Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional perturbations caused by SV40 large T antigen and its fragments


ABSTRACT: The small genome of polyomaviruses encodes a limited number of proteins that are highly dependent on interactions with host cell proteins for efficient viral replication. The SV40 large T antigen (LT) contains several discrete functional domains that contribute to the viral life cycle, including the DNA binding and helicase domains. In addition, the LT the C-terminal region is required for lytic infection in certain restrictive cell types. To understand how LT affects the host cell to facilitate viral replication, we expressed full-length or functional domains of LT in cells and identified interacting cellular proteins and performed expression profiling. LT perturbed the expression of p53 target genes and subsets of cell-cycle dependent genes regulated by the DREAM and the B-Myb-MuvB complexes. To examine transcriptome perturbations directly in human cells, we generated expression constructs of each LT fragment. Full length and truncated LT containing N-terminal HA and FLAG epitope tags were expressed from the pMSCV retroviral vector and introduced into U-2 OS cells. Total RNA was isolated from three biological replicate U-2 OS stable cell lines and gene expression was assayed on Affymetrix Human Gene U133 Plus 2.0 arrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Megha Padi 

PROVIDER: E-GEOD-40567 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


The small genome of polyomaviruses encodes a limited number of proteins that are highly dependent on interactions with host cell proteins for efficient viral replication. The SV40 large T antigen (LT) contains several discrete functional domains including the LXCXE or RB-binding motif, the DNA binding and helicase domains that contribute to the viral life cycle. In addition, the LT C-terminal region contains the host range and adenovirus helper functions required for lytic infection in certain r  ...[more]

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