Caspases are cysteine-proteases with key roles in the execution phase of apoptosis. Additional cellular activities, unrelated to cell death seem to be influenced by these enzymes. Identification of genes co-regulated with caspases could help to ascertain new biological roles for these proteases.To identify genes and pathways under the influence of caspase-2 we silenced its expression in U87MG glioblastoma cell line. Transcriptional expression profiles of cells transfected with caspase-2 siRNA or control siRNA were compared.
Transcriptomic analysis unveils correlations between regulative apoptotic caspases and genes of cholesterol homeostasis in human brain.
Cell line, Treatment
View SamplesLong noncoding RNAs (lncRNAs) have been implicated in numerous cellular processes including brain development. Yet the in vivo expression dynamics and molecular pathways regulated by these molecules are less well understood. Here, we leveraged a cohort of 13 lncRNA null-mutant mouse models to investigate the spatio-temporal expression of lncRNAs in the developing and adult brain. We observed a wide range of different spatio-temporal expression profiles in the brain. Several lncRNAs are differentially expressed both in time and space, and others present highly restricted expression in only selected brain regions. We further explore the consequent transcriptome alterations after loss of these lncRNA loci, and demonstrate altered regulation of a large variety of cellular pathways and processes. We further found that 6/13 lncRNA null-mutant strains significantly affect the expression of several neighboring protein-coding genes, in a cis-like manner. This resource provides insight into the expression patterns and potential effect of lncRNA loci in the developing and adult mammalian brain, and allows future examination of the specific functional relevance of these genes in neural development, brain function, and disease. We have sequenced wildtype and mutant whole brains from a cohort of 13 lncRNA knockout mouse strains at two developmetal timepoints (E14.5 and adult). Overall design: Comparison between wildtype and mutant whole brains transcriptomes in 13 lncRNA mutant strains at two different timepoints. Please note that for each knockout strain there are KO_E14.5 and KO_Adult samples, however for WT, each KO strain was compared to a cohort of 14 WTs (N3 background) and 3 WTs (N2.5 background) at either Adult or E14.5 timepoint. So in total there are 14 WT_Adult and 14 WT_E14.5 and in each differential analysis the 2 or 3 KOs (in N3 background) were compared to this entire cohort at the respective timepoint; a cohort of 3 WT_adult (N2.5) or 3 WT_E14.5 samples compared to other N2.5 KO samples at the respective timepoint. Thus, each processed data file was generated by comparing each KO strain to a cohort of WTs (at either Adult or E14.5 timepoint; ko_vs_WT_Adult or ko_vs_WT_embryonic). The mouse strain (background) used in these experiments a cross between 129 and C57BL/6 in the third generation (N3) of breeding in the C57BL/6 line, with the exception of the KANTR mice, which are N2.5.
Spatiotemporal expression and transcriptional perturbations by long noncoding RNAs in the mouse brain.
No sample metadata fields
View SamplesWe conducted RNA-Seq (using Direct Ligation of Adapters to first strand cDNA) in neurons from E16.5 mouse embryonic cortices from WT and SMCX KO mice and harvested after 10 days in vitro culture. Overall design: We sequenced RNA samples after 10 days in vitro cultures in biological and technical duplicates. 4 RNA samples from WT and SMCX KO neurons. We also sequenced RNA samples from same neurons after stimulation with KCl for 60 mins. So a total of 8 RNA-Seq samples.
A Mouse Model of X-linked Intellectual Disability Associated with Impaired Removal of Histone Methylation.
No sample metadata fields
View SamplesWe sequenced RNA from Pre-frontal cortex (PFC) and Amygdala from 3-6 month old adult mice. Overall design: The amygdala and the frontal cortex were dissected from three adult mice for each genotype (WT and SMCX KO) and homogenized in trizol. RNA was purified using Qiagen RNEasy kit and ribosomal RNA was depleted using Ribominus Eukaryote v2 kit from Life Technologies. RNA-Seq libraries were prepared using Direct Ligation of Adapters to first strand cDNA (DLAF) and subjected to 50 base sequencing on Illumina HiSeq2000.
A Mouse Model of X-linked Intellectual Disability Associated with Impaired Removal of Histone Methylation.
Sex, Specimen part, Subject
View SamplesWe sought to find a gene-expression multigene predictor of response to infliximab therapy in Rheumatoid Arthritis patients. Using internal and external cross-validation systems we have built and validated an 8-gene predictor for response to infliximab.
An eight-gene blood expression profile predicts the response to infliximab in rheumatoid arthritis.
Sex, Specimen part, Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Gene expression profiling reveals renin mRNA overexpression in human hypertensive kidneys and a role for microRNAs.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MicroRNA networks in mouse lung organogenesis.
Sex
View SamplesWe performed miRNA and mRNA profiling over a 7-point time course, encompassing all recognized stages of lung development and explore dynamically regulated miRNAs and potential miRNA-mRNA interaction networks specific to mouse lung development
MicroRNA networks in mouse lung organogenesis.
Sex
View SamplesThe regulation of necrotic death and its relevance in anti-cancer therapy are largely unknown. Here we have investigated the pro-apoptotic and pro-necrotic activities of two ubiquitin-proteasome system inhibitors (UPSIs): bortezomib and G5. The present study points out that the glioblastoma cell lines U87MG and T98G are useful models to study the susceptibility to apoptosis and necrosis in response to UPSIs. U87MG cells are resistant to apoptosis induced by bortezomib and G5 but susceptible to necrosis induced by G5. On the opposite T98G cells are susceptible to apoptosis induced by both inhibitors but show some resistance to G5-induced necrosis. By comparing the transcriptional profiles of the two cell lines, we have found that the resistance to G5-induced necrosis could arise from differences in glutathione synthesis/utilization and in the microenvironment. In particular collagen IV, which is highly expressed in T98G cells, and fibronectin, whose adhesive function is counteracted by tenascin-C in U87MG cells, can restrain the necrotic response to G5. Collectively, our results provide an initial characterization of the molecular signals governing cell death by necrosis in glioblastoma cell lines.
Characterization of caspase-dependent and caspase-independent deaths in glioblastoma cells treated with inhibitors of the ubiquitin-proteasome system.
Cell line
View SamplesDAP12 is a transmembrane protein, expressed as a disulfide-bonded homodimer and bears an immunoreceptor tyrosine-based activation motif (ITAM). DAP12 is broadly expressed in hematopoietic cells and associates with a variety of cell surface receptors in lymphoid and myeloid cells. Macrophages express several DAP12-associated receptors including triggering receptors expressed by myeloid cells (TREM)-1,2 and 3, myeloid DAP12-associating lectin (MDL)-1, CD200R like proteins CD200R3/R4 and CD300C/D/E .
Essential role of DAP12 signaling in macrophage programming into a fusion-competent state.
No sample metadata fields
View Samples