This SuperSeries is composed of the SubSeries listed below.
Continuous expression of the transcription factor e2-2 maintains the cell fate of mature plasmacytoid dendritic cells.
Specimen part, Cell line, Time
View SamplesThe interferon-producing plasmacytoid dendritic cells (PDC) share common progenitors with antigen-presenting classical dendritic cells (cDC), yet they possess distinct morphology and molecular features resembling those of lymphocytes. It is unclear whether the unique cell fate of PDC is actively maintained in the steady state. We report that the deletion of transcription factor E2-2 from mature peripheral PDC caused their spontaneous differentiation into cells with cDC properties. This included the loss of PDC markers, increase in MHC class II expression and T cell priming capacity, acquisition of dendritic morphology and induction of cDC signature genes. Genome-wide chromatin immunoprecipitation revealed direct binding of E2-2 to key PDC-specific and lymphoid genes, as well as to certain genes enriched in cDC. Thus, E2-2 actively maintains the cell fate of mature PDC and opposes the default cDC fate, in part through direct regulation of lineage-specific gene expression programs.
No associated publication
Specimen part, Time
View SamplesThe gene expression of bone marrow cells of mice enriched for
Gremlin 1 identifies a skeletal stem cell with bone, cartilage, and reticular stromal potential.
Sex, Specimen part
View SamplesThis represents an unbiased evaluation of the transcriptional response in the prefrontal cortex and hippocampus areas in the Df(16)A/+ mice, a mouse model of human 22q11 microdeletion syndrome. These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1
Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11-deletion mouse model.
No sample metadata fields
View SamplesMost human B cell lymphomas (B-NHL) are derived from germinal centers (GCs), the structure where B-cells undergo class switch recombination (CSR) and somatic hypermutation (SHM) and are selected for high-affinity antibody production. The pathogenesis of B-NHL is associated with distinct genetic lesions, including chromosomal translocations and aberrant somatic hypermutation, which appear to arise from mistakes occurring during CSR and SHM. To ascertain the role of CSR and SHM in lymphomagenesis, we crossed three oncogene-driven (MYC, BCL6, MYC/BCL6) mouse models of B cell lymphoma with mice lacking activation-induced cytidine deaminase (AID), the enzyme required for both processes.
AID is required for germinal center-derived lymphomagenesis.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Metabolic reprogramming induces resistance to anti-NOTCH1 therapies in T cell acute lymphoblastic leukemia.
Specimen part
View SamplesBackground
Glioblastoma models reveal the connection between adult glial progenitors and the proneural phenotype.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Reprogramming of the microRNA transcriptome mediates resistance to rapamycin.
Specimen part, Cell line
View SamplesIn mammals, expansion of adipose tissue mass induces accumulation of adipose tissue macrophages (ATMs). We isolated CD11c- (FB) and CD11c+ (FBC) perigonadal ATMs from SVCs of lean (C57BL/6J Lep +/+) and obese leptin-deficient (C57BL/6J Lep ob/ob) mice.
No associated publication
Specimen part
View SamplesSHS exposure during pregnancy has adverse effects on offspring.
In utero exposure to second-hand smoke aggravates the response to ovalbumin in adult mice.
Sex, Specimen part
View Samples