We noticed that ThPOK repression is readily abrogated upon in vitro TCR stimulation of peripheral CD8 T cells. This observation prompted us to investigate a role of ThPOK in the CD8 T cell response to an acute viral infection. We observed that clonal expansion is significantly less in both primary and secondary CD8 T cell responses in the absence of functional ThPOK. To approach this mechanism, we carried out a microarray analysis for comparison of gene expression between ThPOKhd/hd and ThPOKwt/wt P14 memory T cells.
ThPOK derepression is required for robust CD8 T cell responses to viral infection.
No sample metadata fields
View SamplesGene expression changes between outside and inside of biofilms were investigated. The gene expression was compared between the outside and inside of the biofilms. At the same time, the gene expressions were also compared with exponential phase and stationary phase in planktonic cells. The gene expression analysis showed that the physiological activities were higher at the outside of the biofilms than those at the inside of the biofilms. The genes induced at the ouside of the biofilms included genes involved in the stress responses and adhesions.
Localized expression profiles of rpoS in Escherichia coli biofilms.
No sample metadata fields
View SamplesWe sought to identify genes regulated by the transcription factor Th-POK (Zbtb7b) in liver Va14i NKT cells, by RNA microarray analysis of global gene expression in Va14i NKT cells from mice homozygous for the Th-POK-inactivating hd point mutation as compared with the same cell population isolated from heterozygous or wild-type age-matched mice.
The transcription factor Th-POK negatively regulates Th17 differentiation in Vα14i NKT cells.
No sample metadata fields
View SamplesTranscripts upregulated or downregulated by HOXB7-MEK signaling were identified for use on the microarray using the Affymetrix GeneChip WT PLUS Reagent Kit in comparison with HOXB7-knockdown S2-013 cells that were transfected with rescue-HOXB7 plasmid and treated with MEK inhibitor, and HOXB7-knockdown S2-013 cells that were transfected with rescue-HOXB7 plasmid but not treated with MEK inhibitor.
The transcription factor HOXB7 regulates ERK kinase activity and thereby stimulates the motility and invasiveness of pancreatic cancer cells.
Specimen part
View SamplesIn skeletal muscle, the pattern of electrical activity regulates the expression of proteins involved in synaptic transmission, contraction and metabolism. Disruptions in electrical activity, resulting from prolonged bed-rest, cast-immobilization or trauma, inevitably lead to muscle atrophy. The mechanisms that regulate muscle atrophy are poorly understood, but it seems likely that changes in gene expression play a key role in initiating and maintaining a muscle atrophy program. Previously, we found that Runx1, a transcription factor previously termed AML1, was substantially induced in muscle following denervation. More recently, we sought to determine whether this increase in Runx1 expression may be causally related to the morphological changes in skeletal muscle that accompany muscle disuse, notably muscle atrophy. We found that Runx1 is indeed required to sustain muscle and to minimize atrophy following denervation. Experiments described here are designed to identify the genes that are regulated by Runx1 in skeletal muscle with the particular goal of identifying genes that regulate muscle atrophy.
Runx1 prevents wasting, myofibrillar disorganization, and autophagy of skeletal muscle.
No sample metadata fields
View SamplesConstitutive CD8 expression drives innate CD8+ T cell differentiation via induction of iNKT2 subset. Overall design: Analysis of RNA from Cd8ab transgenic mice by RNA-seq.
Constitutive CD8 expression drives innate CD8<sup>+</sup> T-cell differentiation via induction of iNKT2 cells.
Specimen part, Subject
View SamplesGene expression profiles of Cbfb-deficient and control Treg cells were compared.
Indispensable role of the Runx1-Cbfbeta transcription complex for in vivo-suppressive function of FoxP3+ regulatory T cells.
Sex, Age, Specimen part
View SamplesComparison of transcriptome between wild type, CD4 cre conditional knock-out and Bcl11b mutant mice. Overall design: Five replicates from wt newborn thymus, three replicates mutant new born thymus and four replicate of Bcl11bfl/fl: Cd4-Cre mice.
Priming of lineage-specifying genes by Bcl11b is required for lineage choice in post-selection thymocytes.
Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Direct recruitment of polycomb repressive complex 1 to chromatin by core binding transcription factors.
Specimen part, Cell line
View SamplesPolycomb repressive complexes (PRCs) play key roles in developmental epigenetic regulation. Yet the mechanisms that target PRCs to specific loci in mammalian cells remain incompletely understood. In this study, we show that Bmi1, a core component of Polycomb Repressive Complex 1 (PRC1), binds directly to the Runx1/CBFbeta transcription factor complex. Genome-wide studies in megakaryocytic cells demonstrate considerable chromatin occupancy overlap between the PRC1 core component Ring1b and Runx1/CBFbeta and functional regulation of a significant fraction of commonly bound genes. Bmi1/Ring1b and Runx1/CBFbeta deficiency generate partial phenocopies of one another in vivo. We also show that Ring1b occupies key Runx1 binding sites in primary murine thymocytes and that this occurs via Polycomb Repressive Complex 2 (PRC2) independent mechanisms. Genetic depletion of Runx1 results in reduced Ring1b binding at these sites in vivo. These findings provide evidence for site-specific PRC1 chromatin recruitment by core binding transcription factors in mammalian cells.
Direct recruitment of polycomb repressive complex 1 to chromatin by core binding transcription factors.
Specimen part, Cell line
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