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ZXR-1 could translocate into cells, target on the mitochondria and induce cell apoptosis, while ZXR-2 directly targeted on the cell membranes and caused membrane lysis.
Further, the protein leakage study revealed that the Micrococcus luteus cells treated with compound 5l caused membrane permeability which resulted in protein leakage and subsequent bacterial cell death.
An examination of foulants components by wavelength dispersive X-ray fluorescence showed that the combination of organic foulants and inorganic compounds enhanced the formation of gel layer and thus caused membrane fouling.
The KCl application caused membrane depolarization, and as a consequence, opening of voltage-dependent calcium channels.
This was also confirmed by TEM where CXCL9 irrespective of SpeB-treatment caused membrane disruption and disintegration of bacterial chains (Fig 2B, CXCL9, Buffer / SpeB).
Samples were prepared and loaded according to standard Novex gel protocols with the exception that the samples were incubated at room temperature prior to loading, as boiling caused membrane protein aggregation.
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The accumulation of H2O2 then begins and exacerbates membrane lipid peroxidation, causing membrane damage.
Copper oxide (CuO) nanoparticles cause membrane damage to Escherichia coli as demonstrated by K+ leakage [15].
ZnO-NPs are bactericidal and thus disrupt membrane causing membrane dysfunction, resulting in their internalization into the bacteria (Fig. 5a).
This change allows the amphiphilic α-helical peptide to bind to the endosomal membrane, causing membrane disruption.
The molecular level interaction between the cell membrane and the dGNPs that causes membrane rupture remains to be established.
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