The experiment was designed to generate a time series for epithelial model during development. Each time point had 3 replicates. The data set contained 5 time points over 10 days. They are day0, day3, day5,day7,day10.
Dynamic and physical clustering of gene expression during epidermal barrier formation in differentiating keratinocytes.
Age, Specimen part, Time
View SamplesNOD mice are an inbred strain that display enhanced MZ B cell differentiation from an early age. Interestingly, several lines of evidence implicate MZ B cells in this strain as important contributors to the T cell mediated beta cell destruction associated with the development of type 1 diabetes (T1D). In order to develop a better understanding of the underlying causes for augmented MZ B cell production in NOD mice, we obtained the transcriptional profiles of FO and MZ subsets and TR precursors from NOD mice and compared them to those of the B6 strain.
Intrinsic molecular factors cause aberrant expansion of the splenic marginal zone B cell population in nonobese diabetic mice.
Sex, Age, Specimen part
View SamplesFailures to produce neutralizing antibodies upon HIV-1 infection result in part from B cell dysfunction due to unspecific B cell activation. How HIV-1 affects antigen-specific B cell functions remains elusive. Using an adoptive transfer mouse model and ex vivo HIV infection of human tonsil tissue we found that expression of the HIV-1 pathogenesis factor NEF in CD4 T cells undermines their helper function and impairs cognate B cell functions including mounting of efficient specific IgG responses. NEF interfered with T cell help via a specific protein interaction motif that prevents polarized cytokine secretion at the T cell - B cell immune synapse. This interference reduced B cell activation and proliferation and thus disrupted germinal center formation and affinity maturation. These results identify NEF as a key component for HIV-mediated dysfunction of antigen-specific B cells. Therapeutic targeting of the identified molecular surface in NEF will facilitate host control of HIV infection.
HIV-1 infection of CD4 T cells impairs antigen-specific B cell function.
Specimen part
View SamplesType 1 Diabetes (T1D) in humans and the non-obese diabetic (NOD) mouse model results from autoreactive T cell destruction of pancreatic beta cells. A pathogenic role for B lymphocytes (B cells) in T1D first became evident when NOD mice made deficient in this population through introduction of an inactivated Ig heavy chain gene (NOD.Ignull) or chronic treatment with anti-IgM antibodies were strongly protected from disease. We produced an NOD background strain developing a greatly decreased T1D incidence due to a NOR-derived 44.31Mb congenic region from rs3674285 to D4Mit127 on distal Chr. 4 (termed NOD.NOR-Chr4 (NR4)) containing disease resistance alleles decreasing the pathogenic activity of autoreactive B cells. Microarrays were conducted on B cells purified from spleens of NOD and NR4 mice to highlight differentially expressed genes within the distal Chr. 4 locus. B cells were either cultured in media alone (unstimulated) or with BCR cross-linking anti-IgM-F(ab)2 fragments (stimulated) for 2h before RNA was extracted for transcript analysis.
Subcongenic analyses reveal complex interactions between distal chromosome 4 genes controlling diabetogenic B cells and CD4 T cells in nonobese diabetic mice.
Sex, Age, Specimen part
View SamplesBackground: Although TNF inhibitors are used to treat chronic inflammatory diseases, there is little information about how long-term inhibition of TNF affects the homeostatic functions that TNF maintains in the intact CNS. TNF is known to modulate neurogenesis by decreasing cell proliferation, increasing apoptosis of precursor cells, and impairing neuronal differentiation. TNF can also influence the formation of the hippocampus, with long-lasting effects on cognition. Materials and methods: To clarify whether developmental TNF deficiency causes alterations in the naïve CNS, we estimated the number of proliferating cells, microglia, and neurons in the brains of E13.5, P7, and adult TNF +/+ and TNF-/- mice and measured changes in gene and protein expression and monoamine levels in adult TNF+/+ and TNF-/- mice. To evaluate long-term effects of TNF inhibitors, we treated healthy adult C57BL/6 mice with either saline, selective soluble TNF inhibitor XPro1595, or nonselective TNF inhibitor etanercept. We estimated changes in cell number and protein expression after two months of treatment. We assessed the effects of TNF deficiency on cognition by testing adult TNF+/+ and TNF-/- mice and anti-TNF treated mice with behavioral tasks.
TNF deficiency causes alterations in the spatial organization of neurogenic zones and alters the number of microglia and neurons in the cerebral cortex.
Sex, Specimen part
View SamplesmiRNA-1343 is an uncharacterized miRNA predicted to target a number of genes involved in epithelial cell function including TGF-beta signaling, cell adhesion, and cell proliferation. We transiently overexpressed miRNA-1343 or a non-targeting control miRNA in A549 and 16HBE14o- human airway cell lines. As predicted, RNA-seq following miRNA-1343 overexpression showed significant downregulation of genes involved in these pathways. Furthermore, genes involved in cholesterol and lipid biosynthesis were found to be significantly upregulated by miRNA-1343 overexpression. Overall design: mRNA profiles from A549 and 16HBE14o- cells transiently transfected with miRNA-1343 or a negative control (NC) miRNA, in quintuplicate.
miR-1343 attenuates pathways of fibrosis by targeting the TGF-β receptors.
No sample metadata fields
View SamplesARC (NSC 188491, SMA-491), 4-amino-6-hydrazino-7-beta-d-ribofuranosyl-7H-pyrrolo-(2,3-d)-pyrimidine-5-carboxamide, is a nucleoside analog with profound in vitro anti-cancer activity. First identified in a high-throughput screen for inhibitors of p21 mRNA expression, subsequent experiments showed that ARC also repressed expression of hdm2 and survivin, leading to its classification as a global inhibitor of transcription 1. The following Hu U133 plus 2.0 arrays represent single time point (24 hour) gene expression analysis of transcripts altered by ARC treatment. Arrays for the other compounds (sangivamycin and doxorubicin) are included as comparators.
ARC (NSC 188491) has identical activity to Sangivamycin (NSC 65346) including inhibition of both P-TEFb and PKC.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Clockwork Orange is a transcriptional repressor and a new Drosophila circadian pacemaker component.
No sample metadata fields
View SamplesPurpose: The goal of this study is to compare the differential expression of transcripts in control kidneys compared to kidneys lacking the miR-17~92 cluster in nephron progenitors and their derivatives by RNA-seq to identify potential miRNA targets in the mutant kidneys. Overall design: mRNA profiles of control and mutant (=Six2-TGC; miR-17~92 flx/flx) embryonic day 16 kidneys were generated by deep sequencing, in triplicate, using Illumina HiSeq2000
MicroRNA-17~92 is required for nephrogenesis and renal function.
No sample metadata fields
View SamplesCLK targets from fly heads using the TIM-GAL4; UAS-CLKGR line
Clockwork Orange is a transcriptional repressor and a new Drosophila circadian pacemaker component.
No sample metadata fields
View Samples