Project description:Different osteoprogenitors (SSC, BCSP, Thy+) were sorted after 2 days of JUN induction, followed by RNA extraction and microarray analysis
Project description:To further dissect whether and how activated JUN reconfigures the chromatin landscape, we performed Chromatin Immunoprecipitation (ChIP)-seq analyses for H3K4me1 and H3K27ac. Based on the significant increase of H3K27ac levels at H3K4me1+ sites, we identified 3,017 JUN-activated enhancers in JUN WT cells. In contrast, JUN AA fails to significantly induce H3K27ac accumulation at these regions. Their enrichment levels at JUN-activated enhancers were significantly decreased after JNKi treatment. Besides, these enhancers are directly driven by JUN, especially phosphorylated JUN.
Project description:We found that JUN expression is increased in many human fibrotic diseases and that systemic induction of Jun in mice resulted in development of fibrosis of multiple organs. To identify the changes in chromatin accessibility associated with JUN, we worked with primary human fibrotic lung fibroblasts that have normal or Knock-out levels of JUN expression and performed ATAC-seq analysis in both of them. Meanwhile we also modified primary human normal lung fibroblasts with or without JUN over-expression induction, then processed ATAC-seq and ChIP-seq analysis.
Project description:The oncogene c-Jun plays a key role in development and cancer. Yet, its role in cell fate decision remains poorly understood at the molecular level. Here we report that c-Jun confers different fate decisions upon mouse embryonic stem cells (mESCs) in adhesion vs suspension. We developed a Tet-on system for temporal induction of c-Jun expression by Doxycycline treatment in mESCs. We show that mESCs carrying the inducible c-Jun TetOn remain pluripotent and grow slowly in suspension with induction of c-Jun, while undergoing differentiation with normal proliferative potentials in adherence upon c-Jun induction. Apparently, c-Jun pushes mESCs in suspension into cell cycle arrest at G1/S, through the induction of Cdkn1a/b and Cdkn2/a/b/c. Despite cell cycle arrest, they can re-enter cell cycle upon plating on adhesive surface and grow into typical mESC colonies albeit at lower efficiency. These results demonstrate that mESCs respond to c-Jun differently in suspension or adherence. Our results suggest that cells in suspension may be more resistant to differentiation than in adherence.
Project description:We found that JUN and SHH expression is increased in many human fibrotic diseases and that systemic induction of Jun in mice resulted in development of fibrosis of multiple organs. To identify the changes in chromatin accessibility associated with JUN and SHH, we worked with primary SSCL dermal fibroblasts that have normal or Knock-out levels of JUN expression and vismodegib treatment then performed ATAC-seq analysis in all of them.
Project description:Time course analysis of c-Jun expression at 24h resulted in upregulation of a number of well-known fibrogenesis-associated factors. We compared the global gene expression pattern of mouse whole bone marrow after c-Jun induction in vivo at 24h with no induction and applied to standard Affymetrix mouse arrays.
Project description:To examine the effects of phosphorylated JUN-mediated enhancers activation on gene expression, we conducted RNA-seq analysis in JUN wildtype (WT) or JUN inactive mutant (JUN AA) overexpressed MRC5 cells. The expression levels of genes associated with JUN-activated enhancers are significantly upregulated in JUN WT cells rather than in JUN AA cells. To quantify the effects of JUN inactivation on gene expression, we also performed RNA-seq analysis in JNKi-treated induced CAFs (iCAFs). We observed that JNKi significantly reduced expression levels of JUN-activated enhancers-associated genes.
Project description:To determine target genes, biological functions of Jun and mechanisms of gene regulation by Jun in regenerating neurons, gene expression profiling was carried out of axotomized and uninjured facial motor neurons in floxed c-Jun mice crossed with nestin-cre mice. Nestin-promoter-driven Cre ensures deletion of Jun in the central nervous system including facial motor neurons. KO animals were Jun Flox/Fox Cre+, while WT animals were Jun Flox/Flox, Cre-.
Project description:This SuperSeries is composed of the following subset Series: GSE39928: Murine livers post DEN treatment: c-Jun f/f vs. c-Jun Dli [35MM] GSE39929: Murine livers post DEN treatment: c-Jun f/f vs. c-Jun Dli [40MM] GSE39930: Murine livers post DEN treatment: c-Jun f/f vs. c-Jun Dli [41MM] GSE39931: Murine livers post DEN treatment: c-Jun f/f vs. c-Jun Dli [43MM] Refer to individual Series ** Six samples in each Series represent the same set of biological source material hybridized to 4 different arrays (named IMP internal: 35MM, 40MM, 41MM, and 43MM).
Project description:Interventions: Control:FOLFOX or CAPEOX chemtherapy;Experimental group 1:Si-Jun-Zi decoction;Experimental group 2:enteral nutrition combine with Chemotherapy;Experimental group 3:Si-Jun-Zi decoction + enteral nutrition
Primary outcome(s): Intestinal barrier function
Study Design: Parallel
