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These interactions are implicated in the modulation of virus replication and the induction of host defense responses.
More data are needed to determine whether modulation of virus load by therapeutic agents affects clinical outcomes.
More data are needed on whether modulation of virus load by therapeutic agents can affect clinical outcomes.
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We screened the newly identified ISGs for those participating in the modulation of virus-induced innate immune activation.
Viruses with larger genomes encode multiple proteins with dedicated functions in the modulation of virus-host interaction at different levels rather than direct roles in virus reproduction [ 2- 5].
While its role in the reverse transcription process implies interaction with the nuclear form of the DNA repair enzyme UNG2 for modulation of the virus mutation rate [4] [6], it was suggested that Vpr participates in the DNA nuclear import process through docking to the nuclear envelope (NE) by interaction with components of the nuclear pore complex [7] [10], such as the nucleoporin hCG1.
Many of these signaling events have been shown to be important for post-binding virus entry steps, for example modulation of microtubules, movement of virus in the cytoplasm and nuclear delivery of viral DNA [48].
However, the role of DELLA proteins in the modulation of signaling events during virus infection has not been characterized yet.
Although the DELLA proteins have been reported to be central players in hormone cross-talk, their role in the modulation of hormone signaling during virus infections remains unknown.
In addition to its crucial role in virus entry and trafficking, many viruses activate PI3K signalling for modulation of post-internalization events such as virus replication and assembly (highlighted in Diehl and Schaal, 2013).
Once again, these results show a diferential modulation of protein level by viruses belonging to different families.
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