Project description:BRG1-SWI/SNF complex is an important chromatin remodeling complex that involved in various biological processes. Here we described the genome-wide binding of histone acetylation upon BRG1 depletion in mouse embryonic stem cells. Mouse embryonic stem cells were treated with either scrambled siRNA or siRNA against BRG1 for 48 h, and each treatment has three replicates.
Project description:BRG1-SWI/SNF complex is an important chromatin remodeling complex that involved in various biological processes. Here we described the genome-wide binding of histone acetylation upon BRG1 depletion in human embryonic stem cells. Human embryonic stem cells were treated with either scrambled siRNA or siRNA against BRG1 for 48 h, and each treatment has three replicates.
Project description:CD44 expression has been shown to be enhanced in the liver and white adipose tissue (WAT) during obesity, suggesting a possible regulatory role for CD44 in metabolic syndrome. To study this hypothesis, we compared the gene expression profiles in liver and in WAT between WT and CD44 knockout (CD44KO) mice fed a high-fat diet (HFD) for 21 weeks. This analysis demonstrated that several genes associated with triglyceride synthesis and accumulation, including Mogat2, Cidea, Cidea, Apoa4, and Elovl7, were decreased in the livers of CD44KO mice compared to WT mice. Many genes encoding pro-inflammatory chemokines and chemokine receptors also were decreased in the livers of CD44KO mice. Analysis with WAT showed that genes associated with triglyceride accumulation, including Fasn, Elovl6 and Mogat2, were increased in WAT of CD44KO(HFD) mice compared to WT(HFD) mice. Moreover, many genes associated with inflammation, including cytokines (Cxcl14, Cxcl12, Il33, and Il2), cytokine receptors (Ccr1, Il6ra, Il10rb), trypases (Tpsb2, Tpsab1, Tpsg1), and cellular matrix proteins (Integrin ?4 (Itga4), ItgaM, Itgb2), were decreased in WAT of CD44(HFD) compared to WT(HFD) mice. This study indicates that CD44 plays a critical role in regulating several aspects of metabolic syndrome. Liver and white adipose tissue (WAT) total RNAs were purified from 5 WT and 5 CD44 knockout mice fed with a high-fat diet for 21 weeks. Then, samples were applied on Agilent mouse genome chips.
Project description:We show that Glis3 is expressed in gonocytes, SSCs and SPCs, but not in differentiated spermatogonia or subsequent stages of spermatogenesis nor in Sertoli or Leydig cells. We further demonstrate that Glis3-deficiency causes a severe impairment in spermatogenesis in mice. Although the number of gonocytes was slightly diminished in Glis3KO testis, the number undifferentiated, PLZF+ spermatogonia was dramatically reduced leading to a virtual block in the progression of spermatogenesis. Gene expression profiling showed that the expression of a number of genes associated with self-renewal and differentiation of spermatogonial cells was significantly decreased in 1-week-old Glis3KO2 testis. These included a set of GDNF-dependent genes, such as Etv5, Bcl6b, Lhx1, Brachyury, Id4, and Pou3f1, and GDNF-independent genes, such as FoxO1, Oct4, and Zbtb16. Impairment of the nuclear localization of FoxO1 may be in part responsible for the reduced expression of Ret, Lhx1, and Sall4 in Glis3KO2 testis. Our study identifies Glis3 as a novel and critical regulator of early stages of spermatogenesis. Testis total RNAs were purified from 4 WT and 4 Glis3KO2 at 1 week old age, and 3WT and 3 Glis3KO2 at 3 week-old age. Then the samples were applied to Agilent mouse genome chip.
Project description:We used AAV as a vector to deliver hGRβ to the liver of GR Liver Knockout mice. We collected liver samples for microarray analysis to investigate any phenotype as well as the underlying specific signaling pathway. In particular, we would like to determine if and how hGRβ overexpression in liver affects mGRαâs gene transcription profile in GR Liver Knockout mice. GR Liver Knockout mice were treated with PBS, AAV-GFP and AAV-hGRB, respectively. Each treatment group has four replicates.
Project description:We proposed an experiment that determines liver gene regulation profiles in GRLKO. By comparison to the wide type C57BL/6 mouse, we determined the contribution of GR on liver gene expression either at basal level or after Dexamethasone (DEX) injection. WT and GR knockout mice were divided into two groups, one with dexamethasone treatment and one with out. Each group has four replicates.
Project description:We used AAV as a vector to deliver hGRβ to C57BL/6 mouse liver. We collected liver samples for microarray analysis to investigate any phenotype as well as the underlying specific signaling pathway. In particular, we would like to determine if and how hGRβ overexpression in liver affects mGRαâs gene transcription profile in C57BL/6 mice. Three replicates for each group: untreated WT liver, AAV-GFP treated liver, and AAV-hGRB treated liver.
Project description:To investigate the role of HES1 during glucocorticoid signaling in the liver, we employed whole-genome microarray expressions in liver mRNA extracted from control and Hes1-liver knockout male mice (HESKOL) that had been adrenalectomized to remove endogenous glucocorticoids. RNA isolated from the liver of control and HESKOL animals either untreated or treated with 1mg/kg of synthetic glucocorticoid (dexamethasone) for 6hours. Each group had an n of 3 mice.
Project description:Gene expression analysis was conducted on lung RNA from C57BL/6J mice and compared to lung RNA from B6.129S2-Trp53tm1Ty/J mice (p53 NULL) to observe differences in baseline gene expression in mice with p53 deficiency. Lung RNA was isolated at baseline (saline airway exposure) in a total of 5 biological reps for both C57BL/6J (WT) and p53-deficient mice.