Project description:WT mice and mPGES-1 KO mice were treated with 120 mikrogram/kg LPS and sacrificed 5 h later. The preoptic region was dissected by LCM and analyzed using GeneChip Mouse Genome 430 2.0 arrays (Affymetrix). Groups: WT LPS-treated versus mPGES-1 KO LPS-treated mice.
Project description:WT mice and mPGES-1 KO mice were treated with 120 mikrogram/kg LPS and sacrificed 5 h later. The preoptic region was dissected by LCM and analyzed using GeneChip Mouse Genome 430 2.0 arrays (Affymetrix).
Project description:Cmtm4 Knockout mouse was constructed by CRISPR-Cas9 technology, and the KO mice showed male infertility. A proteomic anlaysis of sperm proteins was performed by comparing KO and WT mice.
Project description:To confirm the changed gene expression profiles in GPR15 knock out (KO) macrophages, we applied a SurePrint G3 Mouse Gene Expression service from Takara Bio Inc (Kusatsu, Shiga, Japan) to analyze gene expression profiles in lipopolysaccharide (LPS)-stimulated GPR15KO macrophages, comparing with wild type (WT) macrophages. Most significantly up-regulated genes in GPR15KO macropahges included Il6, Il17a, Il23, Tnfsf8, Il1b, Ifna2 and Ccnd2. On the contrary, several inflammation-related genes, including Ccl17, Itgax, Nrp1 and Rasgrf2, were down-regulated in WT macrophages, compared to GPR15 KO macrophages. Abdominal macrophages from WT and GPR15 KO mice were stimulated with PBS or LPS (100 ng/ml) for 4 hrs. Total RNA were extracted using a TRIzol-chloroform based method.
Project description:Bone marrow was harvested from Rosa26CreER; Stk40+/+ (WT; n = 3) and Rosa26CreER; Stk40loxp/loxp (Stk40 KO; n = 3) mice and differentiated for 6 days in the presence of 100 nM 4-OHT to generate WT and Stk40 KO bone-marrow derived macrophages (BMDMs). 2. On day 7 following differentiation BMDMs were treated with 100 ng x ml-1 LPS and harvested at 0 hrs, 6 hrs, 16 hrs, and 32 hrs following LPS exposure. 3. The cells were snap-frozen at the time of harvest. RNA was extracted using the Qiagen RNeasy mini kit as per manufacturer’s protocol including the on-column DNase digestion. Groups: There are cells from 3 mice x 2 genotypes x 4 time points G1: WT 0 hr LPS G2: WT 6 hr LPS G3: WT 16 hr LPS G4: WT 32 hr LPS G5: Stk40 KO 0 hr LPS G6: Stk40 KO 6 hr LPS G7: Stk40 KO 16 hr LPS G8: Stk40 KO 32 hr LPS
Project description:IL-6 has been described to be a critical cytokine in mediating the febrile response because neither IL-6 knockout mice injected with peripheral lipopolysaccharide (LPS) or IL-1M-NM-2, nor animals treated with IL-6 antiserum develop fever. However, the fever response is developed in IL-6 KO mice following intracerebroventricular administration of Prostaglandin E2 which is the principal mediator of the febrile response. We performed a genome-wide microarray expression comparison between LPS-treated WT and IL-6 KO mice to evaluate if there were any differentially expressed genes in mice devoid of IL-6 that can explain the absence of fever response.
Project description:We studied the impact of a PGE2 signaling on tumor progression in the PyMT mammary carcinoma mouse model. To gain insight into the reasons underlying altered tumor development, whole transcriptome profiling of FACS-isolated cancer-associated fibroblasts (CAFs) from WT and mPGES-1 KO tumors were generated via next generation mRNA sequencing, in triplicates, on a NextSeq 550 high-throughput bench top sequencer.
Project description:To confirm the changed gene expression profiles in GPR15 knock out (KO) macrophages, we applied a SurePrint G3 Mouse Gene Expression service from Takara Bio Inc (Kusatsu, Shiga, Japan) to analyze gene expression profiles in lipopolysaccharide (LPS)-stimulated GPR15KO macrophages, comparing with wild type (WT) macrophages. Most significantly up-regulated genes in GPR15KO macropahges included Il6, Il17a, Il23, Tnfsf8, Il1b, Ifna2 and Ccnd2. On the contrary, several inflammation-related genes, including Ccl17, Itgax, Nrp1 and Rasgrf2, were down-regulated in WT macrophages, compared to GPR15 KO macrophages.
Project description:Transcriptional profiling of mouse pituitary tissue comparing WT with Brdt KO mice. Goal was to determine the effects of Brdt absence on pituitary gene expression.
