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Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1 [array]

ABSTRACT: Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1 [array]

PROVIDER: PRJNA543487 | ENA |

REPOSITORIES: ENA

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Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1 [RNA-seq]

Project description:We identified RNF123 (KPC1) ubiquitin E3 ligase is involved in glioblastoma progression through NF-kB-target SerpinE1. The goal of the RNA-Seq analysis is to determine the gene expression profile in LN18 cells overexpressing RNF123 compare to control empty vector (EV) cells. By integration of reverse-phase protein array (RPPA) and RNA-Seq data in glioblastoma cells, we determined NF-kB1-target genes that significantly changed by RNF123 overexpression.

2020-06-17 | GSE131400 | GEO

Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1

Project description:Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1

| PRJNA543481 | ENA

Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1 [RNA-seq]

Project description:Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1 [RNA-seq]

| PRJNA543485 | ENA

Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1 [array]

Project description:Two glioblastoma cell lines (LN18 and HS863) were stable transfected with control empty vector (EV) or RNF123-vector (KPC1). The objective of this experiment was to determine NFKB1-targets regulated by RNF123 overexpression in glioblastoma cell lines. To do that LN18 and HS863 cell lines with RNF123 overexpression were compared to control empty vector. In the present study, we utilized the combination of RPPA and RNA-Sequencing. By comparing both datasets, we identified commonly proteins and genes differentially expressed in control versus RNF123-overexpressing cells.

2020-06-17 | GSE131399 | GEO

Downregulation of the Ubiquitin-E3 Ligase KPC1 promotes glioblastoma progression through upregulation of SerpinE1

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-17 | GSE131402 | GEO

Downregulation of the Ubiquitin-E3 Ligase RNF123 Promotes Upregulation of the NF-?B1 Target SerpinE1 in Aggressive Glioblastoma Tumors.

Project description:This study examined the role of the ubiquitin E3-ligase RNF123 in modulating downstream NF-?B1 targets in glioblastoma (GB) tumor progression. Our findings revealed an oncogenic pathway (miR-155-5p-RNF123-NF-?B1-p50-SerpinE1) that may represent a new therapeutic target pathway for GB patients with isocitrate dehydrogenase 1 and 2 (IDH) WT (wild type). Mechanistically, we demonstrated that RNF123 is downregulated in IDH WT GB patients and leads to the reduction of p50 levels. RNA-sequencing, reverse-phase protein arrays, and in vitro functional assays on IDH WT GB cell lines with RNF123 overexpression showed that SerpinE1 was a downstream target that is negatively regulated by RNF123. SERPINE1 knockdown reduced the proliferation and invasion of IDH WT GB cell lines. Both SerpinE1 and miR-155-5p overexpression negatively modulated RNF123 expression. In clinical translational analysis, RNF123, SerpinE1, and miR-155-5p were all associated with poor outcomes in GB patients. Multivariable analysis in IDH WT GB patients showed that concurrent low RNF123 and high SerpinE1 was an independent prognostic factor in predicting poor overall survival (p < 0.001, hazard ratio (HR) = 2.93, 95% confidence interval (CI) 1.7-5.05), and an increased risk of recurrence (p < 0.001, relative risk (RR) = 3.56, 95% CI 1.61-7.83).

| S-EPMC7281601 | biostudies-literature

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

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

Interactions between Yeast Proteins and Rsp5 Ubiquitin Ligase

Project description:To identify substrates of the ubiquitinating E3 enzyme Rsp5 we applied purified Rsp5 to duplicate protein arrays. The Rsp proteins were expressed as fusion proteins to GST. We used as a control Ubr1, a RING domain containing E3 ligase We analyzed Rsp5 from S.cerevisiae on duplicate arrays, with four control chips, two without Rsp5 and two with Ubr1.

2008-12-30 | E-GEOD-14218 | biostudies-arrayexpress

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

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