Fig. 7: Infection-induced silencing of HPnc4160 upregulates target gene expression and promotes bacterial-host adaptation and, potentially, oncogenesis during chronic H. pylori infection. | Nature Communications

Fig. 7: Infection-induced silencing of HPnc4160 upregulates target gene expression and promotes bacterial-host adaptation and, potentially, oncogenesis during chronic H. pylori infection.

From: A bacterial small RNA regulates the adaptation of Helicobacter pylori to the host environment

Fig. 7

H. pylori infection in vivo leads to elongation of T-repeats upstream of the HPnc4160 sRNA coding region, which results in decreased expression of HPnc4160 sRNA. Gene silencing of HPnc4160 results in increased target gene expression, coding for OMPs and CagA. As a result, bacterial colonization and CagA translocation into the attached host cells increase, promoting bacterial adaptation to the host and, possibly, oncogenesis.

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