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EDF1 binds collided ribosomes and facilitates recruitment of translational repressors GIGYF2/EIF4E2 and initiates JUN-mediated transcriptional response

ABSTRACT: RNA-seq analyses of wild-type and DEDF1 cell lines show that the immediate-early JUN-dependent transcriptional response to collisions is dependent on EDF1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE149565 | GEO | 2020/08/02

REPOSITORIES: GEO

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EDF1 binds collided ribosomes and facilitates recruitment of translational repressors GIGYF2/EIF4E2 and initiates JUN-mediated transcriptional response

Project description:EDF1 binds collided ribosomes and facilitates recruitment of translational repressors GIGYF2/EIF4E2 and initiates JUN-mediated transcriptional response

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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.

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

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

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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-.

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Murine livers post DEN treatment: c-Jun f/f vs. c-Jun Dli

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).

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The effect and mechanism of Si-Jun-Zi decoction on the function of intestinal mucosal barrier during chemotherapy for colorectal cancer

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PRR7 is a novel NMDA-dependent inhibitor of c-Jun ubiquitination in neurons

Project description:Elevated c-Jun levels result in apoptosis and are evident in neurodegenerative disorders such as Alzheimer's disease and dementia and after global cerebral insults such as stroke and epilepsy. NMDA receptor (NMDAR) antagonists block c-Jun upregulation and prevent neuronal cell death following excitotoxic insults. However, little is known about the molecular mechanisms that regulate c-Jun abundance in neurons. Here we show that PRR7, a component of synaptic junctions, can upregulate c-Jun levels by inhibiting its ubiquitination in neurons. PRR7 interacts with the GLUN1 subunit of NMDARs and is upregulated in the nucleus following NMDAR activation. We show that PRR7 interacts with the E3 ligase SCFFBW7 (FBW7) and blocks the FBW7-mediated ubiquitination of c-Jun. PRR7 overexpression increases c-Jun-dependent transcriptional activity and promotes neuronal death. Microarray assays indicate that both Prr7 knockdown or overexpression alter the abundance of c-Jun-regulated transcripts associated with cellular viability as well as synaptic function. Moreover, Prr7 knockdown attenuates NMDA-mediated excitotoxicity in primary neuronal cultures. Our results show that PRR7 links NMDAR activity to c-Jun function and provide insight into the processes that underlie NMDA-dependent excitotoxicity. Four biological replicas of each of the four conditions: NO = not transduced with virus; NT = transduced with control lentiviruses containing a non-targeting shRNA sequence; KD = transduced with lentiviruses expressing PRR7-specific shRNAs; OE= transduced with lentiviruses to overexpress PRR7.

2014-10-25 | E-GEOD-62686 | biostudies-arrayexpress

Transcriptome analysis of JUN overexpressed or JUN inactivated fibroblasts

Project description:Transcriptome analysis of JUN overexpressed or JUN inactivated fibroblasts

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Stk40 deletion enhances c-Jun protein stability and compromises mesoderm differentiation

Project description:Serine/threonine kinase 40 (Stk40) was previously identified as a direct target gene of pluripotency-associated transcription factor Oct4 and its overexpression could facilitate differentiation of mouse embryonic stem cells (mESCs) towards the extraembryonic endoderm. Stk40-/- mice are lethal at the perinatal stage, displaying multiple organ failures. However, the molecular mechanisms underlying the physiological functions of Stk40 remain elusive. Here, we report that Stk40 ablation compromises the mesoderm differentiation from mESCs in vitro and in embryos. Mechanistically, Stk40 interacts with both mammalian constitutive photomorphogenic protein 1 (Cop1) and c-Jun, promoting degradation of c-Jun. Consequently, Stk40 knockout leads to c-Jun protein accumulation, which, in turn, might suppress the Wnt signaling activity and impair the mesoderm differentiation process. Overall, this study reveals that Stk40, together with Cop1, represent a novel axis for modulating c-Jun protein levels within an appropriate range during mesoderm differentiation from mESCs. Our finding provides new insight into the molecular mechanism regulating c-Jun protein stability and may have potential for managing related cellular disorders.

2019-05-14 | PXD012579 | Pride

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