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RPL12A/B double deletion strains: Control vs. Wt RPL12B or Mutant RPL12B-R66K Transformed

ABSTRACT: Transcriptional and translational profiling of RPL12A/B double deletion comparing control untransformed RPL12B strains with transformed with a pESC-RPL12B wild type or muated RPL12B-R66K gene. Keywords: Genetic modification

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE13894 | GEO | 2008/12/18

SECONDARY ACCESSION(S): PRJNA110299

REPOSITORIES: GEO

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RPL12A/B double deletion strains: Control vs. Wt RPL12B or Mutant RPL12B-R66K Transformed

Project description:Transcriptional and translational profiling of RPL12A/B double deletion comparing control untransformed RPL12B strains with transformed with a pESC-RPL12B wild type or muated RPL12B-R66K gene. Keywords: Genetic modification Two-condition experiment, Transcriptional experiments from total mRNA and Translational experiments from polysomal mRNA from three strains including deleted RPL12A/B, retransformed WT RPL12B and mutated RPL12B-R66K strain. Biological replicates: independently grown and harvested. double, triple or more replication per array.

2008-12-17 | E-GEOD-13894 | biostudies-arrayexpress

Differential gene expression in Ki-RAS and Ha-RAS cell lines.

Project description:Comparison of gene expression in Ha-RAS transformed cells versus untransformed Caco-2. Comparison of gene expression in Ki-RAS transformed cells versus untransformed Caco-2.

2009-04-07 | GSE12203 | GEO

Transcription profiling of baby rat kidney cells transformed with the non-oncogenic Ad5 E1 or oncogenic Ad12 E1 region, as well as primary untransformed BRK cells

Project description:Multiple rat microarrays were used to compare RNA transcript levels from 15,481 genes of baby rat kidney (BRK) cells transformed with the non-oncogenic Ad5 E1 or oncogenic Ad12 E1 region, as well as primary untransformed BRK cells.

2008-06-20 | E-MTAB-30 | biostudies-arrayexpress

The chromatin assembly factor complex 1 (CAF1) and 5-Azacytidine (5-AzaC) affect cell motility in Src-transformed human epithelial cells

Project description:Tumor invasion into surrounding stromal tissue is a hallmark of high-grade, metastatic cancers. Oncogenic transformation of human epithelial cells in culture can be triggered by activation of v-Src kinase, resulting in increased cell motility, invasiveness and tumorigenicity and provides a valuable model for studying how changes in gene expression cause cancer phenotypes. Here, we show that epithelial cells transformed by activated Src show increased levels of DNA methylation and that the methylation inhibitor, 5-AzaC, potently blocks the increased cell motility and invasiveness induced by Src activation. A proteomic screen for chromatin regulators acting downstream of activated Src identified the replication-dependent histone chaperone CAF1 as an important factor for Src-mediated increased cell motility and invasion. We show Src causes a 5-AzaC-sensitive decrease in both mRNA and protein levels of the p150 (CHAF1A) and p60 (CHAF1B), subunits of CAF1. Depletion of CAF1 in untransformed epithelial cells using siRNA was sufficient to recapitulate the increased motility and invasive phenotypes characteristic of transformed cells without activation of Src. Maintaining high levels of CAF1 by exogenous expression suppressed the increased cell motility and invasiveness phenotypes when Src was activated. These data identify a critical role of CAF1 in the dysregulation of cell invasion and motility phenotypes seen in transformed cells and also highlight an important role for epigenetic remodeling through DNA methylation for Src-mediated induction of cancer phenotypes.

2016-12-20 | PXD005494 | Pride

Comparison of primary MEF vs HRasV12 + Twist transformed MEF

Project description:MEF cells were sequentially infected with H-RasV12 and Twist (Twist1 or Twist2) expression retroviral constructs. Gene expression profiles of the resulting transformed cell lines were compared to the gene expression profile of primary MEF cells

2008-07-11 | GSE11756 | GEO

MicroRNA levels in non-transformed and transformed lung cells

Project description:MicroRNA levels in non-transformed BEAS-2B bronchial epithelial cells, two lines of mycoplasma transformed BEAS-2B cells, and A549 lung adenocarcinoma cells were measured. Microarray analyses of 1145 microRNAs in A549 lung adenocarcinoma cells and two other transformed lung cell types relative to BEAS-2B bronchial epithelial cells were performed. 106 miRNAs were down-regulated and 69 miRNAs were up-regulated in all three transformed lines

2014-03-11 | GSE55748 | GEO

The effect on gene expression of Smchd1 deletion in primary MEFs, transformed MEFs and MEF tumours

Project description:Smchd1 appears to act as a tumour suppressor in the transformed fibroblast model. We find gene expression differences are most pronounced in the transformed MEFs. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis.

2012-09-30 | GSE40734 | GEO

Transcription profiling of Arabidopsis Col-0 vs. AtAOX1a antisense treated plants

Project description:Leaf transcriptome comparison of untransformed Col-0 Arabidopsis plants with plants transformed to be anti-sense for AtAOX1a (alternative oxidase). Two âbio-replicatesâ were sampled, for a total of four microarray chipsâCol-0 and anti-sense leaf tissue from a first planting (samples GSM45208 and GSM45231, respectively), and from a second planting made one week later (samples GSM45209 and GSM45278, respectively). See sample descriptions for growth conditions and microarray procedure.

2008-06-12 | E-GEOD-2406 | biostudies-arrayexpress

Deinococcus radiodurans R1: wildtype strains vs. DR0199-deletion strains

Project description:Transcriptional profiling of comparing wildtype strains with DR0199-deletion strains under normal growth conditions.

2012-03-29 | GSE33758 | GEO

Deinococcus radiodurans R1: wildtype strains vs. DR1790-deletion strains

Project description:Transcriptional profiling of comparing wildtype strains with DR1790-deletion strains under normal growth contidions. Keywords: Genetic modification

2010-09-10 | GSE22628 | GEO

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