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Little change in host cell protein expression was observed (Fig. 10B, left); the efficiency of silencing was confirmed by Western blots (Fig. 10B, right).
Excretory/secretory proteins of pathogens change the host cell environment by suppressing the immune system, to aid the proliferation of infection.
Viruses change the host cell's genetic material from its normal function to producing the virus itself.
Phosphorylation of the identified potential human PknB targets would result in significant changes in host cell signal transduction.
Changes in host cell transcription can directly induce bradyzoite specific gene expression [10], showing that T. gondii can also sense signals inside the host cell.
This modulation may be due to changes in host cell signalling pathways [ 33, 37].
The observed changes in host cell function are partially explained by alterations in granulocyte gene transcription [ 9– 11].
The assays used did not detect significant changes in host cell viability, suggesting AEPa was specific for the protozoa.
This suggested that distinct changes in host cell transcriptome occurred at early and late stages in infection.
Changes in host cell metabolism as a consequence of nutrient scavenging by intracellular B. pseudomallei have never been studied.
Changes in host cell gene expression that accompany the infection process are highly dynamic and reflect a wide array of responses to a specific host-pathogen relationship [ 6].
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