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Role of the COP1 E3 ligase in ERalpha signaling

ABSTRACT: Our study defines the E3 ligase COP1 as a positive modulator of ERalpha-dependent gene transcription. We carried our RNA-Seq experiments with total RNAs from control or COP1-depleted MCF7 cells treated or not with estrogens and identified a signature of genes known to be regulated by estrogens whose transcription is deregulated upon COP1 deficiency.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183753 | GEO | 2022/01/01

REPOSITORIES: GEO

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Role of the COP1 E3 ligase in ERalpha signaling

Project description:Role of the COP1 E3 ligase in ERalpha signaling

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In Vivo CRISPR Screens Identify E3 Ligase Cop1 as a Modulator of Macrophage Infiltration and Cancer Immunotherapy Target

Project description:Cop1 regulates stability of transcription factors. We found that Cop1 can regulate the proteasomal degradation of Cebpd. We generated 4T1 breast cancer cells with CRISPR/Cas9 mediated Cop1 (gene symbol RFWD2) knockout. We used Cebpd antibody to pulldown the DNA fragments binding with Cebpd and did ChIP-seq.

2021-05-23 | GSE175332 | GEO

In Vivo CRISPR Screens Identify E3 Ligase Cop1 as a Modulator of Macrophage Infiltration and Cancer Immunotherapy Target

Project description:In Vivo CRISPR Screens Identify E3 Ligase Cop1 as a Modulator of Macrophage Infiltration and Cancer Immunotherapy Target

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Transcriptomic profiling of Cop1-deficient embryos

Project description:In order to assess the physiological role of Cop1 in vivo we generated mice that do no longer express the protein. Cop1KO mice die at around E10.5 of embryonic development. In order to gain insights into the molecular mechanisms that cause the embryonic death we compared the genome-wide gene expression profile of E9.5 wild-tytpe and Cop1-null embryos. The data do not support a role for Cop1 in the regulation of the p53 pathway in vivo and highlight a role for Cop1 in cardiovascular development and/or angiogenesis. The abstract of the associated publication is as follows:Biochemical data have suggested conflicting roles for the E3 ubiquitin ligase Cop1 in tumourigenesis. Here we present the first in vivo investigation of the role of Cop1 in cancer aetiology. We used an innovative genetic approach to generate an allelic series of Cop1 and show that Cop1 hypomorphic mice spontaneously develop malignancy at a high frequency in their first year of life and are highly susceptible to radiation-induced lymphomagenesis. Biochemically, we show that Cop1 regulates c-Jun oncoprotein stability and modulates c-Jun/AP1 transcriptional activity in vivo. Cop1-deficiency stimulates cell proliferation in a c-Jun-dependent manner. We conclude that Cop1 is a tumour suppressor that antagonizes c-Jun oncogenic activity in vivo. RNA from 6 different control embryos (+/+ or +/-) were mixed and subdivided into control pool 1 and pool 2. RNA from 6 different Cop-null embryos were mixed and subdivided into KO pool 1 and pool 2.

2011-01-13 | E-GEOD-18636 | biostudies-arrayexpress

Ubiquitin ligase COP1 suppresses microglia-mediated inflammation

Project description:Dysregulated microglia are intimately involved in neurodegeneration including Alzheimer’s disease (AD) pathogenesis, but the mechanisms controlling pathogenic microglial gene expression remain poorly understood. The transcription factor CCAAT/enhancer binding protein beta (c/EBPß) regulates pro-inflammatory genes in microglia and is upregulated in AD. We show expression of c/EBPß in microglia is regulated post-translationally by the ubiquitin ligase COP1 (also called RFWD2). Ubiquitination of c/EBPß by COP1 targets it for proteasomal degradation. In the absence of COP1, c/EBPß accumulates rapidly and drives a potent pro-inflammatory and ApoE gene-expression program, evidenced by increased neurotoxicity in microglia-neuronal co-cultures. Antibody blocking studies reveal that neurotoxicity is almost entirely attributable to complement. Remarkably, loss of a single allele of Cebpb prevented the pro-inflammatory phenotype. COP1-deficient microglia markedly accelerated tau-mediated neurodegeneration in a mouse model where elevated ApoE plays a deleterious role. Collectively, these results identify c/EBPß as a potential therapeutic target for inflammation-driven neurodegeneration.

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Project description:ChIP followed by deep sequencing was performed with antibodies to ERalpha in U2OS-ERalpha cells treated with 17beta-estradiol.

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Structural Basis for Substrate Selectivity of the E3 Ligase COP1.

Project description: Not available

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COP1 controls light-dependent chromatin remodeling in Arabidopsis [ChIP-Seq]

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