Ask about this productRelated genes to: OGG1 antibody
- Gene:
- OGG1 NIH gene
- Name:
- 8-oxoguanine DNA glycosylase
- Previous symbol:
- -
- Synonyms:
- HMMH, HOGG1, OGH1, MUTM
- Chromosome:
- 3p25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-22
- Date modifiied:
- 2016-10-05
Related products to: OGG1 antibody
Related articles to: OGG1 antibody
- Previously, it was thought that ultraviolet radiation (UV) carcinogenesis was caused by accumulation of mutations related to cancer, including oncogenes and tumor suppressor genes. These genetic changes found in skin cancers are considered to be induced by UV, based on the findings that "UV-signature mutations" are predominant. However, recent findings revealed that UV carcinogenesis includes a more complicated process, and the importance of inflammation is emphasized. It is evident that DNA lesions cause inflammation. We showed that Ogg1 knockout mice, which fail to repair 8-OxoG, a representative oxidative DNA lesion, manifest a much higher frequency of UV-induced skin cancers without increasing p53 mutations. Gene expression analysis in this system revealed that 8-oxoG upregulates inflammatory pathway genes. Furthermore, a mice model of xeroderma pigmentosum, a DNA repair disorder, where patients manifest severe sunburn and high frequency of skin cancers, was demonstrated to express an extremely high level of CXCL1, an inflammatory chemokine. Inhibiting CXCL1 decreased the development of UV-induced skin cancers without repairing dipyrimidine photoproducts. Additionally, some anti-inflammatory medicines suppress the development of UV-induced skin cancers. The enhancement of photosensitive medications, including voriconazole and hydrochlorothiazide on UV carcinogenesis, has been indicated both epidemiologically and experimentally. - Source: PubMed
Publication date: 2026/05/08
Nishigori Chikako - Acute Myocardial Infarction (AMI) is a significant contributor to cardiovascular death, with rising prevalence in Bangladesh. Although DNA damage contributes to AMI pathogenesis, the role of DNA damage repair (DDR) genes remains poorly characterized. This study aims to identify key DDR genes associated with AMI, and develop a machine learning-based risk prediction model for the Bangladeshi population. Differentially expressed DDR genes in AMI were identified via bioinformatics analysis, with WGCNA revealing AMI-associated hub genes. These candidates were validated by qRT-PCR in Bangladeshi patients. A machine learning model using demographic and gene expression data was then trained using five classifiers. Differential expression and WGCNA identified Nibrin (NBN) and 8-Oxoguanine glycosylase (OGG1) as key dysregulated DDR genes. RT-qPCR confirmed a ~ 2.78-fold upregulation of OGG1 (p < 0.001) in AMI patients, while NBN expression was significantly higher in smokers (p < 0.05). Feature selection identified age, smoking, hypertension, diabetes, BMI, and OGG1 as critical AMI risk predictors. Logistic regression showed the best performance (accuracy 87.3%, AUC = 0.903). This study provides novel evidence linking DDR genes to AMI and presents a strong ML-based risk stratification model for the first time, integrating transcriptomic and clinical data from Bangladeshi patients to advance personalized AMI management. - Source: PubMed
Publication date: 2026/05/07
Zahin HasnatSaba Abdullah AlRipon Rifat HossainNabi A H M NurunYasmin Tahirah - Long non-coding RNAs (lncRNA) play important regulatory roles during embryonic genome activation (EGA) in porcine early embryonic development. However, whether promoter-associated lncRNAs exert key functions in EGA and their underlying regulatory mechanisms remain largely unclear in pigs. In this study, we identified a highly expressed promoter-associated long non-coding RNA during the 4-cell stage of porcine embryos and named it pancEIF4G3. pancEIF4G3 is a nuclear-localized lncRNA that lacks protein-coding capacity and exhibits an expression pattern similar to its neighboring gene EIF4G3. The study found that interference with either pancEIF4G3 or EIF4G3 led to developmental arrest of porcine embryos at the 4-cell stage, indicating their crucial role in early embryogenesis. Further investigation revealed that pancEIF4G3, which is located upstream of EIF4G3, regulates both its RNA and protein expression levels through binding to OGG1. Downregulation of pancEIF4G3 and EIF4G3 resulted in reduced chromatin accessibility, decreased nascent RNA synthesis, and significant downregulation of multiple EGA marker genes and core transcription factors. In summary, this study is the first to reveal a novel mechanism in porcine early embryos whereby the promoter-associated lncRNA pancEIF4G3 regulates the expression of the translation initiation factor EIF4G3, thereby influencing the process of embryonic genome activation. This finding enriches the regulatory network of early embryonic development in pigs and also provides a potential molecular target for optimizing in vitro embryo culture and reproductive techniques. - Source: PubMed
Publication date: 2026/04/29
He TianyaoLu HuiqinZhang ChenyuanZhang ShanlongLi HanZhang ShichaoLiu DongsongZhu YanlongSun Jing-TaoWang JiaqiangLiu ZhonghuaJin Jun-Xue - The stamens of L., often discarded as floral waste, are rich in flavonoids and phenolics. This study investigated their toxicological safety, antigenotoxic potential, and molecular mechanisms of protection against cyclophosphamide (CP)-induced genotoxicity. Hydroethanolic and hydromethanolic extracts were prepared, and acute oral toxicity was assessed in mice following the Organization for Economic Co-operation and Development guideline 423. Genotoxicity and its amelioration were evaluated in rat and mouse leukocytes by employing the alkaline comet assay. Oxidative stress markers, including superoxide dismutase activity, as well as malondialdehyde and glutathione levels, in hepatic and renal tissues were quantified. In parallel, nine major metabolites were identified in the extracts and were molecularly docked with key enzymes involved in CP bioactivation (CYP2B6), aldehyde detoxification (ALDH1A1), DNA repair (OGG1), and oxidative stress regulation (Keap1-Kelch domain; Protein Data Bank ID: 7K2A). The extracts were non-toxic up to 4,000 mg/kg and did not exhibit any genotoxicity. Pre-treatment with extracts (200 mg/kg body weight) significantly attenuated CP-induced DNA damage and restored antioxidant enzyme levels. Docking results supported these observations: rutin demonstrated a high affinity for CYP2B6 (-11.2 kcal/mol) and favorable binding to 7K2A (-9.7 kcal/mol); catechin gallate bound tightly to ALDH1A1 (-10.0 kcal/mol) and OGG1 (-9.2 kcal/mol). These findings suggest reduced CP activation, but enhanced detoxification and DNA repair. In conclusion, the extracts of stamens are safe and possess robust antioxidant and antigenotoxic properties, confirmed by molecular docking. These findings highlight their potential as natural protective agents against chemotherapy-induced genotoxicity. - Source: PubMed
Publication date: 2026/04/13
Mamri SamiraBaddaoui SanaeKhibech OussamaOuahhoud SabirKhoulati AmineChoukri MohammedAsehraou AbdeslamSaalaoui Ennouamane - Genetic predisposition without doubt is one of the risk factors of cancer initiation. It is known that single nucleotide polymorphisms (SNP) of genes that maintain the genome stability, including SNP of DNA repair, may contribute to the initiation of carcinogenesis. Single-nucleotide polymorphisms of genes that support genome stability, including SNP of DNA repair genes, can contribute to cancer initiation. Polymorphism of the excision repair gene OGG1 causes interest of leading scientific groups from various countries. It is assumed that there is relationship between the rs1052133 polymorphism in the gene and predisposition to cancer initiation. The objective of this study was to establish association between rs1052133 polymorphism of base excision repair gene OGG1 and the risk of cancer initiation in people chronically exposed to ionizing radiation. Residents (888 people) of the Techa riverside settlements, chronically exposed to low or medium dose radiation from the Techa River and the East-Urals Radioactive Trace were included in the study. The study allowed researchers to establish that exposed to chronic radiation people, carriers of the rs1052133*G allele, have increased risk of malignant neoplasm initiation: OR = 1.38; 95% CI [1.05-1.83], p = 0.023. The multifactorial synergistic interactions between the dose to the red bone marrow and the rs1052133 polymorphism of the OGG1 gene was found: Testing Balanced Accuracy (TBA) = 0.56; Cross Validation Consistency (CVC) = 10/10; p = 0.01). The study found that the rs1052133 polymorphism may be considered as genetical marker of risk of cancer initiation in people chronically exposed to radiation with doses ranged from 0.74 to 3507.07 mGy (average 523.10 ± 33.89 mGy). It was found that the presence of the rs1052133*G in combination with radiation exposure can modify the risk of solid cancers initiation, as it is indicated by the synergistic relationship between the SNP and the radiation dose. - Source: PubMed
Publication date: 2026/04/20
Yanishevskaya M ABlinova E AKorechenkova A VAkleyev A V