This chemical screen showed that a compound known as digoxin — a plant - derived cardiac toxin often used to treat various heart conditions —
inhibited wild type HIV - 1 more than the mutated strain.
Not exact matches
These are the same T cell genes
inhibited by digoxin, and since replication of integrated HIV - 1 requires transcription of nearby genes, this provides an explanation for why
wild type HIV - 1 is more susceptible to digoxin: digoxin represses the genes that the virus more frequently targets for integration.
Moreover, purified Qβ virions
inhibited wild -
type MurA, but not the mutant MurA, in vitro.
Binding to the COX - 2 promoter sequence could be specifically
inhibited by excess amount of cold
wild -
type probes, but not by STAT6 binding site - mutant probes (Figure 6b and c).
Using this treatment scheme, we observed a robust difference on day 9 in the disease activity indices of
wild -
type and Rassf1a knockout mice that was significantly
inhibited with the use of the RIPK2 inhibitors, especially RIPK2 inhibitor 1 (Fig. 6B; Table 2).