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E3 ubiquitin ligase NEDD4-1 suppresses acetaminophen-induced liver injury in mouse by targeting the degradation of VDAC1

ABSTRACT: E3 ubiquitin ligase NEDD4-1 suppresses acetaminophen-induced liver injury in mouse by targeting the degradation of VDAC1

PROVIDER: PRJNA819441 | ENA |

REPOSITORIES: ENA

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E3 ubiquitin ligase NEDD4-1 suppresses acetaminophen-induced liver injury in mouse by targeting the degradation of VDAC1

Project description:Acetaminophen (APAP) overdose provokes various degrees of liver injury, whose pathogenesis involves multiple pathological events, such as mitochondrial damage and necrosis. E3 ubiquitin ligase neural precursor cell expressed developmentally downregulated 4-1 (NEDD4-1) plays vital roles in regulating a wide spectrum of physiological processes, and has been implicated in the pathogenesis of numerous liver disease. However, studies about the regulation of NEDD4-1 on APAP-induced liver injury (AILI) is still deficient. Thus, the aim of this study is to determine whether and how NEDD4-1 plays a role in AILI. Thus, we performed transcriptomic studies comparing liver samples of APAP-treated Flox or APAP-treated hepatocyte-specific Nedd4-1 (HepKO) deficiency mice,

2022-03-29 | GSE199353 | GEO

The E3 Ubiquitin Ligase AFF1 targets ARF19 to the proteasome

Project description:The E3 Ubiquitin Ligase AFF1 targets ARF19 to the proteasome

| PRJNA723009 | 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

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

EGFR is a target of the tumor suppressor E3-ligase FBXW7

Project description:FBXW7 is and E3 ubiquitin ligase and is highly mutated in colorectal cancer. We used human colon organoids with engineered FBXW7 hotspot mutations to investigate novel targets of E3 ligase activity with a combined transcriptomic and proteomic approach uncovering the EGFR-MAPK pathway as highly regulated by the E3 ligase activity.

2024-04-03 | GSE246896 | GEO

TUBE-based approach coupled with ligase trapping for identification of E3 ubiquitin ligase substrates

Project description:an E3 ligase substrate-trapping strategy by fusing a tandem ubiquitin-binding entity (TUBE) with an anti-ubiquitin remnant antibody for effectively identifying ubiquitinated substrates

2020-08-06 | PXD020658 | JPOST Repository

The E3 ubiquitin ligase Siah2 contributes to castration-resistant prostate cancer by regulation of androgen receptor transcriptional activity

Project description:Analysis of gene expression altered upon knockdown of Siah2 in prosate cancer cells. The objective is to elucidate which signaling pathways or transcription factors are regulated by the E3 ubiquitin ligase Siah2 in human prostate cancer cells. CWR22Rv1 cells were in fected with pLKO.1 control or Siah2 shRNA, and selected with 1ug/ml of puromycin to get stable transfectants. Total RNA was extracted for micorarray analysis to compare the diffentially expressed genes between pLKO.1 control and Siah2 knockdown cells.

2013-03-19 | E-GEOD-38851 | biostudies-arrayexpress

The E3 ubiquitin ligase Siah2 contributes to castration-resistant prostate cancer by regulation of androgen receptor transcriptional activity

2013-03-19 | GSE38851 | GEO

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

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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