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The results of studies with a HeLa cell model revealed that VacA also can enter cells, traffic to the mitochondria, and then modulate mitochondrial membrane permeability by a mechanism affecting channel activity.
Inhibiting Fyn kinase did not indicate any significant loss of cell viability (Supplementary Figure S2b) and also did not appear to modulate mitochondrial membrane polarity.
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Moreover, in vitro results also shown that, SA protects H9c2 cells from oxidative stress and modulates mitochondrial membrane permeability transition (MPT).
In contrast, EPO (10 ng/ml) could not maintain mitochondrial membrane potential during gene reduction of Wnt1, illustrating that Wnt1 modulates mitochondrial membrane potential for EPO.
Viruses and bacteria have evolved strategies to modulate mitochondrial outer membrane permeabilization either by regulating the levels of host Bcl-2 family proteins or by the release of effector proteins to host cell cytosol to directly influence mitochondrial outer membrane permeabilization [38].
Recombinant PINK1 can protect from apoptosis, modulate the mitochondrial membrane potential [1], localize to mitochondrial cristae [6] and was reported to phosphorylate the mitochondrial chaperone TRAP1 [7] and the mitochondrial protease HTRA2 [8].
DAPK1 has been shown to regulate mitochondrial integrity and to modulate the mitochondrial membrane potential but, to the best of our knowledge, no work has been carried out in this respect with regard to DAPK2.
The observation that pharmacological antagonism of the RyR in neurons exposed to Tat modulated both mitochondrial membrane potential and Ca2+ stores lead us to ask whether we could observe RyR that localize to the mitochondria.
As Bax deletion did not inhibit DNA-damage-induced caspase activation and apoptotic cell death, we investigated whether the absence of Bax modulates the mitochondrial membrane permeabilization.
It has been known that the ratio of Bcl-2 to Bax determines the response to a death signal via modulating the mitochondrial membrane permeability transition (MTP) pore formation [ 23].
Recent studies have revealed the important role of Mcl-1 in modulating mitochondrial outer membrane permeabilization as destabilizing Mcl-1 can induce the release of cytochrome c from the mitochondria [39].
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