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.
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.
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.
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.
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.
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
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
Project description:Comparison between gene expression profiles of splenic stroma from wild type and lymphotoxin beta receptor knockout mice. The goal was to identify a set of genes which expression in splenic stroma is under lymphotoxin control and which can potentially be important for proper stroma development and function in secondary lymphoid organs.
