The gene expression patterns in the dentate gyrus of wild-type mice during postnatal development were examined using Affymetrix GeneChip arrays.
Transcriptomic immaturity inducible by neural hyperexcitation is shared by multiple neuropsychiatric disorders.
Specimen part
View SamplesWe previously found that mice with heterozygous knockout of the alpha-isoform of calcium/calmodulin-dependent protein kinase II (alpha-CaMKII HKO mice) show various dysregulated behaviors, including cyclic variations in locomotor activity (LA), suggesting that alpha-CaMKII HKO mice may serve as an animal model showing infradian oscillation of mood. We performed gene expression microarray analysis of dentate gyrus from alpha-CaMKII HKO mice. Mice were selected for the sampling such that their LA levels varied among the mice.
Circadian Gene Circuitry Predicts Hyperactive Behavior in a Mood Disorder Mouse Model.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
Specimen part
View SamplesSchnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of dentate gyri from Shn-2 knockout and wild-type control mice.
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
Specimen part
View SamplesSchnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of prefrontal cortices from Shn-2 knockout and wild-type control mice.
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
Specimen part
View SamplesSchnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of hippocampi from Shn-2 knockout and wild-type control mice.
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
Sex, Specimen part
View Samples<Objective> To compare gene expression in labial salivary glands (LSG) of IgG4-related disease (IgG4-RD) with Sjgrens syndrome (SS).
DNA microarray analysis of labial salivary glands in IgG4-related disease: comparison with Sjögren's syndrome.
Sex, Specimen part
View SamplesWe reported that NRP-1 expression on CD4+ T cells was probably induced by NRP-1 transfer from macrophages to T cells. In HER2+ BC, NRP-1 expressing TIIs correlated with better clinical outcomes. Overall design: Examination of monocytes and monocyte derived macrophages.
Downregulation of neuropilin-1 on macrophages modulates antibody-mediated tumoricidal activity.
No sample metadata fields
View SamplesHere we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, yin-yang regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage.
Opposing activities of DRM and MES-4 tune gene expression and X-chromosome repression in Caenorhabditis elegans germ cells.
Sex
View SamplesPoly(A)+ RNAs were fragmented and sequenced. Poly(A)+ RNAs were fragmented and sequenced.
Position-dependent and neuron-specific splicing regulation by the CELF family RNA-binding protein UNC-75 in Caenorhabditis elegans.
No sample metadata fields
View Samples