Project description:The rapid decline of ovarian function in TAF4b-null mice begins in early postnatal life and follicle depletion is completed by sixteen weeks. To uncover differences in gene expression that may underlie accelerated ovarian aging, we compared genome-wide expression profiles of three week old, pre-pubescent TAF4b-null and wild-type ovaries.
Project description:We report that colonic lamina propria anti-inflammatory macrophages from Il10rb-/- (KO) mice at 12 weeks possessed significantly high levels of proinflammatory transcripts compared to the ones from Il10rb+/- (het) controls. While the transcriptional profile between macrophages from KO and het mice was comparable at 1 weeks and did not possess significant levels of proinflammatory transcripts, we show that the macrophages from KO mice were enriched for proinflammatory transcripts at 3 weeks compared to the ones from 3 week old het controls. These data indicate that the anti-inflammatory signature of colonic lamina propria macrophages from Il10rb-/- mice is compromized at 3 weeks.
Project description:The rapid decline of ovarian function in TAF4b-null mice begins in early postnatal life and follicle depletion is completed by sixteen weeks. To uncover differences in gene expression that may underlie accelerated ovarian aging, we compared genome-wide expression profiles of three week old, pre-pubescent TAF4b-null and wild-type ovaries. Total RNA from 9, 3-week-old mice (3 wild-type, 3 TAF4b-heterozygous, 3 TAF4b-null) was obtained as described as above. RNA quality was checked using a Bioanalyzer, and concentration determined using a Nanodrop. 300 ng of each RNA sample was used in the Affymetrix Whole-transcript Sense Target Labeling Assay (Rev 3) followed by hybridization to a GeneChip® Mouse Gene 1.0 ST Array. 9 GeneChips were used to provide biological triplicates of each genotype. The Affymetrix Expression Console (v 1.1) was used to normalize data and determine signal intensity (RMA-Sketch).
Project description:RNA-seq of WT, Tet2-het and Tet2-KO mTSCs in stem-state, RNA-seq of WT and Tet2-KO mTSCs in vitro differentiation, (h)MeDIP of WT and Tet2-KO mTSCs in stem-state
Project description:RNA-seq of WT, Tet2-het and Tet2-KO mTSCs in stem-state, RNA-seq of WT and Tet2-KO mTSCs in vitro differentiation, (h)MeDIP of WT and Tet2-KO mTSCs in stem-state
Project description:We report the genome-wide binding sites of the NK homeodomain transcription factor, Nkx3-1, in mouse prostate. Three different mouse genotypes were used: Nkx3-1 wild-type (WT), Nkx3-1 heterozygote (HET), and Nkx3-1 knock-out (KO). Two biological replicates were performed for WT and HET, and one replicate for KO. The mice used were a recombinant inbred C57BL6/J x 129 strain. The KO dataset was used as a control in lieu of an IgG. Examination of Nkx3-1 binding sites in Nkx3-1+/+ (WT), +/- (HET) and -/- (KO) mouse prostates
Project description:WT and Q175 heterozygous (het) mice treated orally twice a day with vehicle (10% HPβCD), and Q175 mice treated with either 30 or 100 mg/kg orally twice a day CHDI-00390576. CHDI-00390576 is a Class IIa HDAC inhibitor. Mice were dosed from 4 weeks to 6 months of age.
Project description:We investigated the biological function of INSIG1 in acute (CCl4) and chronic (NASH) liver damage. Male whole-body Insig1 wild-type (WT), Heterozygous (HET) and Knock-out (KO) mice were: 1) challenged with Olive Oil or CCl4 single IP injection and sacrificed 4 days after the treatment; 2) fed Low Fat Diet (LFD) or Western Diet plus Sugar Water (WDSW) and sacrificed after 12 weeks of the challenge. Hepatic RNA was extracted and studied by Next Generation Sequencing to highlight changes in the transcriptome driven by the challenges and genotype-associated differences.
Project description:We report the genome-wide binding sites of the NK homeodomain transcription factor, Nkx3-1, in mouse prostate. Three different mouse genotypes were used: Nkx3-1 wild-type (WT), Nkx3-1 heterozygote (HET), and Nkx3-1 knock-out (KO). Two biological replicates were performed for WT and HET, and one replicate for KO. The mice used were a recombinant inbred C57BL6/J x 129 strain. The KO dataset was used as a control in lieu of an IgG.
Project description:Hepatocyte Nuclear Factor 4 alpha (HNF4α), a master regulator of hepatocyte differentiation, and circadian regulator Aryl Hydrocarbon-Like Receptor-Like 1 (ARNTL, or BMAL1) though robustly co-expressed in healthy liver, are incompatible within the context of HCC. Differential expression of Bmal1 and Hnf4α may control susceptibility to liver disease and ultimately, hepatocellular carcinoma. We compared gene expression profiles under conditions of inducible loss of hepatic Hnf4α and inducible loss of Hnf4a and Bmal1 in this RNA-seq experiment. Hepatic Hnf4a (H-KO) or Hnf4a and Bmal1 (BH-KO) were inducibly knocked out after 5 days tamoxifen treatment in eight week-old mice (H-KO) or (BH-KO) followed by vivarium chow or high fat feeding (BH-HF-KO). Littermate control mice (H-WT, BH-WT and BH-HF-WT ) were also treated with tamoxifen at eight weeks of age, but since they lacked the Cre transgene, Hnf4a and Bmal1 expression remained intact. Livers were harvested at 10 weeks of age (BH-WT/KO, H-WT/KO) or 45 weeks ( BH-HF-WT/KO) of age after high fat diet feeding, and liver tissue was flash frozen in liquid nitrogen.