Real-time quantitative PCR analysis of pro-inflammatory gene expression in Human embryonic kidney cells 293 (HEK293)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE119929 | GEO | 2018/10/02
REPOSITORIES: GEO
Similar Datasets
Project description:Balb/cJ mouse received control RNAi or RNAi to 8-oxoguanine DNA glycosylase (Ogg1) intranasally prior to the exposure for 1 h to a) glucose oxidase (1 mU) to induce OGG1-BER or b) OGG1-BER product 8-oxoguanine (1 μM). We used SABiosciences Mouse Inflammatory Cytokines & Receptors PCR Array (PAMM-011A) to quantitate inflammatory gene expression dependent on OGG1 and its product 8-oxoguanine.
2014-08-26 | GSE60711 | GEO
Project description:MLE12 cells were treated with 8-oxoguanine DNA glycosylase 1 (OGG1) inhibitor with or without TNF to evaluate its effect on pro-inflammatory gene expression. We used SA Biosciences Mouse Inflammatory Cytokines & Receptors PCR Array (PAMM-011Z) to quantitate inflammatory gene expression dependent on OGG1 .
2018-07-06 | GSE106785 | GEO
Project description:Balb/cJ mouse received control RNAi or RNAi to 8-oxoguanine DNA glycosylase (Ogg1) intranasally prior to the exposure for 1 h to a) glucose oxidase (1 mU) to induce OGG1-BER or b) OGG1-BER product 8-oxoguanine (1 M-NM-<M). We used SABiosciences Mouse Inflammatory Cytokines & Receptors PCR Array (PAMM-011A) to quantitate inflammatory gene expression dependent on OGG1 and its product 8-oxoguanine. After intranasal challenge with glucose oxidase or 8-oxoguanine, mice were sacrificed and lungs were collected and processed to obtain RNA. Total pooled (n=5) RNA (1 M-NM-<g) was reverse transcribed into cDNA using SuperscriptM-BM-. III First Strand Synthesis System (Invitrogen), mixed with equal amounts of 2X SYBR Green Supermix (Qiagen) and 20 M-NM-<l of reaction mixture was added to each well of the PAM-011A array. The reaction was evaluated using an ABI PRISMM-BM-. 7000 Sequence Detection System using recommended settings by SABiosciences.
2014-08-26 | E-GEOD-60711 | biostudies-arrayexpress
Project description:Altered oncogene expression in cancer cells causes loss of redox homeostasis resulting in oxidative DNA damage, e.g., 8-oxoguanine (8-oxoG), repaired by base excision repair (BER). PARP1 coordinates BER and relies on the upstream 8-oxoguanine-DNA glycosylase (OGG1) to recognise and excise 8-oxoG. Here we hypothesize that OGG1 may represent an attractive target to exploit reactive oxygen species (ROS) elevation in cancer. Although OGG1 depletion is well tolerated in non-transformed cells, we report here that OGG1 depletion obstructs A3 T-cell lymphoblastic acute leukemia growth in vitro and in vivo, validating OGG1 as a potential anti- cancer target. In line with this hypothesis, we show that OGG1 inhibitors (OGG1i) target a wide range of cancer cells, with a favourable therapeutic index compared to non-transformed cells. Mechanistically, OGG1i and shRNA depletion cause lost mitochondrial function leading to S- phase DNA damage, replication stress and proliferation arrest or cell death, representing a novel mechanistic approach to target cancer. This study adds OGG1 to the list of BER factors, e.g., PARP1, as potential targets for cancer treatment. _x000B_
2020-08-07 | GSE155782 | GEO
Project description:Effect of 8-oxoguanine DNA glycosylase 1 (OGG1) inhibitor on pro-inflammatory gene expression.
| PRJNA662307 | ENA
Project description:Effect of 8-oxoguanine DNA glycosylase 1 (OGG1) inhibitor on pro-inflammatory gene expression.
| PRJNA480274 | ENA
Project description:To investigate the role of 8-oxo-7, 8-dihydroguanine (8-oxoguanine) accumulation in DNA or nucleotide pools during the development of AD pathology, we introduced a Mth1/Ogg1-double deficiency into homozygous triple-transgenic AD model (3xTg-AD-H) mice. Mth1 encodes 8-oxo-7, 8-dihydro-2'-deoxyguanosine-5'-triphosphatase (8-oxo-dGTPase) and Ogg1 encodes 8-oxoguanine DNA glycosylase 1. One-way eBays ANOVA of microarray data from hippocampi revealed that the gene expression profiles are most significantly altered in the hippocampi of 3xTg-AD-H with Mth1/Ogg1-double deficient (ADH/TO-DKH) mice compared to non-Tg control (NT) mice. Comparative analysis between 3xTg-AD-H (ADH/WT) and ADH/TO-DKH mice showed that the expression of genes involved in neuroprotection are significantly altered. Among them, expression of the AD-related genes including Ttr, Enpp2, Kcnj13 and Kl was significantly downregulated in ADH/TO-DKH mice.
2021-03-24 | GSE83996 | GEO
Project description:Respiratory syncytial virus (RSV), along with other prominent respiratory RNA viruses such as influenza and SARS-CoV-2, significantly contributes to the global incidence of respiratory tract infections. These pathogens induce the production of reactive oxygen species (ROS), which play a crucial role in the onset and progression of respiratory diseases. However, the mechanisms by which viral RNA manages ROS-induced base oxidation remain poorly understood. Here we reveal that 8-oxo-7,8-dihydroguanine (8-oxoGua) is not merely an incidental byproduct of ROS activity but serves as a strategic adaptation of RSV RNA to maintain genetic fidelity within host cells. Through 8-oxoguanine DNA glycosylase 1 (OGG1) immunoprecipitation and LC_MS/MS, we discovered that RSV nucleoprotein is a principal partner of OGG1. Further investigation revealed that viral ribonucleoprotein complexes specifically hijack OGG1. Importantly, inhibiting OGG1's ability to recognize 8-oxoGua significantly reduces RSV progeny production. Our results underscore the viral replication machinery's adaptation to oxidative challenges, suggesting that inhibiting OGG1's reading function could be a novel strategy for antiviral intervention.
2024-10-09 | PXD053262 | Pride
Project description:Interstitial lung diseases such as idiopathic pulmonary fibrosis (IPF) are caused by persistent micro-injuries to alveolar epithelial tissues accompanied by aberrant repair processes. Despite substantial advancement in our understanding of IPF progression, numerous questions remain concerning disease pathology. IPF is currently treated with pirfenidone and nintedanib, compounds which slow the rate of disease progression but fail to target underlying pathophysiological mechanisms. The DNA repair enzyme 8-oxoguanine DNA glycosylase-1 (OGG1) is upregulated following TGF-β1 exposure in several fibrosis-associated cell types. Currently, no pharmaceutical solutions targeting OGG1 have been utilized in the treatment of IPF. In this study, administration of Ogg1-targetting siRNA, mitigated bleomycin-induced pulmonary fibrosis in mice, thereby highlighting OGG1 as a tractable target in lung fibrosis. The novel small molecule OGG1 inhibitor, TH5487, decreased myofibroblast transition and associated pro-fibrotic markers in fibroblast cells. In addition, TH5487 decreased pro-inflammatory cytokine production, inflammatory cell infiltration, and lung remodeling in a murine model of bleomycin-induced pulmonary fibrosis. OGG1 and SMAD7 interact to induce fibroblast proliferation and differentiation, with both increased in fibrotic murine and IPF patient lung tissue. Taken together, these data strongly suggest that TH5487 is a potent, specific, and clinically-relevant treatment for IPF. This DIA-MS dataset entails the raw data and peptide-centric DIA-NN search results of both, lung tissue and bronchoalveolar lavage fluid of n=5 mice profiled across the treatment groups bleomycin combined with TH (BTH), dexamethasone (DEX), TH alone (TH) and vehicle control (V) relative to bleomycin alone (B) as control. Different animals within protein groups were considered biological replicates of the respective treatment condition.
2023-02-06 | PXD029625 | Pride
Project description:Oxidative DNA damage is recognised by 8-oxoguanine (8-oxoG) DNA glycosylase 1 (OGG1), which excises 8-oxoG, leaving a substrate for apurinic endonuclease 1 (APE1), initiating repair. Here, we describe a small molecule (TH10785) that interacts with the Phe319 and Gly42 amino acids of OGG1, increases the enzyme activity 10-fold and generates a novel β,δ-lyase enzymatic function. TH10785 controls the catalytic activity mediated by a nitrogen base within its molecular structure. In cells, TH10785 increases OGG1 recruitment to and repair of oxidative DNA damage. This alters the repair process, which no longer requires APE1 but instead is dependent on polynucleotide kinase phosphatase (PNKP1) activity. The increased repair of oxidative DNA lesions with a small molecule may have therapeutic applications in various diseases and ageing.
2022-06-24 | GSE188779 | GEO