Schizophrenia is a complex psychiatric disorder encompassing a range of symptoms and etiology dependent upon the interaction of genetic and environmental factors. Several risk genes, such as DISC1, have been associated with schizophrenia as well as bipolar disorder (BPD) and major depressive disorder (MDD), consistent with the hypothesis that a shared genetic architecture could contribute to divergent clinical syndromes. The present study compared gene expression profiles across three brain regions in post-mortem tissue from matched subjects with schizophrenia, BPD or MDD and unaffected controls. Post-mortem brain tissue was collected from control subjects and well-matched subjects with schizophrenia, BPD, and MDD (n=19 from each group). RNA was isolated from hippocampus, Brodmann Area 46, and associative striatum and hybridized to U133_Plus2 Affymetrix chips. Data were normalized by RMA, subjected to pairwise comparison followed by Benjamini and Hochberg False Discovery Rate correction (FDR). Samples derived from patients with schizophrenia exhibited many more changes in gene expression across all brain regions than observed in BPD or MDD. Several genes showed changes in both schizophrenia and BPD, though the magnitude of change was usually larger in schizophrenia. Several genes that have variants associated with schizophrenia were found to have altered expression in multiple regions of brains from subjects with schizophrenia. Continued evaluation of circuit-level alterations in gene expression and gene-network relationships may further our understanding of how genetic variants may be influencing biological processes to contribute to psychiatric disease.
STEP levels are unchanged in pre-frontal cortex and associative striatum in post-mortem human brain samples from subjects with schizophrenia, bipolar disorder and major depressive disorder.
Sex, Age, Specimen part, Disease, Disease stage, Race
View SamplesWe present a microarray analysis of primary mouse astrocytes exposed to HIV-1 in culture. Results are compared with previous genomic studies of HIV-1 effect in human astrocytes and human and macaque brains.
Gene expression profiles of HIV-1-infected glia and brain: toward better understanding of the role of astrocytes in HIV-1-associated neurocognitive disorders.
Specimen part, Treatment
View SamplesMutant embryos lacking maternal and zygotic HOW exhibit defects in mesoderm development. How is an RNA binding protein that regulates the levels of mRNAs by controling RNA metabolism.
Post-transcriptional repression of the Drosophila midkine and pleiotrophin homolog miple by HOW is essential for correct mesoderm spreading.
No sample metadata fields
View SamplesThe objective of this study is to determine how inhibition of microRNA 10b affects gene expression in neurospheres cultures of glioblastoma stem-like cells.
Therapeutic potential of targeting microRNA-10b in established intracranial glioblastoma: first steps toward the clinic.
Treatment
View SamplesGene expression profiling of 82 patients with cervical cancer was performed. The expression data were correlated with copy number alterations of the same patients, as assessed with array CGH in a separate study, in order to identify drivers of cervical cancer carcinogenesis.
Gene network reconstruction reveals cell cycle and antiviral genes as major drivers of cervical cancer.
Specimen part
View SamplesWe identified LAMP3 as a key driver gene of anti-viral subnetwork genes in cervical cancer patients. Therefore we tested this prediction using an in vitro system. This is the first direct demonstration of LAMP3 regulatory role in interferon-dependent immune response.
Gene network reconstruction reveals cell cycle and antiviral genes as major drivers of cervical cancer.
Disease, Cell line, Treatment, Time
View SamplesAntiretroviral therapy (ART) has reduced morbidity and mortality in HIV infection; however HIV-1-associated neurocognitive disorders (HAND) persist despite treatment. We used microarray analysis in post-mortem brain tissues to determine ART effectiveness in the brain and to identify molecular signatures of HAND under ART.
Significant effects of antiretroviral therapy on global gene expression in brain tissues of patients with HIV-1-associated neurocognitive disorders.
Specimen part, Disease, Disease stage, Treatment
View SamplesSignal intensity data for rpd3 delete, H3delta(1-28), H3(K4,9,14,18,23,27Q), H4delta(2-26), H4(K5,8,12,16Q), rpd3 delete H3delta(1-28), and rpd3 delete H4(K5,8,12,16Q) yeast grown in rich (YPD) media
Genome-wide analysis of the relationship between transcriptional regulation by Rpd3p and the histone H3 and H4 amino termini in budding yeast.
No sample metadata fields
View SamplesTranscription termination and mRNA export from the nucleus are closely regulated and coordinated processes. Nuclear export factors are recruited to actively transcribed genes through their interactions with protein complexes associated with transcription and co-transcriptional pre-mRNA processing. We determine a new role for the kinase WNK1 in the cross-talk of transcription termination and mRNA export. WNK1 was previously attributed a cytoplasmic role as a regulator of ion transport. However, we now show a nuclear function for this kinase where it is required for efficient mRNA export along with the transcription termination factor PCF11. Finally, we identify the phosphorylation of the CID domain of PCF11 as an important step for the release of the mRNA from the transcription locus, thus allowing efficient mRNA export to the cytoplasm. Overall design: RNA from cytoplasmic and nuclear extracts of HeLa cells was obtained, upon depletion of WNK1 kinase or from control cells. Upon pA selection, libraries were generated and sequenced. A duplicate experiment was performed for each sample.
WNK1 kinase and the termination factor PCF11 connect nuclear mRNA export with transcription.
Cell line, Subject
View SamplesWe undertook a survey of gene expression changes in primary microglial cultures with and without neurovirulent (FrCasE) and non-neurovirulent (Fr57E) virus infection to identify physiological changes that could be relevant to the induction of spongiform neurodegeneration. These gene expression analyses were performed using Affymetrix 430A mouse GeneChips (5 chips for each of the three experimental conditions, representing over 14,000 murine genes and ESTs. RNA from 5 separate microglial culture preparations were analyzed for Control (mock infected), Fr57E-, and FrCasE-infected microglia. Present/absent calls were based on MicroArray Suite 5.0 from Affymetrix. Affymetrix CEL files were analyzed using dChip software after normalization of the data between all 15 arrays. Statistical analyses were performed using ANOVA.
Gene expression profiling of microglia infected by a highly neurovirulent murine leukemia virus: implications for neuropathogenesis.
Specimen part
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