Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of NEDD4 E3s in CD4+ T cell activation

ABSTRACT: Itch and WWP2 belongs to NEDD4 E3 family, and highly share the structural homology. However it remains elusive whether there are redundant or distinct roles in helper CD4+ T cell differentiation. Here we performed RNA seq analysis using WT, single and double knockout CD4+ T cells, and demonstrated the cooperative effect of the two E3s on Th2 differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE114021 | GEO | 2018/05/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Role of NEDD4 E3s in CD4+ T cell activation

Project description:Role of NEDD4 E3s in CD4+ T cell activation

| PRJNA454898 | ENA

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 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

2013-08-07 | GSE49027 | GEO

H3K9ac occupancy of Nedd4- or control-knockdown Hep3B cells

Project description:H3 Nedd4

2017-06-12 | GSE66340 | GEO

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

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

2017-06-12 | GSE66341 | GEO

Itch attenuates CD4 T cell proliferation in mice by limiting WBP2 protein stability

Project description:To mount an anti-pathogen response, CD4 T cells must undergo rapid cell proliferation. However, poorly controlled expansion can result in diseases such as autoimmunity. One important regulator of T cell activity is the E3 ubiquitin ligase Itch. Itch deficient patients suffer from extensive autoinflammation. Similarly, Itch deficient mice exhibit inflammation characterized by high numbers of activated CD4 T cells. While the role of Itch in limiting CD4 T cell cytokine production has been extensively studied, it is less clear whether and how Itch regulates proliferation of these cells. We determined that Itch deficient CD4 T cells are hyperproliferative in vitro and in vivo, due to increased S phase entry. Whole cell proteomics analysis of Itch deficient primary mouse CD4 T cells revealed increased abundance of the -catenin co-activator WW domain binding protein 2 (WBP2). Furthermore, Itch deficient cells demonstrate increased WBP2 protein stability, and Itch and WBP2 interact in CD4 T cells. Knockdown of WBP2 in CD4 T cells caused reduced proliferation. Together, our data support that Itch attenuates CD4 T cell proliferation by promoting WBP2 degradation. This study identifies novel roles for Itch and WBP2 in regulating CD4 T cell proliferation, providing insight into how Itch may prevent inflammation.

2021-01-07 | PXD019272 | Pride

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

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

Gene expression changes in NCU10K cells lacking Nedd4

Project description:Gene expression changes in NCU10K cells lacking Nedd4

| PRJNA811254 | ENA