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MARCKS and lnc-MARCKS act as inflammation regulators

ABSTRACT: The goals of this study are to reveal the target transcriptome of MARCKS and lnc-MARCKS in TLR2 signaling pathway. We knocked down MARCKS, or over-expressed lnc-MARCKS in THP1-derived macrophages stimulated with Pam3CSK4 for 8 hours. And compared the transcriptomes of the editing cells with control cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE108680 | GEO | 2019/01/09

REPOSITORIES: GEO

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MARCKS and lnc-MARCKS act as inflammation regulators

Project description:MARCKS and lnc-MARCKS act as inflammation regulators

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Effect of a long non-coding RNA, lnc-FANCI-2 on host transcriptome.

Project description:To seek the function of lnc-FANCI-2 in high-risk HPV infected cancer cells, we knocked out lnc-FANCI-2 in CaSki cells (HPV16 positive) using CRISPR/Cas9 system.

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lnc-EAPV binding proteins in C57BL/6J BMDMs

Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.

2018-11-07 | PXD011577 | Pride

Human dendritic cell microRNA profile after NOD2 and / or TLR2 stimulation

Project description:microRNA expression in human monocyte-derived DCs following stimulation with NOD2 ligand MDP, TLR2 ligand Pam3CSK4, or both. 4 condition experiment with two timepoints, and 4 biological replicates. Conditions: unstimulated; MDP stimulated; Pam3CSK4 stimulated; MDP + Pam3CSK4 stimulated. Timepoints: 4 hours and 24 hours.

2013-06-01 | E-GEOD-44785 | biostudies-arrayexpress

Crosslinking Proteomics Indicates Effects of Simvastatin on the TLR2 interactome and Reveals ACTR1A as a Novel Regulator of the TLR2 Signal Cascade

Project description:Toll-like receptor 2 (TLR2) is a pattern recognition receptor that, upon ligation by microbial molecules, interacts with other proteins to initiate pro-inflammatory responses by the cell. Statins (hydroxymethylglutaryl coenzyme A reductase inhibitors), drugs widely prescribed to reduce hypercholesterolemia, are reported to have both pro- and anti-inflammatory effects upon cells. Some of these responses are presumed to be driven by effects on signaling proteins at the plasma membrane, but the underlying mechanisms remain obscure. We reasoned that profiling the effect of statins on the repertoire of TLR2-interacting proteins might provide novel insights into the mechanisms by which statins impact inflammation. In order to study the TLR2 interactome, we designed a co-immunoprecipitation (IP)-based cross-linking proteomics study. A hemagglutinin (HA)-tagged-TLR2 transfected HEK293 cell line was utilized to precipitate the TLR2 interactome upon cell exposure to the TLR2 agonist Pam3CSK4 and simvastatin, singly and in combination. To stabilize protein interactors, we utilized two different chemical cross-linkers with different spacer chain lengths. Proteomic analysis revealed important combinatorial effects of simvastatin and Pam3CSK4 on the TLR2 interactome. After stringent data filtering, we identified alpha-centractin (ACTR1A), an actin-related protein and subunit of the dynactin complex, as a potential interactor of TLR2. The interaction was validated using biochemical methods. RNA interference studies revealed an important role for ACTR1A in induction of pro-inflammatory cytokines. Taken together, we report that statins remodel the TLR2 interactome, and we identify ACTR1A, a part of the dynactin complex, as a novel regulator of TLR2-mediated immune signaling pathways.

2019-06-24 | PXD012759 | Pride

biotin RNA pulldown assay of lnc-GD2H and mass spectrometry

Project description:Vectors carrying lnc-GD2H and antisense lnc-GD2H were linearized with the corresponding restriction enzymes to prepare template DNAs for in vitro transcription. Biotinylated RNAs were mixed with proteins extracted from C2C12 cells, followed by targeting of the RNAs with streptavidin beads. After SDS-PAGE following RNA pulldown, the differentially expressed proteins were enzymolyzed and used for MS analysis.

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Comparison of mRNA expression level between AmTARS and Pam3 as a lignad of TLR2 receptor

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2024-09-02 | GSE183968 | GEO

MDP- and Pam3CSK4-induced genes in naïve and tolerant macrophages

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Human dendritic cell microRNA profile after NOD2 and / or TLR2 stimulation

Project description:microRNA expression in human monocyte-derived DCs following stimulation with NOD2 ligand MDP, TLR2 ligand Pam3CSK4, or both.

2013-06-01 | GSE44785 | GEO

Agonistic targeting of TLR1/TLR2 induces p38 MAPK-dependent apoptosis and NfkB-dependent differentiation of AML cells

Project description:Acute myeloid leukemia (AML) is associated with poor survival and there is a strong need to identify disease vulnerabilities that might reveal new treatment opportunities. Here, we found that Toll-like receptor 1 (TLR1) and TLR2 are upregulated on primary AML CD34+CD38- cells relative to corresponding normal bone marrow cells. Activating the TLR1/TLR2 complex by the agonist Pam3CSK4 in MLL-AF9 driven human AML, resulted in induction of apoptosis by p38 MAPK-dependent activation of Caspase 3 and myeloid differentiation in a NFκB-dependent manner. By using murine Trp53-/- MLL-AF9 AML cells, we demonstrate that p53 is dispensable for Pam3CSK4-induced apoptosis and differentiation. Moreover, also murine AML1-ETO9a driven AML cells were forced into apoptosis and differentiation upon TLR1/TLR2 activation, demonstrating that the antileukemic effects observed were not confined to MLL-rearranged AML. We further evaluated whether Pam3CSK4 would exhibit selective antileukemic effects. Ex vivo Pam3CSK4 treatment inhibited murine and human leukemia-initiating cells, whereas murine normal hematopoietic stem and progenitor cells (HSPCs) were relatively less affected. Consistent with these findings, primary human AML cells across several genetic subtypes of AML were more vulnerable for TLR1/TLR2 activation relative to normal human HSPCs. In the MLL-AF9 AML mouse model, treatment with Pam3CSK4 provided proof of concept for in vivo therapeutic efficacy. Our results demonstrate that TLR1 and TLR2 are upregulated on primitive AML cells and that agonistic targeting of TLR1/TLR2 forces AML cells into apoptosis by p38 MAPK-dependent activation of Caspase 3, and differentiation by activating NFκB, thus revealing a new putative strategy for therapeutically targeting AML cells.

2017-10-31 | GSE92744 | GEO

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