diclofenac treatments in vivoresultedin a similar transcriptional signature as Diclofenac treatments in vivo
to delayed DnaA induction activity in PCC9511might have ... contributedto delayed DnaA induction activity in PCC9511
to the activation of the P2X7 purinergic receptorcontributeto the activation of the P2X7 purinergic receptor
in an increase in the ratio of AMP / ATPresultingin an increase in the ratio of AMP / ATP
an increase of Mg2 + concentrationcausesan increase of Mg2 + concentration
to the pathology of this eye disease and other neurodegenerative diseasesmay contributeto the pathology of this eye disease and other neurodegenerative diseases
failure of Na - K pump and sodium - calcium exchangecausingfailure of Na - K pump and sodium - calcium exchange
to a decrease in Na+/K+-ATPase activitywould leadto a decrease in Na+/K+-ATPase activity
to necrosis with cell death in a short timeleadsto necrosis with cell death in a short time
in the increase in ADP / ATP ratiowill resultin the increase in ADP / ATP ratio
in a deformity in the cell membrane from the Biconcave Disc Shape to a Disc - Sphere Shaperesultsin a deformity in the cell membrane from the Biconcave Disc Shape to a Disc - Sphere Shape
in muscle weakness , exercise intolerance , and fatigue in patients with mitochondrial myopathiesoften resultingin muscle weakness , exercise intolerance , and fatigue in patients with mitochondrial myopathies
to lysis and cell deathleadsto lysis and cell death
immobilization and death of the wormcausesimmobilization and death of the worm
adjacent glial cells to release hydrogen ions , which raise the acidity of the immediate extracellular environmentcausesadjacent glial cells to release hydrogen ions , which raise the acidity of the immediate extracellular environment
to osteoarthritis in miceledto osteoarthritis in mice
cell death in mouse hepatocytes and in a hepatoma cell line ( HepG2can ... causecell death in mouse hepatocytes and in a hepatoma cell line ( HepG2
to oxidative stress and chronic inflammationleadsto oxidative stress and chronic inflammation
to activation of AMPK [ 27 - 30leadingto activation of AMPK [ 27 - 30
in increases in Ca2 + in the mitochondria.34 This subsequently induces mitochondrial fragmentation and elevation of mitochondrial permeability , which then initiates the intrinsic apoptotic signaling pathway.10,35,36resultingin increases in Ca2 + in the mitochondria.34 This subsequently induces mitochondrial fragmentation and elevation of mitochondrial permeability , which then initiates the intrinsic apoptotic signaling pathway.10,35,36
to the regulation of the blood flow and studiescontributesto the regulation of the blood flow and studies
to mitochondrial damage [ 24leadsto mitochondrial damage [ 24
thusmay ... leadthus
to increased cytoplasmic Ca from Sarcolesmaleadsto increased cytoplasmic Ca from Sarcolesma
T helper behaviorwould ... influenceT helper behavior
disturbances in protein synthesiscausesdisturbances in protein synthesis
in a decreased saturation of enzymes that use ATP as substratewill resultin a decreased saturation of enzymes that use ATP as substrate
to impairment of ionic pumps , cell swelling , clearing of the cytosolleadingto impairment of ionic pumps , cell swelling , clearing of the cytosol
alsoleadalso
ultimatelyresultsultimately