Trascriptional analysis of CD2 hi and CD25 lo CD4+ effector T cells during acute viral infection. SMARTA cells were transferred into B6 mice, followed by infection with LCMV. At day 5 post-infection, CD25 hi and CD25 lo SMARTA cells were isolated from the spleen by FACS. Consistent with our prior studies showing that CD25 lo early effector cells give rise to both Tfh effector cells and memory T cells, we observed gene expression in the CD25 lo population consistent with Tfh differentiation. Conversely, CD25 hi effector cells expressed markers consistent with Th1 differentiation and short-term survival. Overall design: mRNA profiles of monoclonal transgenic CD4+ T cells with divergent CD25 surface expression 5 days post LCMV infection in mice
TCR signal strength controls the differentiation of CD4<sup>+</sup> effector and memory T cells.
Specimen part, Cell line, Subject
View SamplesEpigenetic changes are crucial for the generation of immunological memory1-4. Failure to generate or maintain these changes will result in poor memory responses. Similarly, augmenting or stabilizing the correct epigenetic states offers a potential method of enhancing immune memory. Yet the transcription factors that regulate these processes are poorly defined, as are the chromatin modifying complexes they recruit and the chromatin modifications they control. Using pathogen infection models and three different mouse models, including a new conditional allele, we find that the widely expressed transcription factor Oct15, and its cofactor OCA-B6,7, are selectively required the in vivo generation of functional CD4 memory. In vitro, both proteins are also required to maintain a poised state at the Il2 target locus in resting but previously stimulated CD4 T cells, and to generate robust Il2 expression upon restimulation. OCA-B is also required for the robust re-expression of other known targets including Il17a, and Ifng. We identify an underlying mechanism involving OCA-B recruitment of the histone lysine demethylase Jmjd1a8 to targets such as Il2 and Ifng. The findings pinpoint Oct1 and OCA-B as unanticipated mediators of CD4 T cell memory. Overall design: Examination of 4 different conditions in 2 genotypes
Oct1 and OCA-B are selectively required for CD4 memory T cell function.
No sample metadata fields
View SamplesCDk4/6 inhibitor activates RB and represses RB/E2F target genes
RB Loss Promotes Prostate Cancer Metastasis.
Cell line, Treatment
View SamplesCDk4/6 inhibitor activates RB and represses RB/E2F target genes
RB Loss Promotes Prostate Cancer Metastasis.
Cell line, Treatment
View SamplesDNA methylation is essential for mammalian development and plays crucial roles in a variety of biological processes. The DNA methyltransferase Dnmt1 serves to maintain parental cell methylation patterns on daughter DNA strands in mitotic cells, however, the precise role of Dnmt1 in regulation of quiescent adult stem cells is not known.
DNA methyltransferase 1 is essential for and uniquely regulates hematopoietic stem and progenitor cells.
Specimen part
View SamplesCidofovir is an acyclic nucleoside phosphonate with strong antiviral activity against a broad spectrum of DNA viruses. Although it has previously been shown that cidofovir exerts an antiproliferative effect on HPV positive cells by the induction of apoptosis, the exact mechanism of action remains to be unraveled. In order to study the activity of cidofovir against HPV, gene expression profiling was performed in cidofovir-treated and cidofovir-resistant HeLa, HaCaT, and PHK cells by means of microarrays (HG-U133 Plus 2, Affymetrix).
Cidofovir selectivity is based on the different response of normal and cancer cells to DNA damage.
Specimen part, Disease, Cell line
View SamplesDespite the scientific and applied interest in anaerobic metabolism of Saccharomyces cerevisiae, not all genes whose transcription is up-regulated under anaerobic conditions have yet been linked to known transcription factors. Experiments with a reporter construct in which the promoter of the anaerobically up-regulated TIR1 gene was fused to LacZ revealed a complete loss of anaerobic up-regulation in a snf7 mutant. Anaerobic up-regulation was restored by expression of a truncated allele of RIM101 that encodes for a constitutively active Rim101p transcription factor. Analysis of LacZ expression in several deletion mutants confirmed that the effect of Snf7p on anaerobic up-regulation of TIR1 involved Rim101p and did not require a functional multi-vesicular body sorting pathway (in which Snf7p also participates). Transcriptome analysis in anaerobic chemostat cultures revealed that 26 additional genes exhibited a Snf7p/Rim101p dependent anaerobic up-regulation. Since, in its activated form, Rim101p is generally known as a transcriptional repressor, its role in anaerobic up regulation of TIR1 and other anaerobic yeast genes must involve additional factors. Further studies with deletion mutants in NRG1, NRG2 and SMP1, which were previously shown to be regulated by Rim101p, showed that these genes were not involved in the regulation of TIR1. However, the aerobic repression mechanism of TIR1 involved the general repressor Ssn6p-Tup1p complex. The physiological relevance of Snf7p/Rim101p-mediated transcriptional up-regulation of several genes in anaerobic yeast cultures was evident from reduced growth of a snf7 under anaerobic conditions.
Involvement of Snf7p and Rim101p in the transcriptional regulation of TIR1 and other anaerobically upregulated genes in Saccharomyces cerevisiae.
No sample metadata fields
View SamplesThis study determined the genes that are differetially expressed when regulatory T cells were stimulated in vitro with IL-2
Selective IL-2 responsiveness of regulatory T cells through multiple intrinsic mechanisms supports the use of low-dose IL-2 therapy in type 1 diabetes.
Specimen part
View SamplesHSF1 is a major transcriptional regulator of heat shock responses. Many cells activate HSF1 in response to heat shock temperatures (>42oC) and other cellular stress causing agents. Unlike other cell types, T cells activate HSF1 in response to T cell activation or when exposed to febrile (40oC) temperatures, suggesting a role for HSF1 beyond the heat-shock response.
Heat shock transcription factor 1 is activated as a consequence of lymphocyte activation and regulates a major proteostasis network in T cells critical for cell division during stress.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A mouse model of conditional lipodystrophy.
Sex, Age, Specimen part
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