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by oxidative damage to lipids and proteins(passive) caused byincreased plasma membrane permeability
Low aquaporin levels , or down - regulated aquaporin expression , accompanied by decreased plant vigourledto decreased plasma membrane permeability
Opening of potassium channelscauseshyperpolarization of the plasma membrane
ATP - sensitive potassium ion channels ( KATP channels ... to closeresultingin plasma membrane depolarization
channel formation ... potassiumcausesplasma membrane depolarization
sodium arsenitecausedaltered hepatocyte plasma membrane permeability
the subsequent efflux of K ionscauseshyperpolarization of the plasma membrane
S - type anion channelscausesin plasma membrane depolarization
the involvement of extracellular calcium in the ABA - induced inhibition of the H+-ATPasecausingthe plasma membrane depolarization
potassiumcausesplasma membrane depolarization
This influx in anionscausesa depolarization of the plasma membrane
Erg inhibitioncausedplasma membrane depolarization
a second componentleadingto the plasma membrane depolarization
Polyaminescauseplasma membrane depolarization
IR - evokedcontributeto plasma membrane depolarization
Modulations of other ion transport systemscould also leadto the plasma membrane depolarization
The opening of these channels ... a stimuluscausesdepolarisation of the plasma membrane
nitric oxide synthaseresultingin plasma membrane depolarization
ABA is thus able to inhibit the proton pumpleadingto the plasma membrane depolarization
by USA300(passive) caused byPMN ) plasma membrane permeability
bacterial toxins , activation of P2X7R by ATP release from necrotic cells(passive) caused byplasma membrane permeability
by impaired ATP production(passive) caused byplasma membrane permeability
by H2O2(passive) caused byplasma membrane permeability
these toxinsdo ... causepermeabilization of the plasma membrane
by the interaction of determinate surroundings(passive) caused byplasma membrane fluidity
by nanotubes interaction(passive) caused byplasma membrane invaginations
nanotubes interaction(passive) caused byplasma membrane invaginations
The formation of the phospholipid bilayerresultsplasma membrane
of proteins in the bilayer(passive) is composedplasma membrane
of lipid and protein(passive) is composedPlasma membrane
of lipids & proteins(passive) is composedPlasma membrane
of lipids and proteins(passive) is composedPlasma membrane
of proteins and lipids(passive) is composedPlasma membrane
of two layers one layer of phospholipids and one layer of proteins(passive) is composedPlasma membrane
receptor mediated signal transductionoriginatingat the plasma membrane
by ROS(passive) caused byplasma membrane
a SNARE complexcomposedof the plasma membrane
of DHA(passive) is composedplasma membrane
Microvesiclesoriginatefrom evagination of the plasma membrane
of a lipid bilayer that is not as rigid as a bacterial cell wall(passive) is composedPlasma membrane
to the formation of TEMscontributeto the formation of TEMs
necrosisultimately causingnecrosis
to reduced cell - cell adhesionleadsto reduced cell - cell adhesion
further increase in intracellular Ca2causesfurther increase in intracellular Ca2
in increased carboxyfluorescein ( CF ) retention derived from the intracellular hydrolysis of carboxyfluorescein diacetate ( CFDAresultingin increased carboxyfluorescein ( CF ) retention derived from the intracellular hydrolysis of carboxyfluorescein diacetate ( CFDA
to influx of Ca2leadingto influx of Ca2
an influx of Ca2causesan influx of Ca2
to the generation of endocytic vesicles larger than those enclosed by the coatleadto the generation of endocytic vesicles larger than those enclosed by the coat
in increased glucose uptakeresultingin increased glucose uptake
in channel internalization and degradationresultsin channel internalization and degradation
to ion leakage from the cellresultsto ion leakage from the cell
to the release of the ILVs to the extracellular space as exosomes ( Mathivanan et al . , 2010leadsto the release of the ILVs to the extracellular space as exosomes ( Mathivanan et al . , 2010
voltage - gated Ca2causesvoltage - gated Ca2
in the era of endocytic vesicles bigger than those enclosed from the coatresultin the era of endocytic vesicles bigger than those enclosed from the coat
in to ion leakage from the cell [ 50resultsin to ion leakage from the cell [ 50
in cellresultsin cell
the opening of intracellular channelscausesthe opening of intracellular channels
in supplementary ATP releaseresultedin supplementary ATP release
massive influx of calciumcausesmassive influx of calcium
to the formation of an early endosome in the cytosolleadsto the formation of an early endosome in the cytosol
vasodilationultimately causingvasodilation
to apoptosisleadingto apoptosis
to the shedding of the vesicles3,4leadsto the shedding of the vesicles3,4
to increased integrin - dependent adhesioncontributesto increased integrin - dependent adhesion
the opening of intracellular channels and enables the introduction of electroporated assetscausesthe opening of intracellular channels and enables the introduction of electroporated assets
in less active membrane - associated permeases , and also in major membrane transport reduction ( Beltran et al . , 2006bresultsin less active membrane - associated permeases , and also in major membrane transport reduction ( Beltran et al . , 2006b
to their trafficking phenotypemay contributeto their trafficking phenotype
an opening of voltage - gated calcium channelspromptingan opening of voltage - gated calcium channels
to calcium influx and cell deathleadingto calcium influx and cell death
to the formation of pre - autophagosomal structurescontributesto the formation of pre - autophagosomal structures
to cytolysis of the cellleadingto cytolysis of the cell
activationresultingactivation
to a change in membrane fluidityleadingto a change in membrane fluidity
of proteins in the bilayeris composedof proteins in the bilayer
of phospholipids and proteinscomposedof phospholipids and proteins
to loss of essential ions ( e.g. K+leadingto loss of essential ions ( e.g. K+
of lipidwas composedof lipid
to the localizationcontributesto the localization
repairwerediscoveredrepairwere
from the three major functional domains of the rat hepatocyte cell surfaceoriginatingfrom the three major functional domains of the rat hepatocyte cell surface