Proteomics

Dataset Information

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TREx-BCBL1-RTA GPRC5A-FLAG Immunoprecipitation LC-MS


ABSTRACT: The epitranscriptomic modification m6A is a ubiquitous feature of the mammalian transcriptome. It modulates mRNA fate and dynamics to exert regulatory control over numerous cellular processes and disease pathways, including viral infection. Kaposi’s sarcoma-associated herpesvirus (KSHV) reactivation from the latent phase leads to redistribution of m6A topology upon both viral and cellular mRNAs within infected cells. Here we investigate the role of m6A in cellular transcripts upregulated during KSHV lytic replication. Results show that m6A is crucial for the stability of the GPRC5A mRNA, whose expression is induced by the KSHV latent-lytic switch master regulator, the replication and transcription activator (RTA) protein. Moreover, we demonstrate that GPRC5A is essential for efficient KSHV lytic replication by directly regulating NFκB signalling. Overall, this work highlights the central importance of m6A in modulating cellular gene expression to influence viral infection.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human) Human Gammaherpesvirus 8

TISSUE(S): B Cell, Cell Culture

SUBMITTER: Timothy Mottram  

LAB HEAD: Adrian Whitehouse

PROVIDER: PXD039669 | Pride | 2023-07-20

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
200421_Fraction_1.raw Raw
200421_Fraction_2.raw Raw
200421_Fraction_3.raw Raw
200421_Fraction_4.raw Raw
GPRC5A_FLAG_2021_05_07_MastersTidy_BM_BA_Ollie_Manners_200421_8Plex_TMT_Proteins.xlsx Xlsx
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Publications


The epitranscriptomic modification <i>N</i><sup>6</sup>-methyladenosine (m<sup>6</sup>A) is a ubiquitous feature of the mammalian transcriptome. It modulates mRNA fate and dynamics to exert regulatory control over numerous cellular processes and disease pathways, including viral infection. Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation from the latent phase leads to the redistribution of m<sup>6</sup>A topology upon both viral and cellular mRNAs within infected cells. Here we invest  ...[more]

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