Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA97599 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hepatic gene expression induced by chromic exposure to low levels of the SV40 LT/st oncoproteins (4P)
2014-12-22 | GSE6232 | GEO
Project description:Hepatic gene expression induced by chromic exposure to high levels of the SV40 LT/st oncoproteins (4P)
2014-12-22 | GSE5958 | GEO
Project description:Hepatic gene expression induced by chromic exposure to high levels of the SV40 LT/st oncoproteins (4P) Affymetrix mouse genome U74Av2 platform was used, duplicate measurements for wild-type and transgenic animals
2014-12-22 | E-GEOD-5958 | biostudies-arrayexpress
Project description:Hepatic gene expression induced by chromic exposure to low levels of the SV40 LT/st oncoproteins (4P) Affymetrix mouse genome U74Av2 platform was used, duplicate measurements for wild-type and transgenic animals
2014-12-22 | E-GEOD-6232 | biostudies-arrayexpress
Project description:Alterations in hepatic gene expression induced by chromic exposure to high levels of the SV40 LT/st oncoproteins (4P)
| PRJNA97421 | ENA
Project description:Merkel cell polyomavirus (MCV) is clonally integrated in over 80% of Merkel cell carcinomas and mediates tumor development through the expression of viral oncoproteins large T (LT) and small T antigens (sT). Viral integration is associated with signature mutations in the T antigen locus that result in deletions of carboxy-terminal replicative functions of the LT antigen. Despite these truncations, the LT LxCxE retinoblastoma (Rb) pocket protein family-binding domain is retained, and the entire sT isoform is maintained intact. To investigate the ability of MCV oncoproteins to regulate host gene expression, we performed microarray analysis on cells stably expressing tumor-derived LT, tumor-derived LT along with sT, and tumor-derived LT with a mutated Rb interaction motif. Gene expression alterations in the presence of tumor-derived LT could be classified into three main groups: genes that are involved in the cell cycle (specifically the G1/S transition), genes involved in DNA replication, and genes involved in cellular movement. The LxCxE mutant LT largely reversed gene expression alterations detected with the wild type LT, while co-expression of sT did not significantly affect these patterns of gene expression. LxCxE-dependent upregulation of cyclin E and CDK2 correlates with increased proliferation in tumor-derived LT expressing cells. We conclude that in hTERT-immortalized human fibroblasts the LXCXE motif of tumor-derived LT enhances cellular proliferation and upregulates cell cycle and immune signaling gene transcription.
2015-09-21 | GSE68503 | GEO
Project description:Merkel cell polyomavirus (MCV) is clonally integrated in over 80% of Merkel cell carcinomas and mediates tumor development through the expression of viral oncoproteins large T (LT) and small T antigens (sT). Viral integration is associated with signature mutations in the T antigen locus that result in deletions of carboxy-terminal replicative functions of the LT antigen. Despite these truncations, the LT LxCxE retinoblastoma (Rb) pocket protein family-binding domain is retained, and the entire sT isoform is maintained intact. To investigate the ability of MCV oncoproteins to regulate host gene expression, we performed microarray analysis on cells stably expressing tumor-derived LT, tumor-derived LT along with sT, and tumor-derived LT with a mutated Rb interaction motif. Gene expression alterations in the presence of tumor-derived LT could be classified into three main groups: genes that are involved in the cell cycle (specifically the G1/S transition), genes involved in DNA replication, and genes involved in cellular movement. The LxCxE mutant LT largely reversed gene expression alterations detected with the wild type LT, while co-expression of sT did not significantly affect these patterns of gene expression. LxCxE-dependent upregulation of cyclin E and CDK2 correlates with increased proliferation in tumor-derived LT expressing cells. We conclude that in hTERT-immortalized human fibroblasts the LXCXE motif of tumor-derived LT enhances cellular proliferation and upregulates cell cycle and immune signaling gene transcription. RNA was isolated from BJ-hTERT cell lines and hybridized to an Illumina chip for global gene expression analysis
2015-09-21 | E-GEOD-68503 | biostudies-arrayexpress
Project description:The SV40 large (LT) and small (st) antigens are produced from a single alternatively spliced pre-mRNA, that when co-expressed, transform a variety of cells in vitro and in vivo. However, 17kT, a relatively uncharacterized third protein that is co-linear with LT for the first 131 amino acids, is also produced from the early viral pre-mRNA by removal of an additional intron from the LT transcript. Here we report a line of transgenic mice expressing a liver-specific dox-inducible viral transcript that fails to yield any detectable LT protein, yet produces abundant 17kT. Comparative analysis of livers of transgenic mice expressing either 17kT or LT demonstrates that while 17kT is a potent stimulator of cell proliferation, it is ineffective at inducing liver tumor development, due in part, to the failure of 17kT to effectively induce the expression of growth regulators and reactivate expression of imprinted and developmentally regulated hepatic genes. These studies highlight key functional differences between LT and 17kT in their ability to transform quiescent primary epithelial cells in vivo, and demonstrate how specific functional domains within LT impact cell-specific gene expression to promote oncogenesis. Keywords: genetic modification, SV40, 17kT, LT, Rb, p53, hepatocellular carcinoma, hepatic hyperplasia, differentiation.
2010-04-01 | GSE5242 | GEO
Project description:The SV40 large (LT) and small (st) antigens are produced from a single alternatively spliced pre-mRNA, that when co-expressed, transform a variety of cells in vitro and in vivo. However, 17kT, a relatively uncharacterized third protein that is co-linear with LT for the first 131 amino acids, is also produced from the early viral pre-mRNA by removal of an additional intron from the LT transcript. Here we report a line of transgenic mice expressing a liver-specific dox-inducible viral transcript that fails to yield any detectable LT protein, yet produces abundant 17kT. Comparative analysis of livers of transgenic mice expressing either 17kT or LT demonstrates that while 17kT is a potent stimulator of cell proliferation, it is ineffective at inducing liver tumor development, due in part, to the failure of 17kT to effectively induce the expression of growth regulators and reactivate expression of imprinted and developmentally regulated hepatic genes. These studies highlight key functional differences between LT and 17kT in their ability to transform quiescent primary epithelial cells in vivo, and demonstrate how specific functional domains within LT impact cell-specific gene expression to promote oncogenesis. Keywords: genetic modification, SV40, 17kT, LT, Rb, p53, hepatocellular carcinoma, hepatic hyperplasia, differentiation. Affymetrix mouse genome 430 A and B platform was used, single measurements for wild-type and transgenic animals.
2010-03-31 | E-GEOD-5242 | biostudies-arrayexpress
Project description:Hepatic gene expression in transgenic mice with conditional liver-specific expression of the SV40 17kT/LT oncoproteins
| PRJNA96457 | ENA