This array set was used to identify the genes that are highly expressed in the mouse suprachiasmatic nucleus (SCN). Because pharmacological inhibition of Gai/o activity with pertussis toxin hampers intercellular synchronization and causes dampened rhythms of the entire SCN, we hypothesized that member(s) of the Regulator of G protein Signaling (RGS) family might contribute to synchronized cellular oscillations in the SCN. To test this hypothesis, we surveyed all known mouse Rgs genes for their expression by using GeneChip and selected the genes that are highly expressed in the SCN for further analysis.
Circadian regulation of intracellular G-protein signalling mediates intercellular synchrony and rhythmicity in the suprachiasmatic nucleus.
Sex, Age, Specimen part, Disease, Treatment, Time
View SamplesMurine prostate epithelial cells (PECs) were obtained from Ccnd1-/- and Ccnd1+/+ FvB mice (2-3 months of age). RNA extracted from PECs (3 technical replicates for each group) was labeled and used to probe Affymetrix 430_2.0 arrays.
Cyclin D1 Promotes Androgen-Dependent DNA Damage Repair in Prostate Cancer Cells.
No sample metadata fields
View SamplesFunctionally polarized CD4+ T helper (Th) cells such as Th1, Th2 and Th17 cells are central to the regulation of acquired immunity. However, the molecular mechanisms governing the maintenance of the polarized functions of Th cells remain unclear. GATA3, a master regulator of Th2 cell differentiation, initiates the expressions of Th2 cytokine genes and other Th2-specific genes. GATA3 also plays important roles in maintaining Th2 cell function and in continuous chromatin remodeling of Th2 cytokine gene loci. However, it is unclear whether continuous expression of GATA3 is required to maintain the expression of various other Th2-specific genes. In this report, genome-wide DNA gene expression profiling revealed that GATA3 expression is critical for the expression of a certain set of Th2-specific genes. We demonstrated that GATA3 dependency is reduced for some Th2-specific genes in fully developed Th2 cells compared to that observed in effector Th2 cells, whereas it is unchanged for other genes. Moreover, effects of a loss of GATA3 expression in Th2 cells on the expression of cytokine and cytokine receptor genes were examined in detail. A critical role of GATA3 in the regulation of Th2-specific gene expression is confirmed in in vivo generated antigen-specific memory Th2 cells. Therefore, GATA3 is required for the continuous expression of the majority of Th2-specific genes involved in maintaining the Th2 cell identity.
Genome-Wide Gene Expression Profiling Revealed a Critical Role for GATA3 in the Maintenance of the Th2 Cell Identity.
Specimen part, Treatment
View SamplesWe used microarray analysis to identify specific molecular mechanisms controlling IL-5 transcription in memory Th2 cells.
Eomesodermin controls interleukin-5 production in memory T helper 2 cells through inhibition of activity of the transcription factor GATA3.
Specimen part
View SamplesTranscription factors that regulate quiescence, proliferation, and homing of lymphocytes are critical for effective immune system function. In the present study, we demonstrated that the transcription factor ELF4 directly activates the tumor suppressor KLF4 downstream of T cell receptor (TCR) signaling to induce cell cycle arrest in nave CD8+ T cells. Elf4- and Klf4-deficient mice accumulated CD8+CD44hi T cells during steady-state conditions and generated more memory T cells after immunization. The homeostatic expansion of CD8+CD44hi T cells in Elf4-null mice resulted in a redistribution of cells to non-lymphoid tissue due to reduced expression of the transcription factor KLF2, and the surface proteins CCR7 and CD62L. This work describes the combinatorial role of lymphocyte-intrinsic factors in the control of T cell homeostasis, activation and homing.
Transcription factor ELF4 controls the proliferation and homing of CD8+ T cells via the Krüppel-like factors KLF4 and KLF2.
Specimen part
View SamplesAnalysis of mouse chondrocytes lacking the microRNA-140. MicroRNAs are genomically encoded small RNAs to regulate the gene expression. miR-140 shows high expression in cartilage. Results provide insight into the molecular mechanisms underlying miR-140 function in chondrocytes.
MicroRNA-140 plays dual roles in both cartilage development and homeostasis.
Specimen part
View SamplesAnalysis of Foxp3(+)epigenetics(-) T cells, Foxp3(-)epigenetics(+) T cells, and Foxp3(+)epigenetics(+) T cells. Results indicate regulatory T cell (Treg) ontogenesis requires two independent processes, expression of the transcription factor Foxp3 and establishment of Treg epigenetic programs induced by T cell receptor (TCR) stimulation.
T cell receptor stimulation-induced epigenetic changes and Foxp3 expression are independent and complementary events required for Treg cell development.
Specimen part
View SamplesIn skeletal muscle differentiation, muscle-specific genes are regulated by two groups of transcription factors, the MyoD and MEF2 families, which work together to drive the differentiation process. Here we show that ERK5 regulates muscle cell fusion through Klf transcription factors. The inhibition of ERK5 activity suppresses muscle cell fusion with minimal effects on the expression of MyoD, MEF2, and their target genes. Promoter analysis coupled to microarray assay reveals that Klf-binding motifs are highly enriched in the promoter regions of ERK5-dependent upregulated genes. Remarkably, Klf2 and Klf4 expression are also upregulated during differentiation in an ERK5-dependent manner, and knockdown of Klf2 or Klf4 specifically suppresses muscle cell fusion. Moreover, we show that the Sp1 transcription factor links ERK5 to Klf2/4, and that nephronectin, a Klf transcriptional target, is involved in muscle cell fusion. Therefore, an ERK5/Sp1/Klf module plays a key role in the fusion process during skeletal muscle differentiation.
ERK5 regulates muscle cell fusion through Klf transcription factors.
Cell line, Time
View SamplesMammary alveologenesis is abrogated in the absence of the transcription factors STAT5A/5B that mediate cytokine signaling. To reveal the underlying causes for this developmental block we studied mammary stem and progenitor cells. While loss of STAT5A/5B did not affect the stem cell population and their ability to form mammary ducts, luminal progenitors were greatly reduced and unable to form alveoli during pregnancy. Temporally-controlled expression of transgenic STAT5A in mammary epithelium lacking STAT5A/5B restored the luminal progenitor population and rescued alveologenesis in a reversible fashion in vivo. Taken together, STAT5A is necessary and sufficient for the establishment of luminal progenitor cells.
Development of mammary luminal progenitor cells is controlled by the transcription factor STAT5A.
Specimen part
View SamplesTarget genes of Fbxl10 during 3T3-L1 adipogenesis was analyzed
The FBXL10/KDM2B scaffolding protein associates with novel polycomb repressive complex-1 to regulate adipogenesis.
Cell line, Treatment
View Samples