Purpose: Diffuse large B cell lymphomas (DLBCL) frequently harbor mutations in the histone acetyltransferase CREBBP, however their functional contribution to lymphomagenesis remains largely unknown. This study aims at elucidating and characterizing the molecular pathways affected by mutations in CREBBP. Methods: U2932, a DLBCL cell line that has wild type expression of CREBBP was manipulated by CRISPR-Cas9 strategy to mutate one allele of CREBBP and examine the pathways affected. RNA was isolated using the NucleoSping RNA Kit (Macherey-Nagel) from five wild type (CREBBP+/+) and five heterozygous clones (CREBBP+/-). RNA quality was assessed by Bioanalyzer 2100 followed by library preparation using the TruSeq RNA Sample Prep Kit v4 (Illumina). Sequencing was subsequently performed on the Illumina HiSeq 2500 instrument. RNA-seq reads were quality-checked with fastqc, which computes various quality metrics for the raw reads. RNA-seq reads were mapped to the GRCh38 reference human genome using STAR and reads were counted according to Ensembl gene annotation using the featureCounts function in the Rsubread Bioconductor package. Statistical analysis of differential expression was conducted with the DESeq2 package. Overall design: Trascriptomic profiles of CREBBP+/+ and CREBBP+/- clones were generated by deep sequencing.
Inactivation of CREBBP expands the germinal center B cell compartment, down-regulates MHCII expression and promotes DLBCL growth.
Subject
View SamplesGlobal gene expression analysis was performed of several cell lines, mostly classical Hodgkin lymphoma, one DLBCL cell line and one NLPHL cell line.
SMAD1 promoter hypermethylation and lack of SMAD1 expression in Hodgkin lymphoma: a potential target for hypomethylating drug therapy.
Cell line
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Inferring causal metabolic signals that regulate the dynamic TORC1-dependent transcriptome.
Treatment
View SamplesDynamic mRNA gene expression from the wildtype YSBN6 during a nutritional downshift from glutamine to proline. Glutamine and proline were initially together in the media, with cells consuming exlusively glutamine (proline utilization inhibited due to nitrogen catabolite repression). The concentration of glutamine was frequently evaluated at-line, and the moment at which glutamine was not detected anymore is referred to as the time of the shift.
Inferring causal metabolic signals that regulate the dynamic TORC1-dependent transcriptome.
Treatment
View SamplesDynamic mRNA gene expression from the wildtype YSBN6 during a rapamycin treatment (rapamycin-induced downshift). Rapamycin was added to yeast cells growing exponentially on glutamine as sole nitrogen source.
Inferring causal metabolic signals that regulate the dynamic TORC1-dependent transcriptome.
Treatment
View SamplesDynamic mRNA gene expression from the wildtype YSBN6 during a nutritional upshift from proline to glutamine. Glutamine was added to yeast cells growing exponentially on proline as the sole nitrogen source.
Inferring causal metabolic signals that regulate the dynamic TORC1-dependent transcriptome.
Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Modulation of microRNA expression in human T-cell development: targeting of NOTCH3 by miR-150.
No sample metadata fields
View SamplesGene expression of Double Positive, and Single Positive CD4+ human thymocytes
Modulation of microRNA expression in human T-cell development: targeting of NOTCH3 by miR-150.
No sample metadata fields
View SamplesWe generated de novo induced pluripotent stem cells (iPSCs) from two Parkinson’s Disease patients (PD) harboring the p.A53T mutation. iPSC-derived mutant neurons displayed disease-relevant phenotypes at basal conditions, including protein aggregation, compromised neuritic outgrowth and contorted axons with swollen varicosities containing aSyn and tau. We have performed RNA Sequencing (RNA-Seq) of neurons from PD patient and control samples. RNA sequencing has also been performed to neurons derived from HUES samples subjected to the same differentiation protocol as reference. Overall design: We have performed RNA Sequencing (RNA-Seq) in neurons PD and control samples (two clones from each individual), along with HUES-derived neurons.
Defective synaptic connectivity and axonal neuropathology in a human iPSC-based model of familial Parkinson's disease.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The cohesin-associated protein Wapal is required for proper Polycomb-mediated gene silencing.
Specimen part
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