To determine the transcriptional profile of Th22 cells and allow comparative analysis with Th17 cells
Th22 Cells Form a Distinct Th Lineage from Th17 Cells In Vitro with Unique Transcriptional Properties and Tbet-Dependent Th1 Plasticity.
No sample metadata fields
View SamplesHematopoietic progenitor and stem cells from bone marrow have been sorted by FACS (LSK, Lineage -, Sca1 + and cKit +) and co-culture during 18h without cytokines with or without extracellular vesicles (EV) secreted by AFT stromal cells.
Extracellular vesicles of stromal origin target and support hematopoietic stem and progenitor cells.
Specimen part
View SamplesThis study investigates three radiation exposure scenarios in BALB/c and C57BL/6 mice: (1) low dose (LD) group -- four weekly doses of 7.5 cGy, (2) high dose (HD) group -- four weekly doses of 1.8 Gy, (3) unexposed group -- four weekly sham exposures. We then used comparative expression profiles of the mouse mammary gland and cardiac blood to build a model of candidate tissue functions associated with LD cancer susceptibility in these strains and murine and human knowledgebases to characterize these tissue functions and their relevance to breast cancer.
Genetic differences in transcript responses to low-dose ionizing radiation identify tissue functions associated with breast cancer susceptibility.
Sex, Age, Specimen part
View SamplesSerial comparison between Th1 and Th17 tumor-specific cells cultured in vitro and ex vivo after transferred into sublethaly irradiated B6.PL mice. Th17-derived cells acquire Th1-like properties in vivo but maintain a distinct molecular profile.
Th17 cells are long lived and retain a stem cell-like molecular signature.
Specimen part, Treatment
View SamplesPaneth cells recide in the intestinal crypt bottom and are part of the innate immunity and of the intestinal stem cell niche.
mTORC1 in the Paneth cell niche couples intestinal stem-cell function to calorie intake.
Age, Specimen part
View SamplesSmall RNAs (sRNA) that act by base pairing with trans-encoded mRNAs modulate metabolism in response to a variety of environmental stimuli. Here, we describe an Hfq-binding sRNA (FnrS) whose expression is induced upon a shift from aerobic to anaerobic conditions and which acts to down regulate the levels of a variety of mRNAs encoding metabolic enzymes. Anaerobic induction in minimal medium depends strongly on FNR but is also affected by ArcA and CRP. Whole genome expression analysis showed that the levels of at least 32 mRNAs are down regulated upon FnrS overexpression, 15 of which are predicted to base pair with FnrS by TargetRNA. The sRNA is highly conserved across its entire length in numerous enterobacteria, and mutation analysis revealed that two separate regions of FnrS base pair with different sets of target mRNAs. The majority of the target genes previously reported to be down regulated in an FNR-dependent manner lack recognizable FNR binding sites. We thus suggest that FnrS extends the FNR regulon and increases the efficiency of anaerobic metabolism by repressing the synthesis of enzymes that are not needed under these conditions.
Reprogramming of anaerobic metabolism by the FnrS small RNA.
No sample metadata fields
View SamplesGene expression profiling in soybean under aluminum stress: genes differentially expressed between Al-tolerant and Al-sensitive genotypes.
Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.
Specimen part, Treatment
View SamplesGene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level.
Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.
Specimen part, Treatment
View SamplesGene expression profiling in soybean under aluminum stress: Transcriptome response to Al stress in roots of Al-tolerant genotype (PI 416937).
Identification of Aluminum Responsive Genes in Al-Tolerant Soybean Line PI 416937.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome Wide Mapping of NR4A Binding Reveals Cooperativity with ETS Factors to Promote Epigenetic Activation of Distal Enhancers in Acute Myeloid Leukemia Cells.
Cell line, Treatment
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