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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 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.

ORGANISM(S): Homo sapiens

SUBMITTER: FLORENCE LE CALVEZ-KELM

PROVIDER: E-GEOD-78858 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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 pLVUT’ TLR9 or GFP where the same number of cells were harvested and RNA extracted after 36 h treatment with doxycyline.

2016-08-02 | GSE78858 | GEO

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

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

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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.

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

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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.

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2022-08-03 | GSE202103 | GEO

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

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TLR9 deficiency promotes CD73 expression in T cells and diabetes protection in NOD mice

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2013-07-11 | GSE48781 | GEO

RNA-seq analysis of follicular (FO), marginal zone (MZ) and 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 SLE

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TLR9 deficiency promotes CD73 expression in T cells and diabetes protection in NOD mice

2013-07-11 | E-GEOD-48781 | biostudies-arrayexpress