This SuperSeries is composed of the SubSeries listed below.
H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-β-Catenin Signaling in Colorectal Cancer.
Cell line, Treatment
View SamplesKnockdown of H19 leads to cell cycle arrest, reduced cell proliferation, and reduced cell migration in HCT116 cells.
H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-β-Catenin Signaling in Colorectal Cancer.
Cell line, Treatment
View SamplesWe used microarrays to detail the global programme of gene expression following CTNNB1 knockdown in HCT116 cells
H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-β-Catenin Signaling in Colorectal Cancer.
Cell line, Treatment
View SamplesWe used microarrays to detail the global programme of gene expression following CDK8 knockdown in HCT116 cells
H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-β-Catenin Signaling in Colorectal Cancer.
Cell line, Treatment
View SamplesKnockdown of H19 leads to cell cycle arrest, reduced cell proliferation, and reduced cell migration in DLD1 cells.
H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-β-Catenin Signaling in Colorectal Cancer.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Comparing effects of mTR and mTERT deletion on gene expression and DNA damage response: a critical examination of telomere length maintenance-independent roles of telomerase.
Sex, Specimen part
View SamplesTelomerase, the essential enzyme that maintains telomere length, contains two core components, TERT and TR. While early studies in yeast and mouse both indicated that loss of telomerase leads to phenotypes that arise after an increased number of generations, due to telomere shortening, recent studies claim additional roles for telomerase components in transcription and the response to DNA damage. To test these telomere length maintenance-independent roles of telomerase components, we examined first generation mTR-/- and mTERT-/- mice with long telomeres. We used gene expression profiling and found no genes that were expressed at significantly different levels when independent mTR-/- G1 mice were compared to mTERT-/- G1 mice and to wild-type mice. In addition, we compared the response to DNA damage in mTR-/-G1 and mTERT-/- G1 mouse embryonic fibroblasts, and found no increase in the response to DNA damage in the absence of either telomerase components compared to wild-type. We conclude that in the wild-type physiological telomere length setting, neither mTR nor mTERT act as a transcription factor or have a role in the DNA damage response.
Comparing effects of mTR and mTERT deletion on gene expression and DNA damage response: a critical examination of telomere length maintenance-independent roles of telomerase.
Sex, Specimen part
View SamplesTelomerase, the essential enzyme that maintains telomere length, contains two core components, TERT and TR. While early studies in yeast and mouse both indicated that loss of telomerase leads to phenotypes that arise after an increased number of generations, due to telomere shortening, recent studies claim additional roles for telomerase components in transcription and the response to DNA damage. To test these telomere length maintenance-independent roles of telomerase components, we examined first generation mTR-/- and mTERT-/- mice with long telomeres. We used gene expression profiling and found no genes that were expressed at significantly different levels when independent mTR-/- G1 mice were compared to mTERT-/- G1 mice and to wild-type mice. In addition, we compared the response to DNA damage in mTR-/-G1 and mTERT-/- G1 mouse embryonic fibroblasts, and found no increase in the response to DNA damage in the absence of either telomerase components compared to wild-type. We conclude that in the wild-type physiological telomere length setting, neither mTR nor mTERT act as a transcription factor or have a role in the DNA damage response.
Comparing effects of mTR and mTERT deletion on gene expression and DNA damage response: a critical examination of telomere length maintenance-independent roles of telomerase.
Sex, Specimen part
View SamplesCCAAT/enhancer binding protein ß (C/EBPß) is a transcription factor that regulates the expression of important pro-inflammatory genes in microglia. Mice deficient for C/EBPß show protection against excitotoxic and ischemic CNS damage but the involvement of the various C/EBPß expressing cell types in this neuroprotective effect is not solved. Since C/EBPß-deficient microglia show attenuated neurotoxicity in culture we hypothesized that specific C/EBPß deficiency in microglia could be neuroprotective in vivo. In this study we have tested this hypothesis by generating mice with myeloid C/EBPß deficiency. Mice with myeloid C/EBPß deficiency were generated by crossing LysMCre and C/EBPßfl/fl mice . Primary microglial cultures from C/EBPßfl/fl (named here as WT) and LysMCre-C/EBPßfl/fl (named here as KO) mice were treated with lipopolysaccharide ± interferon ? (IFN?) for 6 h and gene expression was analyzed by RNA sequencing. LysMCre-C/EBPßfl/fl mice showed an efficiency of C/EBPß deletion of 100% in cultured microglia. Transcriptomic analysis of C/EBPß-deficient primary microglia revealed C/EBPß-dependent expression of 1068 genes, significantly enriched in inflammatory and innate immune responses GO terms. This study provides new data that support a central role for C/EBPß in the biology of activated microglia. Overall design: LysMCre-C/EBPßfl/fl genotype (12 samples): 4 samples treated with LPS, 4 with LPS +IFNg, and 4 vehicle. C/EBPßfl/fl genotype (9 samples): 3 samples treated with LPS, 3 with LPS +IFNg, and 3 vehicle. Design Case (Treatment LPS or LPS +INF) control (No treatment or vehicle) in LysMCre-C/EBPßfl/fl genotype and in C/EBPßfl/fl genotype
RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ.
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View SamplesAuxin is a key phytohormone regulating central processes in plants that include embryo development, lateral root growth and flower maturation among others. Auxin is sensed by a set of F-Box proteins of the TIR1/AFB3 family triggering auxin dependent responses by a pathway that involves an interplay between the Aux/IAA transcription repressors and the ARF transcription factors. We have previously shown that the AFB3 auxin receptor has a specific role in coordinating primary and lateral root growth to external and internal nitrate availability (Vidal et al., 2010). In this work, we used an integrated genomics, bioinformatics and molecular genetics approach to dissect regulatory networks acting downstream AFB3 that are activated by a transient nitrate treatment in Arabidopsis roots. Our systems approach unraveled key components of the AFB3 regulatory network leading to changes in lateral root growth in response to nitrate.
Systems approaches map regulatory networks downstream of the auxin receptor AFB3 in the nitrate response of Arabidopsis thaliana roots.
Specimen part, Treatment
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