• Journal of Life Science
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• v.10 no.1
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• pp.40-44
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• 2000

The SNF2/SW ATPase/helicase family comprises proteins form a variety of species with in vivo functions, such as transcriptional regulation, maintenance of chromosome stability during mitosis, and various types of DNA repair. Here, we reported the characterization of h게2+gene which was iolated by PCR amplification using the conserved domain of SNF2 motifs. Sequence analysis of PCR product showed striking evolutionary conservation among the SNF2 family of proteins. Two transcripts of 6.7 and 3.4 Lb were detected by Northern blot analysis. furthermore, the intensities of these two bands were increased by ultraviolet(UV) irradiation. These results indicate that the hrp2+ is a novel member of the SNF2 family of proteins and is one of the UV-inducible genes in S. pombe. To determine the level of transcripts of hrp2+ gene during cellular growth, Northern blot analysis were performed. This result indicates that the level of hrp2+transcript reached its maximum before cells entered the exponential growth phase. This suggests that hrp2+ gene is experssed mainly at the early stage of cell growth.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.2
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• pp.665-669
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• 2012

Aim: The distribution of DNA repair gene XRCC1 and XRCC3 genotypes was used to assess the potential influence of genetic polymorphisms on risk of colorectal cancer, and interactions with other factors. Methods: a 1:2 matched case-control study was conducted with 485 cases and 970 controls. XRCC1 and XRCC2 genotype polymorphisms were based upon duplex polymerase-chain-reaction with the confronting-two-pairprimer (PCR-CTPP) method. Results:The XRCC1 399Cln allele polymorphism was found to be associated with an increased colorectal cancer risk, while an non-significant inversely association was noted for XRCC3 241Thr/Thr genotype. We also found that individuals with the XRCC1 399 Gln and XRCC3 241Met alleles had an elevated risk, while XRCC3241Thr/Thr was proctective. Conclusion: This study is the first to provide evidence of importance of XRCC1 and XRCC3 gene polymorphisms for risk of colorectal cancer in the Chinese population.

• Clinical and Experimental Pediatrics
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• v.51 no.4
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• pp.435-438
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• 2008

The Cerebro-oculo-facio-skeletal (COFS) syndrome is a rare autosomal recessive disorder characterized by multiple abnormalities that involve the brain, face, eyes, and extremities. COFS syndrome is regarded as a degenerative disorder of the brain and spinal cord caused by a mutation of the DNA repair genes. We report on an 8-month-old girl with COFS syndrome who exhibited growth and developmental delay, hypotonia, microcephaly, nystagmus, cleft palate, widely separated nipples, inguinal hernia, camptodactyly, and rocker-bottom feet with vertical talus.

• Molecular & Cellular Toxicology
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• v.3 no.2
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• pp.98-106
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• 2007

Genotoxic stress triggers a variety of biological responses including the transcriptional activation of genes regulating DNA repair, cell survival and cell death. In this study, we investigated to examine gene expression profiles and genotoxic response in TK6 cells treated with DNA damaging agents MNNG (N-methyl-N'-nitrosoguanidine) and hydrogen peroxide $(H_2O_2)$. We extracted total RNA in three independent experiments and hybridized cRNA probes with oligo DNA chip (Applied Biosystems Human Genome Survey Microarray). We analyzed raw signal data with R program and AVADIS software and identified a number of deregulated genes with more than 1.5 log-scale fold change and statistical significancy. We indentified 14 genes including G protein alpha 12 showing deregulation by MNNG. The deregulated genes by MNNG represent the biological pathway regarding MAP kinase signaling pathway. Hydrogen peroxide altered 188 genes including sulfiredoxins. These results show that MNNG and $H_2O_2$ have both uniquely regulated genes that provide the potential to serve as biomarkers of exposure to DNA damaging agents.

• Journal of Life Science
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• v.16 no.1
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• pp.126-130
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• 2006

The present study intends to characterize the DNA damage-inducible responses in yeast. The fission yeast, Schizosaccharomyces pombe was used in this study as a model system for higher eukaryotes. To study UV-inducible responses in S. pombe, five UV-inducible cDNA clones were isolated from S. pombe by using subtration hybridization method. To investigate the expression of isolated genes, UVI-155, the cellular levels of the transcripts were determined by Northern blot analysis after UV-irradiation. The transcripts of isolated gene (UVI-155) increased rapidly and reached maximum accumulation after UV-irradiation. Compared to the message levels of control, the levels of maximal increase were approximately 5 fold to UV-irradiation. In order to investigation whether the increase of UVI-l55 trascripts was a specific results of UV-irradiation, UVI-155 transcript levels were examined after treating the cells to mthylmethane sulfonate (MMS). The transcripts of UVI-155 were not induced by treatment of $0.25\%$ MMS. These results implied that the effects of damaging agents are complex and different regulatory pathways exist for the induction of these genes. To characterize the UVI-155 gene, gene deletion experiments were analyzed. The deleted strain was not well grown. This result indicated that the UVI-155 gene is essential for cell viability.

• Journal of Radiation Protection and Research
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• v.37 no.2
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• pp.56-62
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• 2012

To determine the biological effects of low-dose-rate radiation ($^{137}Cs$, 2.95 mGy/h) on EL4 lymphoma cells during 24 h, we investigated the expression of genes related to apoptosis, cell cycle arrest, DNA repair, iron transport, and ribonucleotide reductase. EL4 cells were continuously exposed to low-dose-rate radiation (total dose: 70.8 mGy) for 24 h. We analyzed cell proliferation and apoptosis by trypan blue exclusion and flow cytometry, gene expression by real-time PCR, and protein levels with the apoptosis ELISA kit. Apoptosis increased in the Low-dose-rate irradiated cells, but cell number did not differ between non- (Non-IR) and Low-dose-rate irradiated (LDR-IR) cells. In concordance with apoptotic rate, the transcriptional activity of ATM, p53, p21, and Parp was upregulated in the LDR-IR cells. Similarly, Phospho-p53 (Ser15), cleaved caspase 3 (Asp175), and cleaved Parp (Asp214) expression was upregulated in the LDR-IR cells. No difference was observed in the mRNA expression of DNA repair-related genes (Msh2, Msh3, Wrn, Lig4, Neil3, ERCC8, and ERCC6) between Non-IR and LDR-IR cells. Interestingly, the mRNA of Trfc was upregulated in the LDR-IR cells. Therefore, we suggest that short-term Low-dose-rate radiation activates apoptosis in EL4 lymphoma cells.

• Tuberculosis and Respiratory Diseases
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• v.84 no.1
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• pp.55-66
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• 2021

Background: Particulate matter 10 (PM₁₀; airborne particles <10 ㎛) inhalation has been demonstrated to induce airway and lung diseases. In this study, we investigate the effects of PM₁₀ inhalation on RNA expression in lung tissues using a murine model. Methods: Female BALB/c mice were affected with PM₁₀, ovalbumin (OVA), or both OVA and PM₁₀. PM₁₀ was administered intranasally while OVA was both intraperitoneally injected and intranasally administered. Treatments occurred 4 times over a 2-week period. Two days after the final challenges, mice were sacrificed. Full RNA sequencing using lung homogenates was conducted. Results: While PM₁₀ did not induce cell proliferation in bronchoalveolar fluid or lead to airway hyper-responsiveness, it did cause airway inflammation and lung fibrosis. Levels of interleukin 1β, tumor necrosis factor-α, and transforming growth factor-β in lung homogenates were significantly elevated in the PM₁₀-treated group, compared to the control group. The PM₁₀ group also showed increased RNA expression of Rn45a, Snord22, Atp6v0c-ps2, Snora28, Snord15b, Snora70, and Mmp12. Generally, genes associated with RNA splicing, DNA repair, the inflammatory response, the immune response, cell death, and apoptotic processes were highly expressed in the PM₁₀-treated group. The OVA/PM₁₀ treatment did not produce greater effects than OVA alone. However, the OVA/PM₁₀-treated group did show increased RNA expression of Clca1, Snord22, Retnla, Prg2, Tff2, Atp6v0c-ps2, and Fcgbp when compared to the control groups. These genes are associated with RNA splicing, DNA repair, the inflammatory response, and the immune response. Conclusion: Inhalation of PM₁₀ extensively altered RNA expression while also inducing cellular inflammation, fibrosis, and increased inflammatory cytokines in this murine mouse model.

• Journal of Microbiology and Biotechnology
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• v.30 no.2
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• pp.237-243
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• 2020

A novel psychrotolerant Psychrobacillus strain PB01, isolated from an Antarctic iceberg, was comparatively analyzed with five related strains. The complete genome of strain PB01 consists of a single circular chromosome (4.3 Mb) and a plasmid (19 Kb). As potential low-temperature adaptation strategies, strain PB01 has four genes encoding cold-shock proteins, two genes encoding DEAD-box RNA helicases, and eight genes encoding transporters for glycine betaine, which can serve as a cryoprotectant, on the genome. The pan-genome structure of the six Psychrobacillus strains suggests that strain PB01 might have evolved to adapt to extreme environments by changing its genome content to gain higher capacity for DNA repair, translation, and membrane transport. Notably, strain PB01 possesses a complete TCA cycle consisting of eight enzymes as well as three additional Helicobacter pylori-type enzymes: ferredoxin-dependent 2-oxoglutarate synthase, succinyl-CoA/acetoacetyl-CoA transferase, and malate/quinone oxidoreductase. The co-existence of the genes for TCA cycle enzymes has also been identified in the other five Psychrobacillus strains.

• Korean Journal of Microbiology
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• v.50 no.2
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• pp.95-100
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• 2014

Hrq1 is a novel member of RecQ helicase family, found in fungal genomes by bioinformatics analyses. It is most homologous to human RECQL4 and recent genetic and biochemical studies suggested that it may play roles in the maintenance of genome stability. In this study, we investigated yeast two-hybrid interactions between Hrq1 and the yeast genes homologous to the human genes that are known to interact with RECQL4. Among the 11 genes tested, Rad14, a nucleotide excision repair (NER) factor, was found to interact with Hrq1. In addition, pull-down assay with the purified proteins revealed direct protein-protein interaction between Hrq1 and Rad14. The yeast two-hybrid interaction was enhanced by the DNA damage induced by 4-nitroquinoline-1-oxide, which was dependent on the presence of Rad4, a key NER factor. These results suggest that Hrq1 may function in NER through interaction with Rad14.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.114-114
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• 2003

p53 has identified as a tumor suppressor protein to protect cells from DNA damage. p53, also well known for a transcription factor, can activate genes such as p21, bax, gadd45 and induce a number of the responses such as differentiation, senescence, DNA repair, apoptosis and the inhibition of angiogenesis to protect cells. Many mechanisms of p53 activation have been studied.(omitted)