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TranscriptomicsSynergistic, context-dependent and hierarchical functions of hematopoietic progenitor niche components.
Specialized niche environments specify and maintain stem and progenitor cells, but little is known about the identities and functional interactions of niche components in vivo. Here, we describe a modular system for the generation of artificial hematopoietic niches in the mouse embryo. A circumscrib...
ORGANISM(S): Mus musculus 
2012-08-24 | E-GEOD-33268 | biostudies-arrayexpress
UnknownDevelopmental trajectory and evolutionary origin of thymic mimetic cells.
Not available
S-EPMC12286861 | biostudies-literature
GenomicsBLUEPRINT DNA methylation profiles of monocytes, T cells and B cells in type 1 diabetes-discordant monozygotic twins
BLUEPRINT DNA methylation profiles of monocytes, T cells and B cells in type 1 diabetes-discordant monozygotic twins
EGAS00001001598 | EGA
UnknownIL-9 Controls Central Nervous System Autoimmunity by Suppressing GM-CSF Production.
Not available
S-EPMC7197375 | biostudies-literature
UnknownAnalysis of transcriptional regulation of the human miR-17-92 cluster; evidence for involvement of Pim-1.
Not available
S-EPMC3709785 | biostudies-literature
UnknownMouse monocytes express CD127 by immune cells, not LPS.
Not available
S-EPMC11424446 | biostudies-literature
UnknownLamprey <i>FOXN1</i> rescues the block of thymic epithelial cell development in the mouse <i>Foxn1</i>-deficient thymic rudiment.
Not available
S-EPMC12685072 | biostudies-literature
Genomicsena-DATASET-BLUEPRINT-13-09-2016-12:21:58:649-53 - samples
BLUEPRINT DNA methylation profiles of monocytes, T cells and B cells in type 1 diabetes-discordant monozygotic twins (Bisulfite-Seq data).
EGAD00001002682 | EGA
UnknownSIRT1 inactivation switches reactive astrocytes to an antiinflammatory phenotype in CNS autoimmunity.
Not available
S-EPMC9663155 | biostudies-literature
TranscriptomicsGuthrie card methylomics identifies temporally stable epialleles that are present at birth in humans (Methylation BeadChip)
A major concern in common disease epigenomics is distinguishing causal from consequential epigenetic variation. One means of addressing this issue is to identify the temporal origins of epigenetic variants via longitudinal analyses. However, prospective birth-cohort studies are expensive and time-co...
ORGANISM(S): Homo sapiens 
2012-08-27 | E-GEOD-37966 | biostudies-arrayexpress
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