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Quantitative proteomics of cells treated with decaged WZB117-PPG

ABSTRACT: To further understand how cells response to decaged WZB117-PPG, we performed quantitative proteomics of A549 cells under WZB117-PPG treatment (30 μM) with illumination and normal condition by TMT 10 plex labeling

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell

SUBMITTER: Chunrong Liu

LAB HEAD: Chunrong Liu

PROVIDER: PXD043171 | Pride | 2024-01-04

REPOSITORIES: Pride

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Project description:HPIV1 is an important respiratory pathogen in children and the most common cause of viral croup. We performed a microarray-based analysis of gene expression kinetics to examine how wild-type (wt) HPIV1 infection altered gene expression in human respiratory epithelial cells and what role IFN-beta played in this response. We similarly evaluated HPIV1-P(C-), a highly attenuated and apoptosis-inducing virus that does not express any of the four C proteins, and HPIV1-C(F170S), a less attenuated mutant that contains a single point mutation in C and, like wt HPIV1, does not efficiently induce apoptosis, to examine the role of the C proteins in controlling host gene expression. We also used this data to investigate whether the phenotypic differences between the two C mutants could be explained at the transcriptional level. Mutation or deletion of the C proteins of HPIV1 permitted the activation of over 2000 cellular genes that otherwise would be repressed by HPIV1 infection. Thus, the C proteins profoundly suppress the response of human respiratory cells to HPIV1 infection. Cellular pathways targeted by the HPIV1 C proteins were identified and their transcriptional control was analyzed using bioinformatics. Transcription factor binding sites for IRF and NF-kappaB were over-represented in some of the C protein targeted pathways, but other pathways were dominated by less known factors such as forkhead transcription factor FOXD1. Surprisingly, the host response to the C knockout and C(F170S) mutants was very similar, and thus the phenotypic differences between these two viruses could not be explained at the host cell transcriptional level. Keywords: Time course; response to viral infection; response to IFN-beta A549 cells were infected with wt HPIV1, C(F170S), or P(C-) in triplicate, and RNA was isolated at 6, 12, 24, and 48 hours. A549 cells were also treated with IFN-beta in triplicate, and RNA was isolated at 6 and 24 hours. Mock infection/treatment was performed in triplicate at each corresponding time point. Overall, 42 samples and microarrays were analyzed.

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Quantitative proteomics of cells treated with decaged WZB117-PPG

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