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GSE3990
Drosophila melanogaster
6 Downloadable Samples
Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Drosophila males double transcription of their single X chromosome to equalize X-linked gene expression with females, which carry two X chromosomes. Increased transcription requires the Male-Specific Lethal (MSL) complex. One of the primary functions of the MSL complex is thought to be enrichment of H4Ac16 on the male X chromosome, a modification linked to elevated transcription. The roX1 and roX2 RNAs are essential but redundant components of the MSL complex. Simultaneous removal of both roX RNAs reduces MSL X-localization and leads to ectopic binding of these proteins at autosomal sites and to the chromocenter. Some H4Ac16 accumulates at these ectopic sites in roX1- roX2- males, suggesting the possibility of increased expression. The global effect of roX mutations on gene expression was measured by microarray analysis. We found that expression of the X chromosome was decreased by 26% in roX1- roX2- male larvae, supporting the involvement of roX RNAs in the up-regulation of X-linked genes. This finding is broadly comparable to reports of reduced X chromosome expression following msl2 RNAi knockdown in S2 cells. In spite of strong MSL binding and H4Ac16 accumulation at autosomal sites in roX1- roX2- males, enhanced gene expression could not be detected at these sites by microarray analysis or reverse northern blotting. Thus, failure to compensate X-linked genes, rather than inappropriate up-regulation of autosomal genes at ectopic sites of MSL binding, appears to cause male lethality upon loss of roX RNAs.
Publication Title
roX RNAs are required for increased expression of X-linked genes in Drosophila melanogaster males.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 43 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 37 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We studied transcriptional changes by Affymetrix human microarrays in DLBCL cell lines as a result of treatment with GSK126, a potent, highly-selective, SAM-competitive, small molecule inhibitor of EZH2
Publication Title
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We studied transcriptional changes by Affymetrix human microarrays in 2 DLBCL cell lines as a result of shRNA mediated knockdown of EZH2.
Publication Title
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
We disprove that the impaired Myd88-dependent proinflammatory response of neonatal monocytes is a correlate for immaturity and confirm it as display of transient alarmin-mediated stress tolerization. We find a strong inducibility of TRIF-dependent genes in neonatal monocytes by LPS but a barely detectable expression at baseline.
Publication Title
S100-alarmin-induced innate immune programming protects newborn infants from sepsis.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
roX RNAs are involved in the chromosome-wide gene regulation that occurs during dosage compensation in Drosophila. Dosage compensation equalizes expression of X-linked and autosomal genes. Drosophila males increase transcription two-fold from their single X chromosome. This is mediated by the MSL complex, which is composed of the male-specific lethal (MSL) proteins and two noncoding roX RNAs, roX1 and roX2. Upon elimination of both roX transcripts, a global decrease of X-linked gene expression is observed in males. Expression of the genes on the entire 4th chromosome also decreased in the absence of both roX transcripts. roX1 RNA also presents in females in the early stages. To investigate the effect of loss of roX transcripts on gene expression in females, gene expression was analyzed by microarrays in roX1-roX2- female flies. To eliminate inconsistency caused by differences in genetic background, expression of roX1-roX2- females with females of virtually identical genetic background but carrying the [hsp83-roX1+] transgene were compared. Expression of any chromosome did not change in roX1-roX2- females. It was concluded that roX RNAs only effect in males .
Publication Title
Coordinated regulation of heterochromatic genes in Drosophila melanogaster males.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 23 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We performed mRNA expression profiling of lung tumors from C/L858R, C/T790M, and C/L+T mice and from corresponding normal lung tissue.
Publication Title
Dual targeting of EGFR can overcome a major drug resistance mutation in mouse models of EGFR mutant lung cancer.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Although most of the oncogenic phenotypes of PTEN loss have been attributed to AKT activation, AKT alone is not sufficient to induce all of the biological activities associated with PTEN inactivation. We searched for additional PTEN-regulated pathways through gene set enrichment analysis (GSEA) and found that PTEN inactivation causes an enrichment of genes associated with JNK activation. Biochemically, PTEN-null cells exhibit higher JNK activity, and genetic studies demonstrate that JNK functions parallel to and independently of AKT. Furthermore, PTEN deficiency sensitizes cells to JNK inhibition. We also found that negative feedback regulation of PI3K was impaired in PTEN-null cells. These findings implicate JNK in PI3K-driven cancers and demonstrate the utility of GSEA to identify functional pathways using genetically defined systems.
Publication Title
Identification of the JNK signaling pathway as a functional target of the tumor suppressor PTEN.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Expression of DREAM in dorsal root ganglia and spinal cord is related to endogenous control mechanisms of acute and chronic pain. In primary sensory trigeminal neurons high levels of endogenous DREAM protein are preferentially localized in the nucleus, suggesting a major transcriptional role. Here, we show that DREAM participates in the control of trigeminal pain perception through the regulation of prodynorphin and BDNF. Furthermore, genome-wide analysis of trigeminal neurons in daDREAM transgenic mice revealed that cathepsin L (CTSL) and the monoglyceride lipase (MGLL) are new DREAM downstream targets and have a role in the regulation of trigeminal nociception.
Publication Title
Transcriptional repressor DREAM regulates trigeminal noxious perception.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 58 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype.
Sample Metadata Fields
Specimen part
View Samples