Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA185818 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparison of gene expression in NOD versus NOD.NOR-Chr4 (NR4) splenic B cells.
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Project description:Functional liability conferred by gene expression profile can be a possible basis for diseases phenotype. By comparing gene expression profiles in splenic T cells from NOD, C57BL/6 mice and their congenic strains with altered MHCs (NOD.H2^h4 , B6.NOD/Idd1,5/), we identified that the NOD splenic T cells have a strain dependent, tissue specific unique gene expression profile that can be but not necessarily be modulated by alternation of MHC. The NOD splenic T cells gene expression profile indicated a deregulated stress response system, especially heat shock protein family. We demonstrated that NOD splenic T cells have apoptosis defect in vivo and in vitro. Therefore, the gene expression profile may confer liability upon NOD splenic T cells to make them more susceptible to apoptosis, which can be a critical factor to lead to NOD lymphopenia. As recently described, compensatory homeostatic proliferation, driven by lymphopenia, generates autoimmunity in the NOD mouse. Keywords: other
2005-04-14 | GSE2524 | GEO
Project description:Functional liability conferred by gene expression profile can be a possible basis for diseases phenotype. By comparing gene expression profiles in splenic T cells from NOD, C57BL/6 mice and their congenic strains with altered MHCs (NOD.H2^h4 , B6.NOD/Idd1,5/), we identified that the NOD splenic T cells have a strain dependent, tissue specific unique gene expression profile that can be but not necessarily be modulated by alternation of MHC. The NOD splenic T cells gene expression profile indicated a deregulated stress response system, especially heat shock protein family. We demonstrated that NOD splenic T cells have apoptosis defect in vivo and in vitro. Therefore, the gene expression profile may confer liability upon NOD splenic T cells to make them more susceptible to apoptosis, which can be a critical factor to lead to NOD lymphopenia. As recently described, compensatory homeostatic proliferation, driven by lymphopenia, generates autoimmunity in the NOD mouse.
2010-06-10 | E-GEOD-2524 | biostudies-arrayexpress
Project description:Comparison of gene transcription in Ly49G versus Ly49I positive splenic NK cells
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Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.
2019-11-12 | PXD007511 | Pride
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Gene expression profiling of mouse splenic Dendritic cells subsets
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Project description:Gene expression profiles of CD4+CD25+ Tregs from NOD and B6.H2g7 mice
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