publication_authors:Kita Y Results

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Organism

Mus musculus (247)

Technology

Microarray (247)

Platform

Affymetrix Mouse Genome 430 2.0 Array (mouse4302) (247)

Includes Publication

GSE18148

Microarray analysis of Cbfb-deficient regulatory T cells

Mus musculus
6 Downloadable Samples

Description

Gene expression profiles of Cbfb-deficient and control Treg cells were compared.

Publication Title

Indispensable role of the Runx1-Cbfbeta transcription complex for in vivo-suppressive function of FoxP3+ regulatory T cells.

Alternate Accession IDs

E-GEOD-18148

Sample Metadata Fields

Sex, Age, Specimen part

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GSE24574

Expression data from BCL6-YFP-positive Tfh cells, BCL6-YFP-negative Tfh cells, non-Tfh cells, and nave helper T cells.

Mus musculus
1 Downloadable Sample

Description

We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.

Publication Title

Bcl6 protein expression shapes pre-germinal center B cell dynamics and follicular helper T cell heterogeneity.

Alternate Accession IDs

E-GEOD-24574

Sample Metadata Fields

Specimen part

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GSE12637

AC61 Vector vs. pRb

Mus musculus
2 Downloadable Samples

Description

This experiment is to identify genes that are regulated by pRb in AC61 cells. AC61 cells were derived from a C-cell adenocarcinoma developed in an Rb+/-N-ras-/- mouse.

Publication Title

Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation.

Alternate Accession IDs

E-GEOD-12637

Sample Metadata Fields

No sample metadata fields

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GSE15129

Coenzyme Q10-dependent gene expression in SAMP1 mice tissues

Mus musculus
65 Downloadable Samples

Description

Our present study reveals significant decelerating effects on senescence processes in middle-aged SAMP1 mice supplemented for 6 or 14 months with the reduced form (QH2, 500 mg/ kg BW/ day) of coenzyme Q10 (CoQ10). To unravel molecular mechanisms of these CoQ10 effects, a genome-wide transcript profiling in liver, heart, brain and kidney of SAMP1 mice supplemented with the reduced (QH2) or oxidized form of CoQ10 (Q10) was performed. Liver seems to be the main target tissue of CoQ10 intervention, followed by kidney, heart and brain. Stringent evaluation of the resulting data revealed that QH2 has a stronger impact on gene expression than Q10, which was primarily due to differences in the bioavailability. Indeed, we found that QH2 supplementation was more effective than Q10 to increase levels of CoQ10 in the liver of SAMP1 mice (54.92-fold and 30.36-fold, respectively). To identify functional and regulatory connections of the top 50 (p < 0.05) up- and down-regulated QH2-sensitive transcripts in liver (fold changes ranging from 21.24 to -6.12), text mining analysis (Genomatix BiblioSphere, GFG level B3) was used. Hereby, we identified 11 QH2-sensitive genes which are regulated by PPAR- and are primarily involved in cholesterol synthesis (e.g. HMGCS1, HMGCL, HMGCR), fat assimilation (FABP5), lipoprotein metabolism (PLTP) and inflammation (STAT-1). Thus, we provide evidence that QH2 is involved in the reduction of fat and cholesterol synthesis via modulation of the PPAR- signalling pathway. These data may explain, at least in part, the observed effects on decelerated age-dependent degeneration processes in QH2-supplemented SAMP1 mice.

Publication Title

Supplementation with the reduced form of Coenzyme Q10 decelerates phenotypic characteristics of senescence and induces a peroxisome proliferator-activated receptor-alpha gene expression signature in SAMP1 mice.

Alternate Accession IDs

E-GEOD-15129

Sample Metadata Fields

Sex, Age, Specimen part

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GSE6939

CD4+ T cells gene-transduced with AML1, wild type Foxp3, and a Foxp3 mutant defective in binding to AML1

Mus musculus
4 Downloadable Samples

Description

To clarify how Foxp3 regulates its target genes, we performed co-immunoprecipitation experiments and found that Foxp3 physically bound to AML1/Runx1 (Ono, M. et al, Nature, 2007). In this series of study, we compared gene regulations by AML1, wild type Foxp3, and a Foxp3 mutant with defective binding to AML1.

Publication Title

Foxp3 controls regulatory T-cell function by interacting with AML1/Runx1.

Alternate Accession IDs

E-GEOD-6939

Sample Metadata Fields

No sample metadata fields

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GSE98761

DNA microarray analysis of Jmjd1a and/or Jmjd1b knockout embryonic stem cells

Mus musculus
8 Downloadable Samples

Description

Histone H3 lysine 9 (H3K9) methylation is an epigenetic mark of transcriptionally repressed chromatin. During mammalian development, H3K9 methylation levels seem to be spatiotemporally regulated by the opposing activities of methyltransferases and demethylases to govern correct gene expression. However, the combination(s) of H3K9 methyltransferase(s) and demethylase(s) that contribute to this regulation and the genes regulated by them remain unclear. Herein, we demonstrate the essential roles of H3K9 demethylases Jmjd1a and Jmjd1b in the embryogenesis and viability control of embryonic stem (ES) cells. Mouse embryos lacking Jmjd1a/Jmjd1b died after implantation. Depletion of Jmjd1a/Jmjd1b in mouse ES cells induced rapid cell death accompanied with a massive increase in H3K9 methylation. Jmjd1a/Jmjd1b depletion induced an increase in H3K9 methylation in the gene-rich regions of the chromosomes, indicating that Jmjd1a/Jmjd1b removes H3K9 methylation marks in the euchromatin. Importantly, the additional disruption of the H3K9 methyltransferase G9a in a Jmjd1a/Jmjd1b-deficient background rescued not only the H3K9 hypermethylation phenotype but also the cell death phenotype. We also found that Jmjd1a/Jmjd1b removes H3K9 methylation marks deposited by G9a in the Oct4 and Ccnd1 loci to activate transcription. In conclusion, Jmjd1a/Jmjd1b ensures ES cell viability by antagonizing G9a-mediated H3K9 hypermethylation in the gene-rich euchromatin.