Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA119667 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in astrocyte RCG-12 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Astrocyte RCG-12 cells used in this study were derived from primary cultured rat cortical glia cells infecting with a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Of the 15,923 probe sets analyzed, nonpermissive temperature differentially expressed 556 probe sets by >2.0-fold. Keywords: Astrocyte cell; growth arrest; differentiation; temperature-sensitive simian virus 40 large T-antigen; nonpermissive temperature
2007-04-13 | GSE7501 | GEO
Project description:We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in tracheal epithelial RTEC11 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Tracheal epithelial RTEC11 cells used in this study were derived from transgenic rats harboring a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Experiment Overall Design: A rat conditionally immortalized tracheal epithelial cell line, RTEC11, derived from transgenic rats harboring a temperature-sensitive simian virus 40 large T-antigen was used. RTEC11 cells were cultured at permissive (33°C) or nonpermissive (39°C) temperature for 3 days.
2008-06-16 | E-GEOD-8444 | biostudies-arrayexpress
Project description:We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in tracheal epithelial RTEC11 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Tracheal epithelial RTEC11 cells used in this study were derived from transgenic rats harboring a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Keywords: rat tracheal epithelial RTEC11; growth arrest; differentiation; gene expression
2007-07-17 | GSE8444 | GEO
Project description:The use of in vitro cell culture systems has been of central importance for research of physiology, pharmacology, and toxicology, and functions at the cellular and molecular levels. We have developed an immortalized oral epithelial cell line ROE2 from fetal transgenic rats harboring temperature-sensitive simian virus 40 large T-antigen. Here, to identify genes involved in ROE2 cell differentiation, global-scale gene expression analysis was carried out using a GeneChipM-BM-. system. ROE2 cells, an immortalized oral epithelial cell line from transgenic rats harboring temperature-sensitive simian virus 40 large T-antigen, were cultured for 0, 3, 6 and 9 days at 37M-KM-^ZC. Total RNA samples were prepared from the cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was monitored by an Affymetrix GeneChipM-BM-. system with a Rat Genome 230 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturer's instructions.
2013-02-22 | E-GEOD-44560 | biostudies-arrayexpress
Project description:During oncogenic transformation, cells acquire genetic mutations that override the normal mechanisms regulating cellular proliferation. Excessive expression of activating transcription factor 4 (ATF4) is often observed in mammalian malignant tumors. However, little is known about the role of ATF4 in the malignant transformation of normal cells. Here, we show that ATF4 promotes oncogene-induced malignant transformation of murine fibroblasts by suppressing the expression of cellular senescence-associated genes. Ectopic expression of oncogenes, H-rasV12 and simian virus 40 large T-antigen, elicited malignant transformation of embryonic fibroblasts from wild-type mice, but not from Atf4-null (Atf4-/-) mice. The oncogenic stresses induced the expression of both Atf4 and cyclin-dependent kinase inhibitor 2a (Cdkn2a), in wild-type cells. Elevated levels of ATF4 successively suppressed the expression of cdkn2a encoding the cellular senescence-associated proteins, p16INK4a and p19ARF, thereby promoting oncogenic transformation. Conversely, the loss of ATF4 caused cellular senescence resulting from the consistent expression of p16INK4a and p19ARF. These findings reveal a novel function of ATF4: that of promoting oncogenic transformation by suppressing cellular senescence.
2011-08-17 | GSE31405 | GEO
Project description:During oncogenic transformation, cells acquire genetic mutations that override the normal mechanisms regulating cellular proliferation. Excessive expression of activating transcription factor 4 (ATF4) is often observed in mammalian malignant tumors. However, little is known about the role of ATF4 in the malignant transformation of normal cells. Here, we show that ATF4 promotes oncogene-induced malignant transformation of murine fibroblasts by suppressing the expression of cellular senescence-associated genes. Ectopic expression of oncogenes, H-rasV12 and simian virus 40 large T-antigen, elicited malignant transformation of embryonic fibroblasts from wild-type mice, but not from Atf4-null (Atf4-/-) mice. The oncogenic stresses induced the expression of both Atf4 and cyclin-dependent kinase inhibitor 2a (Cdkn2a), in wild-type cells. Elevated levels of ATF4 successively suppressed the expression of cdkn2a encoding the cellular senescence-associated proteins, p16INK4a and p19ARF, thereby promoting oncogenic transformation. Conversely, the loss of ATF4 caused cellular senescence resulting from the consistent expression of p16INK4a and p19ARF. These findings reveal a novel function of ATF4: that of promoting oncogenic transformation by suppressing cellular senescence. Total 2 samples were derived from [1] H-Ras and SV40T expressing vector-transfected wild-type mouse embryonic fibroblasts (MEFs) and [2] H-Ras and SV40T expressing vector-transfected Atf4-/- MEFs
2011-08-16 | E-GEOD-31405 | biostudies-arrayexpress
Project description:The use of in vitro cell culture systems has been of central importance for research of physiology, pharmacology, and toxicology, and functions at the cellular and molecular levels. We have developed an immortalized oral epithelial cell line ROE2 from fetal transgenic rats harboring temperature-sensitive simian virus 40 large T-antigen. Here, to identify genes involved in ROE2 cell differentiation, global-scale gene expression analysis was carried out using a GeneChip® system.
2013-02-22 | GSE44560 | GEO
Project description:We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in astrocyte RCG-12 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Astrocyte RCG-12 cells used in this study were derived from primary cultured rat cortical glia cells infecting with a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Of the 15,923 probe sets analyzed, nonpermissive temperature differentially expressed 556 probe sets by >2.0-fold. Experiment Overall Design: RCG-12 cells were cultured at permissive (33°C) or nonpermissive (39°C) temperature for 3 days. Total RNA samples were prepared from the cells. Gene expression was analyzed by an Affymetrix GeneChip® system with the Rat Expression Array 230A which was spotted with 15,923 probe sets. Sample preparation for array hybridization was carried out as described in the manufactureâ??s instructions.
2008-06-15 | E-GEOD-7501 | biostudies-arrayexpress
Project description:Malignant mesothelioma is an aggressive tumour arising from the mesothelial cells lining the pleura, peritoneum or pericardium. The principal carcinogen associated with malignant mesothelioma is asbestos . A transgenic mouse model, denoted MexTAg, which encodes the Simian Virus 40 (SV40) large T antigen (TAg) downstream of the mesothelin promoter was developed. Inactivation of the tumour suppressors p53 and RB following binding to TAg results. In this model mesothelioma develops in the mesothelial cell compartment after the mice have been exposed to asbestos. The MexTAg transgenic mouse model of mesothelioma model enables analysis of the molecular events associated with asbestos induced mesothelioma and is utilised here to investigate the molecular dynamics of tumours induced in these mice, using gene expression patterns as a read out.
2016-01-30 | E-MTAB-3988 | biostudies-arrayexpress
Project description:We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell differentiation in testicular Sertoli TTE3 cells harboring temperature-sensitive SV40 large T-antigen by using an Affymetrix GeneChip system. Testicular Sertoli TTE3 cells used in the present study were derived from transgenic mice harboring a temperature-sensitive simian virus 40 large T-antigen. In the TTE3 cells, inactivation of the T-antigen by a nonpermissive temperature at 39˚C led to cell differentiation accompanying elevation of transferrin and cyclin-dependent kinase inhibitor CDKN1A. Of the 22, 690 probe sets analyzed, nonpermissive temperature up-regulated 729 probe sets and down-regulated 471 probe sets by >2.0-fold. Keywords: Sertoli cell; differentiation; temperature-sensitive SV40 large T-antigen; nonpermissive temperature
2007-02-23 | GSE6961 | GEO