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As shown in Fig. 2A, VACV WR entry was inhibited by MAb 7D11 in both BS-C-1 and S2 cells.
We demonstrated that entry was inhibited by a MAb to L1 and was dependent on the presence of A28, two of the proteins known to be essential for VACV entry in mammalian cells.
Although virus entry and infection were not inhibited by the dominant-negative dynamin-2 mutant, entry was inhibited by the general dynamin inhibitor, dynasore, indicating that virus entry is dynamin dependent.
In both cases robust Ca2+ release was observed under Ca2+-free conditions, whereas Ca2+ entry was inhibited.
Whereas Ca2+ release was sensitive to both the RyR blocker RuRed and the cADPR antagonist 8-Br-cADPR, Ca2+ entry was inhibited by the non-specific Ca2+ entry blockers Gd3+ and SKF-96365, as well as by 8-Br-cADPR [ 10].
Whereas Ca2+ release was sensitive to both the RyR (ryanodine receptor) blocker RuRed (Ruthenium Red) and the cADPR antagonist 8-Br-cADPR (8-bromo-cyclic ADP-ribose), Ca2+ entry was inhibited by the Ca2+ entry blockers Gd3+ (gadolinium ion) and SKF-96365, as well as by 8-Br-cADPR.
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However, K1F phage entry requires K1 capsule, while T7 phage entry is inhibited by the capsule.
Entry is inhibited by albumin [6] and by cell-specific enzymes like ecto-lipid phosphate phosphohydrolase (LPP) [25].
Both at physiological and at sub-physiological temperatures, this entry mechanism was inhibited by depletion of the intracellular ATP pool.
That acid-induced disruption of EV membranes partly rescued infection in cells with impaired macropinosomal acidification suggested that EV membrane disruption was indeed the step in EV entry that was inhibited by BafA.
For 5-HT we showed that around 60% of the rise in [Ca2+]i it produces is due to L-type Ca2+ entry, as it was inhibited by nifedipine.
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