This SuperSeries is composed of the SubSeries listed below.
HCFC1 is a common component of active human CpG-island promoters and coincides with ZNF143, THAP11, YY1, and GABP transcription factor occupancy.
Cell line, Treatment
View SamplesWe compared in triplicate mRNA levels from cells treated with siRNA against either HCF-1 or, as a negative control, luciferase. We observed that 19% of Refseq annotated genes are differentially expressed (either up or down regulated with a multiple testing corrected p value of 0.05) upon depletion of HCF-1. This large number of differentially expressed genes upon HCF-1 depletion demonstrates a broad role of HCF-1 in the regulation of gene expression.
HCFC1 is a common component of active human CpG-island promoters and coincides with ZNF143, THAP11, YY1, and GABP transcription factor occupancy.
Cell line, Treatment
View SamplesIn vitro studies identified TBC1D4 as an regulator of renal ion and water transporting proteins. However, TBC1D4-deficient mice did not show a defective renal salt and water homeostasis.
Rab-GAP TBC1D4 (AS160) is dispensable for the renal control of sodium and water homeostasis but regulates GLUT4 in mouse kidney.
Sex, Specimen part
View SamplesCell purification technology combined with whole transcriptome sequencing and small molecule agonist of hematopoietic stem cell self-renewal has allowed us to identify the endothelial protein c receptor protein (EPCR) as a surface maker that defines a rare subpopulation of human cells which is highly enriched for stem cell activity in vivo. EPCR-positive cells exhibit a robust multi-lineage differentiation potential and serial reconstitution in immunocompromised mice. In culture, most if not all of the HSC activity is detected in the EPCR+ subset, arguing for the stability of this marker on the surface of cultured cells, a feature not found with more recently described markers such as CD49f. Functionally EPCR is essential for human HSC activity in vivo. Cells engineered to express low EPCR expression proliferate normally in culture but lack the ability to confer long-term reconstitution. EPCR is thus a stable marker for human HSC. Its exploitation should open new possibilities in our effort to understand the molecular bases behind HSC self-renewal. Overall design: Examining 3 cellular subsets: EPCR+, EPCRlow, EPCR- derived form CD34+CD45RA- cord blood cells after 7 day expansion in UM171
EPCR expression marks UM171-expanded CD34<sup>+</sup> cord blood stem cells.
No sample metadata fields
View SamplesThis study examines the extent to which memory CD4+ T cells share immunosurveillance strategies with CD8+ resident memory T cells (TRM). After acute viral infection, memory CD4+ T cells predominantly utilized residence to survey nonlymphoid tissues, albeit not as stringently as observed for CD8+ T cells. In contrast, memory CD4+ T cells were more likely to be resident within lymphoid organs than CD8+ T cells. Migration properties of memory-phenotype CD4+ T cells in non-SPF parabionts were similar, generalizing these results to diverse infections and conditions. CD4+ and CD8+ TRM shared overlapping transcriptional signatures and location-specific features, such as granzyme B expression in the small intestine, revealing tissue-specific and migration property-specific, in addition to lineage-specific, differentiation programs. Functionally, mucosal CD4+ TRM reactivation locally triggered both chemokine expression and broad immune cell activation. Thus, residence provides a dominant mechanism for regionalizing CD4+ T cell immunity, and location enforces shared transcriptional, phenotypic, and functional properties with CD8+ T cells. Overall design: 17 samples were analyzed by RNA-Sequencing: 3 replicates of resident memory SMARTA CD4 cells (CD62L- CD69+) from the female reproductive tract (FRT) , 2 replicates of resident memory SMARTA CD4 cells (CD62L- CD69+) from the small intestine epithelium (IEL), 3 replicates of resident memory SMARTA CD4 cells (CD62L- CD69+) small intestine lamina propria (LP), 3 replicates of resident memory SMARTA CD4 cells (CD62L- CD69+) from the spleen (SLO), 3 replicates of SMARTA CD4 cells (CD62L+ CD69- or TCM) from the spleen of mice, and 3 replicates of SMARTA CD4 cells (CD62L- CD69- or TEM) from the spleen of mice infected with LCMV-Armstrong 54 days prior.
CD4<sup>+</sup> resident memory T cells dominate immunosurveillance and orchestrate local recall responses.
Specimen part, Subject
View SamplesLeanness is associated with increased lifespan and is linked to favorable metabolic conditions promoting life extension.
Deficiency of the lipid synthesis enzyme, DGAT1, extends longevity in mice.
Sex, Specimen part
View SamplesStudy of brain regions from GRN KO, Heterozygous and WT mice at different time points (2-6-9 months)
Functional genomic analyses identify pathways dysregulated by progranulin deficiency, implicating Wnt signaling.
Sex, Time
View SamplesRNASeq data for mPB or CB-derived CD34+ exposed to UM171 Overall design: human mobilized peripheral blood or cord blood-derived CD34(+) cells were cultured for 16 hours with vehicle (DMSO), dose response of UM171 [11.9nM, 19nM, 30.5nM, 48.8nM, 78.1nM and 125nM], SR1 [500nM] and combination of( UM171 [48.8nM]+SR1 [500nM])
UM171 induces a homeostatic inflammatory-detoxification response supporting human HSC self-renewal.
No sample metadata fields
View SamplesMurine embryonic fibroblasts were isolated from WT and DGAT1,DGAT2-KO (D1D2KO) animals. mRNA was isolated from cells untreated (UNDIFF) or treated (DIFF) according to standard differentiation protocol for adipocytes (Harris, C, et al. JLR 2011).
DGAT enzymes are required for triacylglycerol synthesis and lipid droplets in adipocytes.
Specimen part
View SamplesSIRT3 is a mitochondrial NAD(+)-dependent protein deacetylase, which regulates the enzymatic activity of several mitochondrial proteins.
SIRT3 deficiency and mitochondrial protein hyperacetylation accelerate the development of the metabolic syndrome.
Age, Specimen part
View Samples