Project description:this dataset encompasses the cardiac transcriptomic changes elicited in myocardial tissues of 4months-old male mice at 4 hours after a single ZT0 prednisone (1mg/kg i.p.) injection, or vehicle, in cardiomyocyte-GR-WT versus cardiomyocyte-GR-KO conditions (inducible, tamoxifen-driven ablation right prior to drug pulse).
Project description:Homozygous disruption of c-Maf led to embryonic lethality and impaired erythroblastic island formation. c-Maf is expressed in the fetal liver macrophages. It suggests that macrophages are responsible for the lethality of c-Maf knock-out embryos. To search downstream genes of c-Maf, we surveyed genes associated with macrophage function by microarray analysis. keywords: c-Maf, macrophage, erythroblastic islands, WT (c-Maf WT) and c-Maf KO (c-Maf KO) fetal liver macrophages were sorted by a FACSAria cell sorter. Total RNAs from those macrophages were prepared using RNeasy Kit. Genes down-regulated in c-Maf KO macrophages were searched by GeneSpring software.
Project description:The FOXA1 pioneer factor is an essential mediator of steroid receptor function in multiple hormone dependent cancers, including breast and prostate cancers, enabling nuclear receptors such as ER and AR to activate lineage specific growth programs. . Analyzing data from loss-of-function screens, we identified a subset of NSCLC tumor lines where proliferation is FOXA1-dependent. Using rapid immunoprecipitation and mass spectrometry of endogenous protein (RIME) we identified chromatin-localized interaction between FOXA1 and glucocorticoid receptor (GR) in these tumor cells. Knockdown of GR inhibited proliferation of FOXA1-dependent, but not FOXA1-independent NSCLC cells. Here, we utilized ChIP-sequencing to identify a permissive set of genes potentially regulated by FOXA1 and GR to understand potential mechanisms underlying FOXA1-GR dependence in NSCLC.
Project description:Differentially expressed genes of CD11b+Gr-1+ immature myeloid cells (IMCs) in the bone marrow and colonic tumor setting of histidine decarboxylase (HDC)-KO mice were examined by microarray (Affymetrix Mouse 430.2 array). Myeloid differentiation-related candidate genes were sought to be isolated and functionally studied. Total RNA of HDC-expressing CD11b+Gr-1+ IMCs of bone marrow were extracted from HDC-EGFP and HDC-EGFP/HDC-KO mice (3 mice in each group). CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) of colon tumor were sorted from 10-12 colon tumors of WT and HDC-KO mice (5 mice in each group), and pooled to extract total RNA for microarray studies. Two technical replicates for each of the four groups. Four sets of comparisons were performed to screen for upregulated or downregulated genes in the HDC-KO CD11b+Gr-1+ IMCs or MDSCs (experiment group) compared to the WT group: (1) HDC-expressing CD11b+Gr-1+ IMCs of bone marrow of HDC KO mice compared to bone marrow IMCs of WT mice; (2) CD11b+Gr-1+ MDSCs in tumors of HDC-KO mice compared to WT mice; (3) CD11b+Gr-1+ MDSCs of WT colon tumors compared to IMCs in the WT bone marrow; and (4) CD11b+Gr-1+ MDSCs of colon tumors of HDC-KO mice compared to IMCs in the bone marrow of HDC-KO mice.
Project description:Glucocorticoids are primary stress hormones that have been implicated in the pathogenesis of cognitive impairments and psychiatric illnesses. The hippocampus expresses high levels of glucocorticoid (GR) and mineralocorticoid receptors (MR) which both bind glucocorticoids. However, the specific and cooperative roles played by GR and MR in mediating the direct actions of stress on the hippocampus are unknown. To elucidate the function of hippocampal GR and MR, we generated mice with conditional knockout of GR (GREmx1-cre), MR (MREmx1-cre), or both GR and MR (GRMREmx1-cre) in the hippocampus. Genome-wide microarrays were performed on RNA isolated from the whole hippocampus to 1) identify genes subject to regulation by GR alone, MR alone, or both GR and MR and 2) identify the genes responsible for the morphological and behavioral phenotypes observed in these mice.
Project description:The glucocorticoid receptor (GR) regulates adaptive transcriptional programs that alter metabolism in response to stress. Network properties that allow GR to tune gene expression to match specific physiologic demands are poorly understood. We analyzed the transcriptional consequences of GR activation in murine lungs deficient for Klf15, a transcriptional regulator of amino acid metabolism that is induced by glucocorticoids and fasting Wild type and Klf15 KO mice were treated with dexamethsone or saline control for 4 and 8 hours.
Project description:We studied the impact of Ptdss1 knockdown in PyMT mouse mammary tumor cells and of Csf1-driven Mertk KO (macrophage-specfic) on tumor growth and the associated macrophage phenotype in an orthotopic tumor model. To gain insight into the reasons underlying tumor rejection once either Ptdss1 was deleted in tumor cells or Mertk was knocked out in macrophages, whole transcriptome profiling of FACS-sorted tumor-associated macrophages of WT or macrophage-specific Mertk KO mice receiving either control tumor cells or Ptdss1 knockdown tumor cells was performed via next generation mRNA sequencing, at least in triplicates, on a NextSeq 500 high-throughput bench top sequencer.