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TLR9 re-expression in cancer cells extends the S-phase and stabilizes p16INK4a protein expression.

ABSTRACT: Using Illumina HumanHT-12 v4 Expression BeadChips, providing a genome-wide coverage of over 24,000 genes, we have analysed gene expression variation in HNSCC 136 cells transduced with pLVUT’ TLR9 or GFP where the same number of cells were harvested and RNA extracted after 36 h treatment with doxycyline.

ORGANISM(S): Homo sapiens

PROVIDER: GSE78858 | GEO | 2016/08/02

SECONDARY ACCESSION(S): PRJNA314184

REPOSITORIES: GEO

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TLR9 re-expression in cancer cells extends the S-phase and stabilizes p16INK4a protein expression.

Project description:Using Illumina HumanHT-12 v4 Expression BeadChips, providing a genome-wide coverage of over 24,000 genes, we have analysed gene expression variation in HNSCC 136 cells transduced with pLVUTâ TLR9 or GFP where the same number of cells were harvested and RNA extracted after 36 h treatment with doxycyline. Total RNA obtained HNSCC 136 cells transduced with pLVUTâ TLR9 or GFP as controls where the same number of cells were harvested and RNA extracted after 36 h treatment with doxycyline.Diffrential expression analysis was conducted with GFP replicates as reference group.

2016-08-02 | E-GEOD-78858 | biostudies-arrayexpress

Impact of delay to cryopreservation on RNA integrity and genome-wide expression profiles in resected tumor samples.

2013-04-01 | GSE41160 | GEO

TLR9 re-expression in cancer cells extends the S-phase and stabilizes p16(INK4a) protein expression.

Project description: Not available

| S-EPMC4972902 | biostudies-other

Impact of delay to cryopreservation on RNA integrity and genome-wide expression profiles in resected tumor samples.

Project description:Using Illumina HumanHT-12 v3 Expression BeadChips, providing a genome-wide coverage of over 24,000 genes, we have analysed gene expression variation in samples of 3 hepatocellular carcinomas (HCC) and 3 lung carcinomas (LC) cryopreserved at times up to 2 hours after resection. Total RNA obtained 3 frozen Hepatocellular Carcinomas and 3 Lung Carcinomas cryopreserved at 5 min, 15min, 30min and 120min after resection. Tissue samples from the center and the peripheral of the tumours were frozen for each time point.

2013-04-01 | E-GEOD-41160 | biostudies-arrayexpress

Effect of CXCL4 on TLR9-induced B cells

Project description:CXCL4 is a cationic peptide that binds to TLR9-ligand oligonucleotide, resulting in an inhibition of TLR9 response in B cells

2023-06-27 | GSE227639 | GEO

Cell intrinsic expression of TLR9 in autoreactive B cells constrains BCR/TLR7-dependent responses

Project description:Endosomal Toll-like receptors (TLRs) play an important role in the etiology of systemic autoimmune diseases such as SLE, where DNA- and RNA-associated autoantigens activate autoreactive B cells through TLR9- and TLR7-dependent pathways, respectively. Nevertheless, TLR9-deficient autoimmune prone mice develop more severe clinical disease, while TLR7-deficient and TLR7/9-double deficient autoimmune-prone mice develop less severe disease. To determine whether the regulatory activity of TLR9 is B cell intrinsic, we have now directly compared the functional properties of autoantigen activated WT, TLR9-deficient and TLR7-deficient B cells, in an experimental system where proliferation depends on BCR/TLR co-engagement. In vitro, TLR9-deficient cells are less dependent on survival factors for a sustained proliferative response than either WT or TLR7-deficient cells. The TLR9-deficient cells also preferentially differentiate toward the plasma cell lineage, as indicated by expression of CD138, sustained expression of IRF4, and other molecular markers of plasma cells. In vivo, autoantigen-activated TLR9-deficient cells give rise to greater numbers of autoantibody producing cells. Our results identify distinct roles for TLR7 and TLR9 in the differentiation of autoreactive B cells that explain the capacity of TLR9 to limit, and TLR7 to promote, the clinical features of SLE. AM14 WT, Tlr7-/-, Tlr9-/- and Tlr7/9-/- B cells were stimulated with PL2-3 for 0, 6, 24, and 42 hours, for a total of 16 samples.

2015-03-04 | E-GEOD-58756 | biostudies-arrayexpress

Formation of Memory Assemblies through the DNA Sensing Tlr9 Pathway

Project description:As hippocampal neurons respond to diverse types of information a subset assembles into stable microcircuits representing a memory. Those neurons typically undergo energy-intensive molecular adaptations, which occasionally results in transient DNA damage. We found, however, discrete clusters of excitatory hippocampal CA1 neurons showing persistent dsDNA breaks, nuclear envelope ruptures, and perinuclear release of histone and dsDNA fragments for hours after learning. Following these early events, some neurons acquired an inflammatory phenotype involving activation of Toll-like receptor 9 (Tlr9) signaling and accumulation of centrosomal DNA damage repair (DDR) complexes. Neuron-specific knockdown of Tlr9 impaired memory while blunting CFC-induced changes of gene expression in specific clusters of excitatory CA1 neurons. Most notably, Tlr9 played an essential role in centrosome function, including DDR, ciliogenesis, and build-up of perineuronal nets (PNN). We demonstrate a novel cascade of learning-induced molecular events in discrete neuronal clusters undergoing dsDNA damage and Tlr9-mediated repair, resulting in their recruitment to memory circuits. With compromised Tlr9 function, this fundamental memory mechanism becomes a gateway to genomic instability and cognitive impairments, which have been implicated in accelerated senescence, psychiatric disorders, and neurodegenerative disorders. Maintaining the integrity of Tlr9 inflammatory signaling thus emerges as a promising preventive strategy for neurocognitive deficits.

2024-03-01 | GSE254780 | GEO

Cell intrinsic expression of TLR9 in autoreactive B cells constrains BCR/TLR7-dependent responses

2015-03-04 | GSE58756 | GEO

ATAC-seq analysis of aged-associated B cells (ABC) across three TLR9 genotypes (TLR9WT, TLR9-/- and non-signaling TLR9P915H/P915H) isolated from a mixed chimeric setting in the MRL/lpr murine model of systemic lupus erythematosus.

Project description:Purpose: The goal of this study was to assess if TLR9 deficiency (TLR9-/-) or TLR9 incapacity to signal through MyD88 would differentially influence the epigenetic states of ABC, in a B cell intrinsic manner. Methods : Mixed bone marrow chimeras of one-third each TLR9+/+ CD45.1/2, TLR9-/- CD45.1/1 and TLR9P915H/P915H CD45.2/2 were generated on the MRL/lpr background. From each recipient, ABC were sorted with respect to the CD45 congenic markers at [20 weeks] post chimerism. DNA was isolated using a protocol adapted from Corces et al. Samples were sequenced to obtain 20M 2x75 bp paired-end reads using an Illumina NextSeq 550 sequencer (Illumina, Inc, California, USA). Results: The majority of differences in open chromatin regions were observed between TLR9-/- and TLR9P915H ABCs. This must reflect the MyD88-independent regulatory function of TLR9 (lost in TLR9-/- and present in TLR9P915H).

2022-08-03 | GSE202103 | GEO

Enhancement of Human B Cell Differentiation and Function in Lymph Nodes by the TLR9 Agonist MGN1703

Project description:TLR9 agonists are being developed as immunotherapies to increase immune effector cell activity against malignancies and pathogens. However, the in vivo impacts of TLR9 agonism on human B cells are incompletely known and the impacts of such treatments on human lymph node B cells are unknown. These are major knowledge gaps given the high TLR9 expression levels in B cells and the importance of lymph nodes for B cell activity. Therefore, we assessed TLR9 agonist-mediated effects on lymph node B cells as planned secondary endpoints within our clinical trial dosing the TLR9 agonist MGN1703 (Lefitolimod) in the context of developing an HIV cure strategy (NCT02443935).

2019-07-30 | GSE130307 | GEO

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