An assessment of a role of Ebf1 in committed B lineage cells.
Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells.
Specimen part
View SamplesTrimethylated histone H3-lysine 4 is primarily distributed in the form of sharp peaks, extending in neuronal chromatin on average only across 500-1500 base pairs mostly in close proximity to annotated transcription start sites. To explore whether H3K4me3 peaks could also extend across much broader domains, we undertook a detailed analysis of broadest domain cell-type specific H3K4me3 peaks in ChIP-seq datasets from sorted neuronal and non-neuronal nuclei in human, non-human primate and mouse prefrontal cortex (PFC), and blood for comparison. Overall design: We collected separately cortical gray (GM) and subcortical white matter (WM) from 6 adult human subjects without neurological disease and extracted total RNA processed by the RNA-Seq approach.
Deciphering H3K4me3 broad domains associated with gene-regulatory networks and conserved epigenomic landscapes in the human brain.
No sample metadata fields
View SamplesCombined overexpression of miR-125b with miR-99a and/or miR-100 induced VCR resistance in ETV6-RUNX1-positive leukemic cells Reh.
MiR-125b, miR-100 and miR-99a co-regulate vincristine resistance in childhood acute lymphoblastic leukemia.
Disease, Cell line
View SamplesCD27 and CD45RA can be used to split T cells into 4 subsets, nave cells, CD27+CD45RA+, central memory cells CD27+CD45RA-, effector memory cells CD27-CD45RA-, effector memory CD45RA re-expressing cell, CD27-CD45RA+. It is with in this final EMRA subset that it is belived the senenscent T cells reside. Cellular senescence is accompanied by a senescence-associated secretory phenotype (SASP), to date a SASP has not been demonstrated in T cells.
Human CD8<sup>+</sup> EMRA T cells display a senescence-associated secretory phenotype regulated by p38 MAPK.
Sex
View SamplesFemale infertility syndromes are among the most prevalent chronic health disorders in women, but their molecular basis remains unknown because of the complexity of oogenesis and uncertainty regarding the number and identity of ovarian factors controlling the assembly, preservation, and maturation of ovarian follicles. To systematically discover such ovarian fertility factors en masse, we employed a mouse model (Foxo3), where follicles are assembled normally but are then synchronously activated. Gene expression profiling of mutant and normal ovaries led to the identification a surprisingly large set of ovarian factors. The set included the vast majority of known ovarian factors, many of which when mutated produce female sterility phenotypes, but most were novel. Subsequent analyses revealed novel classes of ovarian factors and significant overrpresentation on the X chromosome, among other insights into the general properties of oogenesis genes and their patterns of expression.
Genomewide discovery and classification of candidate ovarian fertility genes in the mouse.
No sample metadata fields
View SamplesWe used microarray to monitor the differentially expresed genes during Jurkat T cell activaiton.
IκB Kinase ε Is an NFATc1 Kinase that Inhibits T Cell Immune Response.
Cell line
View SamplesNeuronal histone H3-lysine 4 methylation landscapes are defined by sharp peaks at gene promoters and other cis-regulatory sequences, but molecular and cellular phenotypes after neuron-specific deletion of H3K4 methyl-regulators remain largely unexplored. We report that neuronal ablation of the H3K4-specific methyltransferase, Kmt2a/Mixed-lineage leukemia 1 (Mll1), in mouse postnatal forebrain and adult prefrontal cortex (PFC) is associated with increased anxiety and robust cognitive deficits without locomotor dysfunction. In contrast, only mild behavioral phenotypes were observed after ablation of the Mll1 ortholog Kmt2b/Mll2 in PFC. Impaired working memory after Kmt2a/Mll1 ablation in PFC neurons was associated with loss of training-induced transient waves of Arc immediate early gene expression critical for synaptic plasticity. Medial prefrontal layer V pyramidal neurons, a major output relay of the cortex, demonstrated severely impaired synaptic facilitation and temporal summation, two forms of short-term plasticity essential for working memory. Chromatin immunoprecipitation followed by deep sequencing in Mll1-deficient cortical neurons revealed downregulated expression and loss of the transcriptional mark, trimethyl-H3K4, at <50 loci, including the homeodomain transcription factor Meis2. Small RNA-mediated Meis2 knockdown in PFC was associated with working memory defects similar to those elicited by Mll1 deletion. Therefore, mature prefrontal neurons critically depend on maintenance of Mll1-regulated H3K4 methylation at a subset of genes with an essential role in cognition and emotion.
Neuronal Kmt2a/Mll1 histone methyltransferase is essential for prefrontal synaptic plasticity and working memory.
Sex, Specimen part
View SamplesWe have previously demonstrated older skin exhibits increased sterile inflammation 6 hours after saline-injection. In this work, we examined whether p38MAPK inhibitor in vivo would attenuate this non-specific inflammatory response towards saline in elder individuals (=65 years). Overall design: Skin mRNA profiles 6 hours after saline injection were studied before and after losmapimod treatment.
Enhancement of cutaneous immunity during aging by blocking p38 mitogen-activated protein (MAP) kinase-induced inflammation.
Specimen part, Treatment, Subject
View SamplesAnalysis of gene expression in two large schizophrenia cohorts identifies multiple changes associated with nerve terminal function.
Analysis of gene expression in two large schizophrenia cohorts identifies multiple changes associated with nerve terminal function.
Sex, Age
View SamplesTranscriptional analysis of the superior temporal cortex (BA22) in schizophrenia: Pathway insight into disease pathology and drug development
Transcription and pathway analysis of the superior temporal cortex and anterior prefrontal cortex in schizophrenia.
Sex, Age, Specimen part, Disease, Disease stage
View Samples