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Many host gene expression levels are not good surrogates [ 63, 74- 76].
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Virus infection activates transcription and translation of many host genes.
Many host genes and proteins responding to WSSV infection were also identified through large scale approaches [ 3– 7].
As discussed later in more detail, many host genes that are required for phagocytosis have been identified using Drosophila in a series of genome-scale cell-based screens.
The TLRs have been shown to be involved in the activation of many host genes, including cytokines, chemokines and antimicrobial peptides such as β-defensin 2 [ 12- 14].
Thus, even though many host genes have been accrued by the phage kingdom as a whole, the vast majority of POGs are phylogenetic characters that are robust against repeated phage-host gene exchange, and may be useful phylogenetic markers.
Our study shows that compared to the wild type, infection of mouse brains by the mutant strain leads to significant up-regulation of many host genes involved in host protective immune response.
Based on this analysis, WRKY33 appears to have a prominent repressive role on the transcription of many specific host genes indicating a negative regulatory function of WRKY33 in mediating immunity to this pathogen.
The largest category is that of genes of unknown function (20 genes), but many host response modifiers or host-range genes (16 genes) were also found.
Viruses, which typically employ many components of the host gene expression machinery, also encode miRNAs.
Over half of the 89 miRNAs (65%) are intragenic; interestingly, many of the host genes have reported roles in cancer.
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