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SRP145589
Homo sapiens
24 Downloadable Samples
Illumina HiSeq 2000
Description
We transfected PC3 cells with 100nM of a scrambled antisense oligonucleotide (AON) and an AON directed against MBNL1 exon 7 (36 basepairs) in order to skip the latter. Cells were harvested at 72h post-transfection and RNAseq was performed with ribozero depletion. Overall design: For RNA-Seq library preparation we followed the Illumina TruSeq RNA Sample Preparation Kit v2 manual. At least 70 million, 75bp long paired end reads were mapped to the GRCh37/hg19 version of the human genome per replicate using STAR 2.4.2a (doi: 10.1093/bioinformatics/bts635) using the default parameters.
Publication Title
MBNL1 alternative splicing isoforms play opposing roles in cancer.
Sample Metadata Fields
Specimen part, Cell line, Subject, Time
View Samples- Arabidopsis thaliana
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
Gene bodies of vertebrates and flowering plants are occupied by histone variant H3.3 and DNA methylation. The origin and significance of these profiles remain largely unknown. The profiles of enrichments in DNA methylation and H3.3 over gene bodies are correlated and both depend similarly on gene transcription levels. This suggests a mechanistic link between H3.3 and gene body methylation. We engineered H3.3 knockdown in Arabidopsis and observed transcription reduction that predominantly affected genes responsive to environmental cues. When H3.3 levels were reduced, gene bodies showed a loss of DNA methylation correlated with transcription levels. To study the origin of changes in DNA methylation profiles when H3.3 levels are reduced, we examined genome wide distributions of several histone H3 marks, H2A.Z, linker histone H1 and nucleosome densities. We observed that in absence of H3.3, H1 distribution increased in gene bodies. This depends on levels of gene transcription. We propose that H3.3 prevents recruitment of H1, which in turn promotes chromatin folding and antagonizes access to DNA methyltransferases responsible for gene body methylation. Thus, gene body methylation is likely shaped by H3.3 dynamics in relation with transcriptional activity. Overall design: Examination of transcription in WT and H3.3 knock down samples by RNA-Seq
Publication Title
The histone H3 variant H3.3 regulates gene body DNA methylation in Arabidopsis thaliana.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
Diffuse large B-cell lymphoma (DLBCL) represents a heterogeneous diagnostic category with distinct molecular subtypes that can be defined by gene expression profiling. However, even within these defined subtypes, heterogeneity prevails. To further elucidate the pathogenesis of these entities, we determined the expression of the tumor suppressor phosphatase and tensin homolog (PTEN) in 248 primary DLBCL patient samples. These analyses revealed that loss of PTEN was detectable in 55% of germinal center B-cell-like (GCB) DLBCLs, whereas this abnormality was found in only 14% of non-GCB DLBCL patient samples. In GCB DLBCL, the PTEN status was inversely correlated with activation of the oncogenic PI3K/ protein kinase B (AKT) pathway in both DLBCL cell lines and primary patient samples. Re-expression of PTEN induced cytotoxicity in PTEN-deficient GCB DLBCL cell line models by inhibiting PI3K/AKT signaling, indicating an addiction to this pathway in this subset of GCB DLBCLs. PI3K/AKT inhibition induced down-regulation of the transcription factor MYC. Re-expression of MYC rescued GCB DLBCL cells from PTEN-induced toxicity, identifying a regulatory mechanism of MYC expression in DLBCL. Finally, pharmacologic PI3K inhibition resulted in toxicity selectively in PTEN-deficient GCB DLBCL lines. Collectively, our results indicate that PTEN loss defines a PI3K/ AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that pharmacologic inhibition of PI3K might represent a promising therapeutic approach in these lymphomas.
Publication Title
PTEN loss defines a PI3K/AKT pathway-dependent germinal center subtype of diffuse large B-cell lymphoma.
Sample Metadata Fields
Sex, Disease, Cell line, Treatment
View Samples- Homo sapiens
- 298 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
A prospective study was conducted in the Neonatal Intensive Care Unit of the University Children's hospital between September 1, 2008 and November 30, 2010. The entry criteria were (1) preterm birth below 32 weeks gestational age, (2) birthweight<1500g (VLBW). During the follow-up period, bronchopulmonary dysplasia (BPD) was diagnosed in 68 (61%) infants, including 40 (36%) children with mild disease, 13 (12%) with moderate and 15 (13%) with severe BPD. Forty-three babies served as a control group (no BPD).
Publication Title
Gene expression profiling in preterm infants: new aspects of bronchopulmonary dysplasia development.
Sample Metadata Fields
Sex, Specimen part
View Samples- Caenorhabditis elegans
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
We report the profiling of induced mRNA transcripts in two C. elegan replicate populations -- WT (N2) and mutant strain with deficient HLH30. Both strains were fed either OP50 strain of e-coli (normal feed) or S. aureus Overall design: Examination of infected versus uninfected wildtype and mutant lawns of animals
Publication Title
Innate host defense requires TFEB-mediated transcription of cytoprotective and antimicrobial genes.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 25 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip, Agilent-014850 Whole Human Genome Microarray 4x44K G4112F (Feature Number version)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
IκB-ζ controls the constitutive NF-κB target gene network and survival of ABC DLBCL.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 13 Downloadable Samples
- Agilent-014850 Whole Human Genome Microarray 4x44K G4112F (Feature Number version), Illumina HumanHT-12 V4.0 expression beadchip
Description
Constitutive activation of the nuclear factor-kappa B (NF-kB) pathway is a hallmark of the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Recurrent mutations of NF-kB regulators that cause constitutive activity of this oncogenic pathway have been identified. However, it remains unclear how specific target genes are regulated. We identified the IkB-like protein NFKBIZ that binds NF-kB subunits and enhances transactivation of some NF-kB target genes while repressing others, to be upregulated in ACB compared to GCB DLBCL primary patient samples (p=5.1 x 10^-37). Knockdown of NFKBIZ by RNA interference was toxic to ABC but not GCB DLBCL cell lines. Gene expression profiling following NFKBIZ knockdown significantly downregulated a large number of NF-kB target genes, suggesting a central role in regulating NF-kB signaling. To further investigate the molecular mechanisms of how NFKBIZ mediates NF-kB signaling in ABC DLBCL, we performed immunoprecipitations and detected an interaction of NFKBIZ with both p50 and p52 NF-kB subunits, indicating that both the canonical and non-canonical NF-kB pathways are regulated by NFKBIZ. Collectively, our data imply that NFKBIZ is required for NF-kB signaling in ABC DLBCL and thus might represent a promising molecular target for future therapies.
Publication Title
IκB-ζ controls the constitutive NF-κB target gene network and survival of ABC DLBCL.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Constitutive activation of the nuclear factor-kappa B (NF-kB) pathway is a hallmark of the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Recurrent mutations of NF-kB regulators that cause constitutive activity of this oncogenic pathway have been identified. However, it remains unclear how specific target genes are regulated. We identified the IkB-like protein NFKBIZ that binds NF-kB subunits and enhances transactivation of some NF-kB target genes while repressing others, to be upregulated in ACB compared to GCB DLBCL primary patient samples (p=5.1 x 10^-37). Knockdown of NFKBIZ by RNA interference was toxic to ABC but not GCB DLBCL cell lines. Gene expression profiling following NFKBIZ knockdown significantly downregulated a large number of NF-kB target genes, suggesting a central role in regulating NF-kB signaling. To further investigate the molecular mechanisms of how NFKBIZ mediates NF-kB signaling in ABC DLBCL, we performed immunoprecipitations and detected an interaction of NFKBIZ with both p50 and p52 NF-kB subunits, indicating that both the canonical and non-canonical NF-kB pathways are regulated by NFKBIZ. Collectively, our data imply that NFKBIZ is required for NF-kB signaling in ABC DLBCL and thus might represent a promising molecular target for future therapies.
Publication Title
IκB-ζ controls the constitutive NF-κB target gene network and survival of ABC DLBCL.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 177 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Perinatal asphyxia is detrimental to the newborn baby and the use of supplemental oxygen during resuscitation may worsen the prognosis of these babies. The mechanism behind hyperoxic injury is not fully understood and our aim was to investigate four oxygen therapies following hypoxia and these effects on transcriptional activity.
Publication Title
Transcriptome profiling of the newborn mouse brain after hypoxia-reoxygenation: hyperoxic reoxygenation induces inflammatory and energy failure responsive genes.
Sample Metadata Fields
Specimen part
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
RIP-chip-SRM : a New Combinatorial Large Scale Approach Identifies a Set of Translationally Regulated bantam/miR 58 Targets in C. elegans
Publication Title
RIP-chip-SRM--a new combinatorial large-scale approach identifies a set of translationally regulated bantam/miR-58 targets in C. elegans.
Sample Metadata Fields
Specimen part
View Samples