Purpose: 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 SamplesTumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-B2 (NF-B2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family). This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo. We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling. As Baff-tg mice display a similar phenotype, and have a genetic modification which acts in the same pathway, yet further up, than TRAF2 and TRAF3, we wished to compare and contrast Baff-tg B cells with TRAF2 and TRAF3 deficient B cells. This analysis should identify genes that are important in B cell survival.
TRAF2 and TRAF3 signal adapters act cooperatively to control the maturation and survival signals delivered to B cells by the BAFF receptor.
Sex, Age
View SamplesRNA expression was measured by RNA-seq in E17 wild type and Sall1-?SRM mutant kidney. Overall design: RNA expression in mutant kidney was compared to wild type stage matched kidney.
A Sall1-NuRD interaction regulates multipotent nephron progenitors and is required for loop of Henle formation.
Specimen part, Subject
View SamplesNIH-3T3 cells transduced with either EBF1-, PPARg2- or empty vector were stimulated with hormones to initiate adipocyte differentiation. RNA extraction was done using TriZol at d0, d2, d4 and d10 after stimulation. Samples were handled according to standard affymetrix protocols.
Gene expression analysis suggests that EBF-1 and PPARgamma2 induce adipogenesis of NIH-3T3 cells with similar efficiency and kinetics.
No sample metadata fields
View SamplesGene expression analysis performed on FACS sort purified GC LZ and DZ cells of either high or low affinity to identify unique gene signatures.
Differentiation of germinal center B cells into plasma cells is initiated by high-affinity antigen and completed by Tfh cells.
Sex, Specimen part
View SamplesGene expression analysis performed on FACS sort purified GC LZ and DZ cells of either high and low affinity to identify unique gene signatures.
Differentiation of germinal center B cells into plasma cells is initiated by high-affinity antigen and completed by Tfh cells.
Sex, Specimen part
View SamplesRegulatory T (Treg) cell activation and expansion during neonatal life and in response to inflammation are critical for immunosuppression, yet the mechanisms governing these events are incompletely understood. We report that the oncogene and transcriptional regulator c-Myc (Myc) controls immune homeostasis through regulation of Treg cell accumulation and functional activation. Myc activity is enriched in Treg cells generated during neonatal life and responding to inflammation. Myc-deficient Treg cells show cell-intrinsic defects in overall accumulation and ability to transition to an activated state during early life or acute inflammation. Consequently, loss of Myc in Treg cells results in a rapid, early-onset autoimmune disorder accompanied by uncontrolled effector CD4+ and CD8+ T cell responses. We also provide evidence that Myc regulates mitochondrial oxidative metabolism but is dispensable for fatty acid oxidation (FAO). Indeed, Treg cell-specific deletion of Cox10, which is required for oxidative phosphorylation, but not Cpt1a, the rate-limiting enzyme for FAO, results in impaired Treg cell function and maturation. Thus, Myc coordinates Treg cell accumulation, transitional activation and metabolic programming to orchestrate immune homeostasis.
Homeostasis and transitional activation of regulatory T cells require c-Myc.
Specimen part
View SamplesTo study mechanisms of long bone growth regulation, p21 misexpression was induced in the left hindlimb of mouse embryos using an intersectional approach that requires both Cre and (r)tTA activity. Doxycycline was provided to the pregnant female at embryonic day (E)12.5 to activate the transgene, and embryos were collected at E17.5. Distal femur and proximal tibia growth plates were dissected out, keeping left and right separated, deprived of perichondrium and flash frozen. After RNA extraction, mRNA libraries were prepared and all samples were deep sequenced in parallel Overall design: 6 samples (left and right growth plates from embryos #386, #387, #388) were sequenced in parallel
Cell-nonautonomous local and systemic responses to cell arrest enable long-bone catch-up growth in developing mice.
Specimen part, Subject
View SamplesSox2 is required to maintain osteosarcoma cell tumor initiation.Knockdown of Sox2 leads tpo loss of tumorigenic properties. To examine gene expression changes upon Sox2 knockdown, we performed microarray analysis on mouse osteosarcoma cells expressing scrambled or Sox2shRNA. We found that genes upregulated upon Sox2 knockdown included osteoblast diffrentiation genes and genes down regulated included cell cycle and RNA processing genes as well as YAP-TEAD target genes.
Sox2 antagonizes the Hippo pathway to maintain stemness in cancer cells.
Specimen part, Cell line
View SamplesChlamydia trachomatis is an obligate intracellular pathogen that causes trachoma and sextually transmitted disease in human. During early stage of infection, Chlamydia secreted bacterial effector proteins into host cell cytoplasm to help its entry and estabilishment of early replicated niche.
The Chlamydia trachomatis type III secretion chaperone Slc1 engages multiple early effectors, including TepP, a tyrosine-phosphorylated protein required for the recruitment of CrkI-II to nascent inclusions and innate immune signaling.
Specimen part, Cell line, Time
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