Chronic opiate use produces molecular and cellular adaptations in the nervous system, leading to tolerance, physical dependence and addiction. Genome-wide comparison of morphine-induced changes in brain transcription of mouse strains with different opioid-related phenotypes provides an opportunity to discover the relationship between gene expression and behavioral response to the drug.
Morphine effects on striatal transcriptome in mice.
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View SamplesTo identify molecular effects of chronic drug treatment, heroin and methamphetamine treated animals were compared with saline treated animals at multiple time-points using microarray technology. Gene expression profile was assessed 14 h after the last dose of 1, 3, 6 or 12 days drug treatment and after 13, 15, 18 or 24 days of withdrawal.
Common transcriptional effects in the mouse striatum following chronic treatment with heroin and methamphetamine.
Specimen part, Compound
View SamplesChronic exposure to opioids induces adaptations in brain function that lead to the formation of the behavioral and physiological symptoms of drug dependence and addiction.
Behavioral and transcriptional patterns of protracted opioid self-administration in mice.
Specimen part
View SamplesIn summary, we characterized genomic signatures of response to drugs of abuse and we found positive correlations between the drug-induced expression and various behavioral effects. These signatures are formed by two dynamically inducible transcriptional networks: (1) CREB/SRF-dependent gene pattern that appears to be related to drug-induced neuronal activity, (2) the pattern of genes controlled at least in part via release of glucocorticoids and androgens that are associated with rewarding and harmful drug effects. The discovery of co-expressed networks of genes allowed for the identification of master-switch controlling factors involved in molecular response to the drugs. Finally, using the pharmacological tools we were able to dissect and inhibit particular gene expression patterns from genomic profile.
The dissection of transcriptional modules regulated by various drugs of abuse in the mouse striatum.
Compound, Time
View SamplesUsing whole-genome Affymetrix microarrays (HG-U133A), we characterized the transcriptome profile of cultured human macrophages stimulated for 4 h with interleukin 1 (IL-1) or interleukin 6 (IL-6). We found that, in distinction to liver cells, IL-1 is much more potent than IL-6 in modifying macrophage gene expression, although considerable heterogeneity in response of macrophages deriving from individual blood donors was observed. The obtained results permitted to identify a large number of cytokine-responsive genes. coding for proteins of unknown function that are now being studied in our laboratory. They may represent novel targets in the anti-inflammatory therapy.
Identification of interleukin-1 and interleukin-6-responsive genes in human monocyte-derived macrophages using microarrays.
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View SamplesHuman PB B cell subsets are functionally distinct and may derive from different developmental pathways, reflected by their differential gene expression profiles.
Functional capacities of human IgM memory B cells in early inflammatory responses and secondary germinal center reactions.
Specimen part
View SamplesRNA-SEQ profiling of dopaminergic neurons from the substantia nigra pars compacta and ventral tegmental area regions of the mouse mid-brain Overall design: Murine midbrain dopaminergic neurons from the SNpc and VTA regions
Identification of neurodegenerative factors using translatome-regulatory network analysis.
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View SamplesRNA-SEQ of dopaminergic neurons from the mid-brain of mice that received one daily intraperitoneal injection of MPTP-HCl (30 mg/kg free base per day) or saline for five consecutive days. Samples were taken 4 days. Overall design: Murine midbrain dopaminergic neurons that were treated with MPTP-HCl
Identification of neurodegenerative factors using translatome-regulatory network analysis.
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View SamplesWe identified a novel recurrent genetic lesion in T-LGL. Mutations of the tumour suppressor gene TNFAIP3 causing amino-acid exchanges or protein truncations were seen in 3/39 cases (8%). Overall design: RNA sequencing (Illumina HiSeq 2500) of 5 index patients with paired tumor and non-tumor samples.
Recurrent alterations of TNFAIP3 (A20) in T-cell large granular lymphocytic leukemia.
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View SamplesPurpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived brain transcriptome profiling (RNA-seq) in neuropathic region specific Gaucher mouse brain compared with WT and Isofagamine treated mice of the same age and background and secondly to identify the DEmiRNA associated with the DEmRNA before and after treatment This will give us some insights to see if miRNA is also involved in the the regulation of the expression of the genes involved in the disease process before and after treatment. Methods: 42-45 days old 4L;C*, wild-type (WT) and Isofagamine treated 4L;C* mouse brain were generated by deep sequencing, in triplicate, using IlluminaHiseq. The sequence reads that passed quality filters were analyzed at the gene level with two methods: Burrows–Wheeler Aligner (BWA) followed and TopHat followed by DESeq. qRT–PCR validation was performed using TaqMan and SYBR Green assays Overall design: Regional brain mRNA profiles of ~42 -days old wild type (WT) and 4L;C* an d Isofagamine treated mice were generated by deep sequencing, in triplicate, using IlluminaHi Seq.
Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer.
No sample metadata fields
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