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Genome-wide CRISPR screening identifies the E3 ubiquitin ligase HERC1 as a modulator of the response to nucleoside analogs in acute myeloid leukemia

ABSTRACT: Genome-wide CRISPR screening identifies the E3 ubiquitin ligase HERC1 as a modulator of the response to nucleoside analogs in acute myeloid leukemia

PROVIDER: PRJNA1142585 | ENA |

REPOSITORIES: ENA

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Genome-wide CRISPR screening identifies the E3 ubiquitin ligase HERC1 as a modulator of the response to nucleoside analogs in acute myeloid leukemia

Project description:We identified the Ubiquitin Ligase HERC1 in the context of cytarabine response in a genome-wide CRISPR screen in murine AML. We hypothesized to detect early transciptomic changes in cytarabine treated murine AML cells genetically targeted by using single guide RNAs targeting HERC1 and Non-targeting Control.

2024-08-02 | GSE273667 | GEO

The search for enzymes responsible for metabolism of nucleoside analogs

Project description:Affymetrix U95Av2 expression data from human intestinal cells (Caco-2) and tissues from all intestinal segments (duodenum, jejunum, ileum, colon). Entries contain the search terms "glycosylase, phosphorylase, cytochrome or nucleoside," which were relevant to our search for enzymes capable of cleaving the N-glycosidic bond of nucleoside analog drugs. Keywords = glycosylase Keywords = phosphorylase Keywords = nucleoside Keywords: parallel sample

2005-10-30 | GSE1862 | GEO

A novel Cereblon E3 ligase modulator with antitumor activity in gastrointestinal cancer

Project description:RNA-seq Data of HCT116 cells treated with a novel Cereblon E3 ligase modulator

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The E3 ubiquitin ligase Siah1 regulates adrenal gland organization and hyperaldosteronism

Project description:Primary and secondary hypertension are major risk factors for cardiovascular disease. Elevated secretion of aldosterone resulting from primary aldosteronism (PA) is a key driver of secondary hypertension. Here, we identify an unexpected role for the ubiquitin ligase Siah1 in adrenal gland development and PA. Siah1a-/- mice exhibit altered adrenal gland morphology, as reflected by dysregulated zonation of the glomerulosa, increased aldosterone levels and aldosterone target gene expression, and reduced plasma potassium levels. Genes involved in catecholamine biosynthesis and cAMP signaling are upregulated in the adrenal glands of Siah1a-/- mice, while genes related to retinoic acid signaling and cholesterol biosynthesis are downregulated. Loss of Siah1 leads to increased expression of PIAS1, an E3 SUMO-protein ligase implicated in the suppression of LXR. Notably, SIAH1 sequence variants which impaired SIAH1 ubiquitin ligase activity, resulting in elevated PIAS1 expression, were identified in patients with PA. The involvement of Siah1–PIAS1 in adrenal gland organization and function points to a possible new therapeutic target for hyperaldosteronism.

2018-05-01 | GSE102963 | GEO

Role of the COP1 E3 ligase in ERalpha signaling

Project description: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.

2022-01-01 | GSE183753 | GEO

Merlin/NF2 Suppresses Tumorigenesis by Inhibiting the E3 Ubiquitin Ligase CRL4DCAF1 in the Nucleus

Project description:Current models imply that the FERM domain protein Merlin, encoded by the tumor suppressor NF2, inhibits mitogenic signaling at or near the plasma membrane. Here, we show that the closed, growth inhibitory form of Merlin accumulates in the nucleus, binds to the E3 ubiquitin ligase CRL4DCAF1, and suppresses its activity. Depletion of DCAF1 blocks the promitogenic effect of inactivation of Merlin. Conversely, enforced expression of a Merlin-insensitive mutant of DCAF1 counteracts the antimitogenic effect of Merlin. Re-expression of Merlin and silencing of DCAF1 induce a similar, tumor-suppressive program of gene expression. Tumor-derived mutations invariably disrupt Merlinâs ability to interact with or inhibit CRL4DCAF1. Finally, depletion of DCAF1 inhibits the hyperproliferation of Schwannoma cells from NF2 patients and suppresses the oncogenic potential of Merlin-deficient tumor cell lines. We propose that Merlin suppresses tumorigenesis by translocating to the nucleus to inhibit CRL4DCAF1. To examine if Merlin controls gene expression through inhibition of CRL4DCAF1, and define the general function of this ligase, we compared the gene expression program activated by expression of Merlin or by depletion of DCAF1 in Merlin-null FC-1801 mouse Schwannoma cells

2010-03-09 | E-GEOD-19305 | biostudies-arrayexpress

The E3 Ubiquitin Ligase AFF1 targets ARF19 to the proteasome

Project description:Auxin critically regulates nearly every aspect of plant growth and development. Auxin-driven transcriptional responses are mediated through the AUXIN RESPONSE FACTOR (ARF) family of transcription factors. Although ARF protein stability is regulated via the 26S proteasome, molecular mechanisms underlying ARF stability and turnover are unknown. Here, we report the identification and functional characterization of an F-Box E3 ubiquitin ligase, which we have named AUXIN RESPONSE FACTOR F-BOX1 (AFF1). AFF1 directly interacts with ARF19 and regulates its accumulation. Mutants defective in AFF1 display ARF19 protein hyperaccumulation, mild auxin resistance, and developmental defects. Together, our data suggest a new mechanism, namely control of ARF protein stability, in regulating auxin responsiveness.

2022-06-09 | GSE172353 | GEO

Quantification of induced RNA mutation by nucleoside analogs in the repRNA-v4 EGFP region

Project description:Quantification of induced RNA mutation by nucleoside analogs in the repRNA-v4 EGFP region

| PRJNA1133798 | ENA

Regulation of metablism by mitochondrial MUL1 E3 ubiquitin ligase

Project description:Regulation of metablism by mitochondrial MUL1 E3 ubiquitin ligase

| PRJNA832764 | ENA

E3 ubiquitin ligase Rfwd2 inactivation effect on embryonic lung development

Project description:Transcriptome analysis by RNA-seq of lungs from control and Rfwd2 epithelial-specific conditional knockout mice at embryonic 13.5 day age. RFWD2, is an E3 ubiquitin ligase that modifies specific target proteins, priming their degradation via the ubiquitin proteasome system. Rfwd2 deficiency led to a striking halt in branching morphogenesis shortly after secondary branch formation. In the mutant lung, two ETS transcript factors essential for normal lung branching, ETV4 and ETV5, were upregulated at the protein, but not transcript level. Introduction of Etv loss-of-function alleles into the Rfwd2 mutant background attenuated the branching phenotype, suggesting that RFWD2 functions at least in part through degrading ETV proteins. As a number of E3 ligases are known to target factors important for lung development, our findings provides a preview of a protein-level regulatory network essential for lung branching morphogenesis.

2016-04-28 | GSE80707 | GEO

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