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Gene expression changes in NCU10K cells lacking Nedd4

ABSTRACT: Gene expression changes in NCU10K cells lacking Nedd4

PROVIDER: PRJNA811254 | ENA |

REPOSITORIES: ENA

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Gene expression changes in NCU10K cells lacking Nedd4

Project description:Nedd4 is an E3 ubiquitin ligase that has essential roles in neural crest cell development. This study aimed to detect the gene expression changes induced by removing Nedd4 in the neural crest cell line, NCU10K, to define the molecular pathways regulated by Nedd4.

2022-03-02 | GSE197631 | GEO

RNA-sequencing of Nedd4+/+ and Nedd4-/- mouse splenic B cells

Project description:Programmed mutagenesis of the immunoglobulin locus of B-lymphocytes during class switch recombination and somatic hypermutation requires RNA polymerase II (RNA polII) transcription complex dependent targeting of the DNA mutator, Activation Induced cytidine Deaminase (AID). AID deaminates cytidine residues on substrate sequences in the immunoglobulin (Ig) locus via a transcription-dependent mechanism and this activity is stimulated by the RNA polII stalling co-factor Spt5 and the eleven-subunit cellular non-coding RNA 3’-5’ exonucleolytic processing complex, RNA exosome. The mechanism by which the RNA exosome recognizes immunoglobulin locus RNA substrates to stimulate AID DNA deamination activity on its in vivo substrate sequences is an important question. Here we report that E3-ubiquitin ligase Nedd4 destabilizes AID-associated RNA polII by a ubiquitination event leading to generation of 3’-end free RNA exosome RNA substrates at the Ig locus and other AID target sequences genome-wide. Using highthrough-out RNA sequencing technology, we find that lack of Nedd4 activity in B cells leads to accumulation of RNA exosome substrates at AID target genes. Moreover, we find that Nedd4-deficient B cells are inefficient in undergoing class switch recombination. Taken together, our study links non-coding RNA processing following RNA polymerase II pausing with regulation of the mutator AID protein. Our study also identifies Nedd4 as a regulator of non-coding RNA that are generated by stalled RNA polII genome-wide. Splenic B cells from Nedd4+/+ and Nedd4-/- B cells fetal liver chimeric mice were were stimulated in culture for IgG1 CSR. Total RNA was isolated and evaluated with whole genome RNA-seq

2013-08-07 | E-GEOD-49027 | biostudies-arrayexpress

Gene expression profiling of Nedd4- or control-knockdown Hep3B cells

Project description:Gene expression profiling of Nedd4 or control knockdown Hep3B cells

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RNA-sequencing of Nedd4+/+ and Nedd4-/- mouse splenic B cells

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Project description:Gene expression profiling and H3K9ac occupancy in Nedd4 knockdown Hep3B cells

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Project description:H3 Nedd4

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Nedd4-2-dependent regulation of astrocytic Kir4.1 and Connexin43 controls neuronal network activity

Project description:Nedd4-2 is an E3 ubiquitin ligase in which missense mutation is related to familial epilepsy, indicating its critical role in regulating neuronal network activity. However, Nedd4-2 substrates involved in neuronal network function have yet to be identified. Using mouse lines lacking Nedd4-1 and Nedd4-2 and an isobaric labeling approach for quantitative comparison of the synaptic membrane proteome, we identified astrocytic channel proteins inwardly rectifying potassium channel 4.1 (Kir4.1) and Connexin43 as upregulated in ubiquitin ligase knockout mice and thus as candidate Nedd4-2 substrates. Kir4.1 and Connexin43 were confirmed as Nedd4-2 substrates by independent methods and their functional role in astrocytes as to modulation of neuronal network activity was established.

2023-11-28 | PXD046450 | Pride

To investigate gene expression changes in neurons lacking cap methyltransferase 1 (CMTR1)

Project description:To investigate gene expression changes in neurons lacking cap methyltransferase 1 (CMTR1)

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