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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE136015 | GEO | 2019/08/20

REPOSITORIES: GEO

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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: Listeria_challenge)

Project description:Lack of Mirc11 significantly reduces NK cell-mediated cytokine production in vivo Mirc11 cluster targets NF-kB and AP-1-mediated gene transcriptions

2019-08-20 | GSE136013 | GEO

Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: IL-2_expanded_NKG2D_stimulation)

Project description:Lack of Mirc11 significantly reduces NK cell-mediated cytokine production in vivo Mirc11 cluster targets NF-kB and AP-1-mediated gene transcriptions

2019-08-20 | GSE136014 | GEO

Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation

Project description:Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation

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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: Listeria_challenge)

Project description:Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: Listeria_challenge)

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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: IL-2_expanded_NKG2D_stimulation)

Project description:Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: IL-2_expanded_NKG2D_stimulation)

| PRJNA560941 | ENA

2-O-Methylhonokiol Suppresses HCV Replication via TRAF6-Mediated NF-kB Activation.

Project description:Hepatitis C virus (HCV) is associated with various liver diseases. Chronic HCV infection is characterized by an abnormal host immune response. Therefore, it is speculated that to suppress HCV, a well-regulated host immune response is necessary. 2-O-methylhonokiol was identified by the screening of anti-HCV compounds using Renilla luciferase assay in Huh 7.5/Con 1 genotype 1b replicon cells. Here, we investigated the mechanism by which 2-O-methylhonokiol treatment inhibits HCV replication using real-time PCR. Our data shows that treatment with 2-O-methylhonokiol activated innate immune responses via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) pathway. Additionally, the immunoprecipitation result shows that treatment with 2-O-methylhonokiol augmented tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) by preventing p62 from binding to TRAF6, resulting in reduced autophagy caused by HCV. Finally, we reproduced our data with the conditioned media from 2-O-methylhonokiol-treated cells. These findings strongly suggest that 2-O-methylhonokiol enhances the host immune response and suppresses HCV replication via TRAF6-mediated NF-kB activation.

| S-EPMC8234778 | biostudies-literature

HOPS/Tmub1 involvement in the NF-kB-mediated inflammatory response through the modulation of TRAF6.

Project description:HOPS/Tmub1 is a ubiquitously expressed transmembrane ubiquitin-like protein that shuttles between nucleus and cytoplasm during cell cycle progression. HOPS causes cell cycle arrest in G0/G1 phase, an event associated to stabilization of p19Arf, an important tumor suppressor protein. Moreover, HOPS plays an important role in driving centrosomal assembly and maintenance, mitotic spindle proper organization, and ultimately a correct cell division. Recently, HOPS has been described as an important regulator of p53, which acts as modifier, stabilizing p53 half-life and playing a key role in p53 mediating apoptosis after DNA damage. NF-κB is a transcription factor with a central role in many cellular events, including inflammation and apoptosis. Our experiments demonstrate that the transcriptional activity of the p65/RelA NF-κB subunit is regulated by HOPS. Importantly, Hops-/- cells have remarkable alterations of pro-inflammatory responses. Specifically, we found that HOPS enhances NF-κB activation leading to increase transcription of inflammatory mediators, through the reduction of IκBα stability. Notably, this effect is mediated by a direct HOPS binding to the E3 ubiquitin ligase TRAF6, which lessens TRAF6 stability ultimately leading increased IKK complex activation. These findings uncover a previously unidentified function of HOPS/Tmub1 as a novel modulator of TRAF6, regulating inflammatory responses driven by activation of the NF-κB signaling pathway. The comprehension on how HOPS/Tmub1 takes part to the inflammatory processes in vivo and whether this function is important in the control of proliferation and tumorigenesis could establish the basis for the development of novel pharmacological strategies.

| S-EPMC7567074 | biostudies-literature

<i>Mirc11</i> Disrupts Inflammatory but Not Cytotoxic Responses of NK Cells.

Project description:Natural killer (NK) cells generate proinflammatory cytokines that are required to contain infections and tumor growth. However, the posttranscriptional mechanisms that regulate NK cell functions are not fully understood. Here, we define the role of the microRNA cluster known as Mirc11 (which includes miRNA-23a, miRNA-24a, and miRNA-27a) in NK cell-mediated proinflammatory responses. Absence of Mirc11 did not alter the development or the antitumor cytotoxicity of NK cells. However, loss of Mirc11 reduced generation of proinflammatory factors in vitro and interferon-γ-dependent clearance of Listeria monocytogenes or B16F10 melanoma in vivo by NK cells. These functional changes resulted from Mirc11 silencing ubiquitin modifiers A20, Cbl-b, and Itch, allowing TRAF6-dependent activation of NF-κB and AP-1. Lack of Mirc11 caused increased translation of A20, Cbl-b, and Itch proteins, resulting in deubiquitylation of scaffolding K63 and addition of degradative K48 moieties on TRAF6. Collectively, our results describe a function of Mirc11 that regulates generation of proinflammatory cytokines from effector lymphocytes.

| S-EPMC7428857 | biostudies-literature

A miR-146a-5p/TRAF6/NF-kB p65 axis regulates pancreatic cancer chemoresistance: functional validation and clinical significance.

Project description:Background: Dysregulated microRNA (miRNA) expression in cancer can act as a key factor that modifies biological processes, including chemoresistance. Our study aimed to identify the miRNAs associated with gemcitabine (GEM) resistance in pancreatic ductal adenocarcinoma (PDAC) and to explore the potential mechanisms. Methods: The miRNA microarray was used to identify miRNAs associated with GEM resistance. Quantitative real-time PCR was used to examine miR-146a-5p expression in paired PDAC and adjacent normal tissues. Bioinformatics analysis, luciferase reporter assays, and chromatin immunoprecipitation assays were used to confirm tumor necrosis factor receptor-associated factor 6 (TRAF6) as a direct target of miR-146a-5p and to explore the potential transcription factor binding and regulation by miR-146a-5p. In vitro and in vivo experiments were performed to investigate the mechanisms. Results: MiR-146a-5p expression was significantly decreased in PDAC tissues compared with adjacent normal tissues, and miR-146a-5p expression correlated with prognosis in PDAC patients. Functional studies indicated that miR-146a-5p suppressed PDAC cell proliferation and sensitized PDAC cells to GEM chemotherapy by targeting the 3'-untranslated region (3'-UTR) of TRAF6. MiR-146a-5p was also observed to downregulate the TRAF6/NF-κB p65/P-gp axis, which regulates PDAC cell growth and chemoresistance. Conclusions: Taken together, the results indicate that the miR-146a-5p/TRAF6/NF-κB p65 axis drives pancreatic chemoresistance by regulating P-gp, suggesting that miR-146a-5p may be utilized as a new therapeutic target and prognostic marker in PDAC patients.

| S-EPMC7086345 | biostudies-literature

TRAF6 promotes spinal microglial M1 polarization to aggravate neuropathic pain by activating the c-JUN/NF-kB signaling pathway.

Project description:BackgroundThe neuropathic pain with complex networks of neuroinflammatory activation severely limits clinical therapeutic research. TNF receptor-associated factor 6 (TRAF6) is associated with multiple inflammatory diseases. However, there remains confusion about the effects and mechanisms of TRAF6 in neuropathic pain.MethodsA chronic constriction injury (CCI) model was developed to simulate neuralgia in vivo. We overexpressed or knocked down TRAF6 in CCI mice, respectively. Activation of microglia by TRAF6, the inflammatory response, and disease progression were inspected using WB, qRT-PCR, immunofluorescence, flow cytometry, and ELISA assays. Moreover, the mechanism of M1/M2 polarization activation of microglia by TRAF6 was elaborated in BV-2 cells.ResultsTRAF6 was enhanced in the spinal neurons and microglia of the CCI mice model compared with the sham operation group.. Down-regulation of TRAF6 rescued the expression of Iba-1. In response to mechanical and thermal stimulation, PWT and PWL were improved after the knockdown of TRAF6. Decreased levels of pro-inflammatory factors were observed in TRAF6 knockdown groups. Meanwhile, increased microglial M1 markers induced by CCI were limited in mice with TRAF6 knockdown. In addition, TRAF6 overexpression has the precise opposite effect on CCI mice or microglia polarization. We also identifed that TRAF6 activated the c-JUN/NF-kB pathway signaling; the inhibitor of c-JUN/NF-kB could effectively alleviate the neuropathic pain induced by upregulated TRAF6 in the CCI mice model.ConclusionIn summary, this study indicated that TRAF6 was concerned with neuropathic pain, and targeting the TRAF6/c-JUN/NF-kB pathway may be a prospective target for treating neuropathic pain.

| S-EPMC11245438 | biostudies-literature

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