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Genome wide chromatin accessibilty changes associated with JUN and SHH expression in human SSCL patients

ABSTRACT: Genome wide chromatin accessibilty changes associated with JUN and SHH expression in human SSCL patients

PROVIDER: PRJNA637779 | ENA |

REPOSITORIES: ENA

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Genome wide chromatin accessibilty changes associated with JUN and SHH expression in human SSCL patients

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.

2020-09-08 | GSE151943 | GEO

Genome wide chromatin accessibilty changes associated with JUN expression in human normal and IPF lung fiborblasts

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.

2020-04-27 | GSE114844 | GEO

Genome wide chromatin accessibilty changes associated with JUN expression in human normal and IPF lung fiborblasts

Project description:Genome wide chromatin accessibilty changes associated with JUN expression in human normal and IPF lung fiborblasts

| PRJNA472802 | ENA

Genome-wide maps of H3K27ac, H3K4me1, JUN and p-JUN in JUN overexpressed or JUN inactivated fibroblasts

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.

2022-12-09 | GSE196345 | GEO

Transcriptome analysis of JUN overexpressed or JUN inactivated fibroblasts

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.

2022-12-09 | GSE196351 | GEO

Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun

Project description:After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during the chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes a significant clinical problem. We find that aging and chronically denervated repair cells express reduced c-Jun protein and the regenerative support provided by these cells is also reduced. In both cases, genetically restoring Schwann cell c-Jun levels restores regeneration to that in controls. We identify potential gene candidates mediating this effect and implicate Shh in the control of Schwann cell c-Jun levels. These experiments reveal that a common mechanism, reduced c-Jun in repair cells, underlies two major reasons for regeneration failure in the PNS. They underscore the central importance of Schwann cell c-Jun as a regulator of nerve repair, and point to molecular pathways that can be manipulated for improving the clinical outcome of nerve injuries.

2020-10-14 | E-MTAB-9640 | biostudies-arrayexpress

Genome-wide mapping of Jun binding site (K562)

Project description:Proto-oncogene c-jun is a leucine-zipper containing transcription factor which has a DNA binding domain and a transactivation domain. Jun dimerizes with another transcription factor Fos to form AP1 transcription factor. The AP-1 complex has been implicated in transformation and progression of cancer. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Map binding sites of transcription factor Jun in the genome of K562 cells. The K562 input data has been deposited in GEO as GSM325934.

2009-12-31 | E-GEOD-19545 | biostudies-arrayexpress

Gene expression profiling of Jun -/- and Jun +/+ facial motor neurons

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-.

2021-11-17 | GSE162977 | GEO

Genome-wide mapping of Jun binding site (K562)

2009-12-31 | GSE19545 | GEO

HHIP-AS1 lncRNA promotes tumorigenicity in human SHH-driven brain tumors

Project description:Long non-coding RNAs (lncRNAs) comprise a diverse class of gene expression regulators with emerging roles in many biological processes including cancer. Here we show that the expression of the lncRNA Hedgehog Interacting Protein Antisense 1 (HHIP-AS1) is a hallmark feature of human SHH-driven tumors. Importantly, loss of HHIP-AS1 leads to reduced tumor growth in SHH-driven tumors in vitro and in vivo. Our results demonstrate the power of cross-entity transcriptome-wide comparisons to identify novel epigenetic–regulatory lncRNA circuitries underlying human cancers.

2022-06-01 | PXD016550 | Pride

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