This SuperSeries is composed of the SubSeries listed below.
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Specimen part, Treatment
View SamplesThis study examined the effect of early pregnancy on the gene expression profiles of stromal and various epithelial mammary cell subpopulations in mice.
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Specimen part
View SamplesThis study examined the gene expression profile of mammary tumors derived from Lgr5- and K8-positive cell-of-origins
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Specimen part
View SamplesThis study examined the effect of mutant PIK3CAH1047R expression in mammary subsets of preneoplastic mammary glands from Lgr5-creERT2/PIK3CA H1047R mice
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Specimen part, Treatment
View SamplesThis study examined the effect of mutant PIK3CAH1047R expression in mammary subsets of preneoplastic mammary glands from K8-creERT2/PIK3CA H1047R mice
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Treatment, Time
View SamplesMissense FBXW7 mutations are prevalent in various tumors, including T-cell acute lymphoblastic leukemia (T-ALL). To study the effects of such lesions, we generated animals carrying regulatable Fbxw7 mutant alleles. We show here that these mutations specifically bolster cancer-initiating cell activity in collaboration with Notch1 oncogenes, but spare normal hematopoietic stem cell function. We were also able to show that FBXW7 mutations specifically affect the ubiquitylation and half-life of c-Myc protein, a key T-ALL oncogene. Using animals carrying c-Myc fusion alleles, we connected Fbxw7 function to c-Myc abundance and correlated c-Myc expression to leukemia-initiating activity.
The ubiquitin ligase FBXW7 modulates leukemia-initiating cell activity by regulating MYC stability.
Age, Specimen part
View SamplesRecurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. In addition, haploinsufficiency for Tet2 confers increased self-renewal and myeloproliferation, suggesting that the monoallelic TET2 mutations found in most TET2-mutant leukemia patients contribute to myeloid transformation. This work demonstrates that absent or reduced Tet2 function leads to enhanced stem cell function in vivo and to myeloid transformation.
Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation.
Specimen part
View SamplesRNA-seq transcriptome profiling of human induced pluripotent stem cells to characterize gene expression variation across individuals and within multiple iPSC lines from the same individual Overall design: Donor erythroblast or activated T-cells were reprogrammed with a Sendai viral vector coding for reprogramming factors. IPSC lines were propagated for ~9 passages before RNA sequencing
Analysis of Transcriptional Variability in a Large Human iPSC Library Reveals Genetic and Non-genetic Determinants of Heterogeneity.
Sex, Age, Race, Subject
View SamplesTranscriptome profiles for innate and adaptive immune stimuli important for host response against mycobacteria. Human monocyte-derived macrophages were stimulated with TLR2/1 ligand and interferon-g, stimuli present during innate and adaptive immune responses, respectively. Overall design: Human monocyte-dervided macrophages from five healthy donors were stimulated with TLR2/1L, IFN-g, or media control for 2, 6, and 24 hours. RNA-sequencing was performed on a total of 45 samples.
S100A12 Is Part of the Antimicrobial Network against Mycobacterium leprae in Human Macrophages.
Specimen part, Subject
View SamplesEscherichia coli 8624 and the isogenic mutants in qseE, qseF and qseG are compared to determine the role that each of the genes play in regulation of the transcriptome. These results are verified by qRT-PCR and reveal the important role of this three-component signaling system.
The two-component system QseEF and the membrane protein QseG link adrenergic and stress sensing to bacterial pathogenesis.
No sample metadata fields
View Samples