Similar Datasets
Project description:mRNA profiling of mouse spleens comparing wild type spleens vs. spleens from mice having deletion of RBP-J in cells of the renin lineage which results in B-cell leukemia We used microarrays to detail the global program of gene expression in wild type and the leukemic spleens which revealed upregulation of genes for cell cycle progression and B cell identity in the leukemic spleens.
2014-02-17 | GSE46229 | GEO
Project description:mRNA profiling of mouse spleens comparing wild type spleens vs. spleens from mice having deletion of RBP-J in cells of the renin lineage which results in B-cell leukemia We used microarrays to detail the global program of gene expression in wild type and the leukemic spleens which revealed upregulation of genes for cell cycle progression and B cell identity in the leukemic spleens. Two condition experiment: wild type vs leukemic; biological replicates: individual mice - 2 wild type, 2 mutant. One replicate per array.
2014-02-17 | E-GEOD-46229 | biostudies-arrayexpress
Project description:ChIP-Seq for H3K4me3 and H3K27me3 in wild type spleens and spleens from mice having deletion of RBP-J in cells of the renin lineage, which results in B-cell leukemia.
2014-02-17 | GSE46566 | GEO
Project description:ChIP-Seq for H3K4me3 and H3K27me3 in wild type spleens and spleens from mice having deletion of RBP-J in cells of the renin lineage, which results in B-cell leukemia. Examination of 2 different histone modifications in wild type and mutant spleens.
2014-02-17 | E-GEOD-46566 | biostudies-arrayexpress
Project description:NEK2 overexpression in the B cell lineage affects B cell development. To determine whether deficiency of NEK2 inhibits B cell malignancies, we crossed Nek2 knockout mice with Eμ-myc transgenic mice, a well-established Myc-driven preclinical model for B cell malignancies. Three genotyping offsprings were obtained: Eμ-myc/Nek2+/+ (NEK2 wild type), Eμ-myc/Nek2+/- (NEK2 heterozygotes), and Eμ-myc/Nek2-/- (NEK2 homozygotes). Bulk RNA-seq was performed on CD19-selected spleen B cells to view the transcriptome differences.
2023-06-01 | GSE226675 | GEO
Project description:To characterize the changes that had occurred in splenic pre-cDCs in the absence of ADAM10, we performed RNA sequencing on sorted pre-cDC1 and 2 from the spleens of wild-type and ADAM10ΔDC mice. Unsupervised hierarchical clustering and principal component analysis of all four groups demonstrated that distinct transcriptomic changes had taken place in ADAM10ΔDC pre-cDC2, while minimal changes were observed for pre-cDC1
2019-11-12 | GSE131264 | GEO
Project description:Extramedullary erythropoiesis is not expected in healthy adult mice, but erythropoietic gene expression was elevated in lineage-depleted spleen cells from cd47−/− mice. Elevated expression of several genes associated with early stages of erythropoiesis was observed in mice lacking CD47 or its signaling ligand thrombospondin-1, consistent with previous evidence that this signaling pathway inhibits expression of multipotent stem cell transcription factors in spleen. In contrast, cells expressing markers of committed erythroid progenitors including erythropoietin receptor, aquaporin-1, glycophorin A, and erythrocyte membrane-associated protein were more abundant in cd47−/− spleens but significantly depleted in thbs1−/− spleens. Single cell transcriptome analysis indicated that loss of CD47 is associated with accumulation and increased proliferation of CD34− committed erythroid progenitors in spleen, consistent with the known function of CD47 to limit turnover of aging erythrocytes. Conversely, loss of thrombospondin-1 delays turnover, which suppresses erythropoiesis in thbs1−/− spleens relative to the basal level in wild type mice.
2024-06-17 | GSE239427 | GEO
Project description:Extramedullary erythropoiesis is not expected in healthy adult mice, but erythropoietic gene expression was elevated in lineage-depleted spleen cells from cd47−/− mice. Elevated expression of several genes associated with early stages of erythropoiesis was observed in mice lacking CD47 or its signaling ligand thrombospondin-1, consistent with previous evidence that this signaling pathway inhibits expression of multipotent stem cell transcription factors in spleen. In contrast, cells expressing markers of committed erythroid progenitors including erythropoietin receptor, aquaporin-1, glycophorin A, and erythrocyte membrane-associated protein were more abundant in cd47−/− spleens but significantly depleted in thbs1−/− spleens. Single cell transcriptome analysis indicated that loss of CD47 is associated with accumulation and increased proliferation of CD34− committed erythroid progenitors in spleen, consistent with the known function of CD47 to limit turnover of aging erythrocytes. Conversely, loss of thrombospondin-1 delays turnover, which suppresses erythropoiesis in thbs1−/− spleens relative to the basal level in wild type mice.
2024-06-17 | GSE239424 | GEO
Project description:Comaprison of the gene expression profiles of the spleen between wild type and Brx haploinsuffieint mice Nuclear factor of activated T-cells 5 (NFAT5) is a transcription factor that regulates hyperosmolarity-responsive genes and helps activated T lymphocytes adapt to and discharge their functions in hyperosmolar environments. We report here that the Rho-type guanine nucleotide exchange factor (GEF) Brx is essential for increased NFAT5 expression in response to osmotic stress in lymphoid tissues. Indeed, brx haploinsufficient mice expressed significantly less NFAT5 in their spleens than wild type controls and their splenocytes had a defective response to osmotic stress in vitro. Haploinsufficient mice also had smaller-sized spleens containing fewer splenocytes, as well as a defective immunoglobulin response to ovalbumin compared to wild type mice. The Brx GEF domain and the p38 mitogen-activated kinase (MAPK) cascade were both required for osmotic stress-mediated induction of NFAT5 in Jurkat cells. Brx physically interacted with the cJun kinase (JNK)-interacting protein (JIP) 4, a scaffold protein for activation of the p38 MAPK cascade that was required for osmotic stress-induced NFAT5 expression. Thus, Brx is a signal integrator for the adaptive response to osmotic stress in the immune system, activating small G proteins, attracting JIP4 and stimulating p38 MAPK, ultimately increasing the expression of NFAT5 and activating hyperosmolarity protective genes, a phenomenon crucial for proper immune function in hyperosmolar environments, such as inflammatory sites and immune organs. Keywords: Genetic modification
2009-02-09 | GSE10117 | GEO