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Notably, the membrane potential appears to be reduced in differentiated cells.

The drop of mitochondrial membrane potential appears to be associated with caspase-3 activation (Fig. 6A).

Control of membrane potential appears also to be important in the regulation of differentiation in nonexcitable cells, as demonstrated in the adipogenic and osteogenic differentiation of mesenchymal stem cells (65).

Since the resting membrane potential appears depolarized in spinal muscular atrophy (related to loss of fast K+ channels as indicated by the modelling), such changes may be at least part of the reason for the increase in τSD.

Although mitochondrial membrane potential appears to be preserved in knockout fruitflies [ 244], stable knockdown of DJ-1 in neuroblastoma cells led to a decrease in mitochondrial membrane potential, increase in mitochondrial fragmentation and accumulation of LC3 around mitochondria.

Similar(55)

The membrane potential appearing with first action potential was significantly reduced (mV, control: 35.5 ± 5.7; BmK I: 11.5 ± 0.9) (Fig. 6H).

However, the dynamics of the membrane potential appeared to be far more complicated than mere damped or limit cycle oscillations even in the absence of oscillatory hair bundles [16].

However, in the case of astrocytes, such rapid oscillations of membrane potential appear meaningless as they do not emulate any known physiological mechanism of astrocytic activation.

As Ca2+ sensitization i.e. alteration of the relationship between force and [Ca2+] appears not to be marked in myometrium under physiological conditions (e.g. [24]), changes in excitability i.e. membrane potential appeared the most likely cause of increased Ca2+ and force with SR Ca2+ depletion.

Although no data on passive membrane properties were presented, the displayed current and membrane potential traces appear equivalent to those of fully mature neurons.

However, as opposed to ROS production generated by reverse electron transport on succinate, reduced membrane potential does not appear to underlie the effect of mitoQ to increase ROS during forward electron transport (respiration on complex I substrates).

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