Relevant bibliographies by topics / Genová indukce

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Genová indukce'

Author: Grafiati
Published: 28 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Genová indukce"

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Hanzelka, P., and F. Kobza. "Genome induced mutation in Callistephus chinensis Ness. – evaluation of plant fertility and seed characteristics." Horticultural Science 31, No. 1 (November 25, 2011): 22–26. http://dx.doi.org/10.17221/3787-hortsci.

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Thousand seed weight (TSW, g), achene size (mm) and fertility were evaluated in polyploid plants of C<sub>0</sub> (1999) and C<sub>1</sub> (2000) generations. The fertility of polyploid plants was usually very low (more than 10&times; compared to diploid plants). Only one plant (genotype A (tm) 1) was found as a tetraploid individual with anomalously high fertility, high TSW and large size of achenes. TSW in polyploid plants was 2.6&ndash;4.13 g, in diploid plants 2.0&ndash;2.3 g. The achene size was mostly about 3.7 mm (diploid plants) and 4.0&ndash;4.8 mm (polyploid plants). Achene (seed) size and thousand seed weight (TSW) can be classified among indirect identification methods (size of stomata, number of chloroplasts in guard cells, etc.) of polyploid plants. &nbsp; &nbsp;
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Chen, Aaron Yun, Yong Luo, Fang Cheng, Yuning Sun, and Jianming Qiu. "Bocavirus Infection Induces Mitochondrion-Mediated Apoptosis and Cell Cycle Arrest at G2/M Phase." Journal of Virology 84, no. 11 (March 24, 2010): 5615–26. http://dx.doi.org/10.1128/jvi.02094-09.

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ABSTRACT Bocavirus is a newly classified genus of the family Parvovirinae. Infection with Bocavirus minute virus of canines (MVC) produces a strong cytopathic effect in permissive Walter Reed/3873D (WRD) canine cells. We have systematically characterized the MVC infection-produced cytopathic effect in WRD cells, namely, the cell death and cell cycle arrest, and carefully examined how MVC infection induces the cytopathic effect. We found that MVC infection induces an apoptotic cell death characterized by Bax translocalization to the mitochondrial outer membrane, disruption of the mitochondrial outer membrane potential, and caspase activation. Moreover, we observed that the activation of caspases occurred only when the MVC genome was replicating, suggesting that replication of the MVC genome induces apoptosis. MVC infection also induced a gradual cell cycle arrest from the S phase in early infection to the G2/M phase at a later stage, which was confirmed by the upregulation of cyclin B1 and phosphorylation of cdc2. Cell cycle arrest at the G2/M phase was reproduced by transfection of a nonreplicative NS1 knockout mutant of the MVC infectious clone, as well as by inoculation of UV-irradiated MVC. In contrast with other parvoviruses, only expression of the MVC proteins by transfection did not induce apoptosis or cell cycle arrest. Taken together, our results demonstrate that MVC infection induces a mitochondrion-mediated apoptosis that is dependent on the replication of the viral genome, and the MVC genome per se is able to arrest the cell cycle at the G2/M phase. Our results may shed light on the molecular pathogenesis of Bocavirus infection in general.
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Brodsky, Michael H., Brian T. Weinert, Garson Tsang, Yikang S. Rong, Nadine M. McGinnis, Kent G. Golic, Donald C. Rio, and Gerald M. Rubin. "Drosophila melanogaster MNK/Chk2 and p53 Regulate Multiple DNA Repair and Apoptotic Pathways following DNA Damage." Molecular and Cellular Biology 24, no. 3 (February 1, 2004): 1219–31. http://dx.doi.org/10.1128/mcb.24.3.1219-1231.2004.

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ABSTRACT We have used genetic and microarray analysis to determine how ionizing radiation (IR) induces p53-dependent transcription and apoptosis in Drosophila melanogaster. IR induces MNK/Chk2-dependent phosphorylation of p53 without changing p53 protein levels, indicating that p53 activity can be regulated without an Mdm2-like activity. In a genome-wide analysis of IR-induced transcription in wild-type and mutant embryos, all IR-induced increases in transcript levels required both p53 and the Drosophila Chk2 homolog MNK. Proapoptotic targets of p53 include hid, reaper, sickle, and the tumor necrosis factor family member Eiger. Overexpression of Eiger is sufficient to induce apoptosis, but mutations in Eiger do not block IR-induced apoptosis. Animals heterozygous for deletions that span the reaper, sickle, and hid genes exhibited reduced IR-dependent apoptosis, indicating that this gene complex is haploinsufficient for induction of apoptosis. Among the genes in this region, hid plays a central, dosage-sensitive role in IR-induced apoptosis. p53 and MNK/Chk2 also regulate DNA repair genes, including two components of the nonhomologous end-joining repair pathway, Ku70 and Ku80. Our results indicate that MNK/Chk2-dependent modification of Drosophila p53 activates a global transcriptional response to DNA damage that induces error-prone DNA repair as well as intrinsic and extrinsic apoptosis pathways.
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Redondo, Elise, Renate Krause-Sakate, Shu-Jun Yang, Hervé Lot, Olivier Le Gall, and Thierry Candresse. "Lettuce mosaic virus Pathogenicity Determinants in Susceptible and Tolerant Lettuce Cultivars Map to Different Regions of the Viral Genome." Molecular Plant-Microbe Interactions® 14, no. 6 (June 2001): 804–10. http://dx.doi.org/10.1094/mpmi.2001.14.6.804.

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Full-length infectious cDNA clones were constructed for two isolates (LMV-0 and LMV-E) of Lettuce mosaic virus (LMV), a member of the genus Potyvirus. These two isolates differ in pathogenicity in susceptible and tolerant-resistant lettuce cultivars. In susceptible plants, LMV-0 induces mild mosaic symptoms, whereas LMV-E induces severe stunting, leaf deformation, and a necrotic mosaic. In plants carrying either of the two probably allelic recessive resistance genes mo11 or mo12, LMV-0 is restricted partially to the inoculated leaves. When a systemic invasion does occur, however, symptoms fail to develop. LMV-E overcomes the protection afforded by the resistance genes, resulting in systemic mosaic symptoms. Analysis of the behavior of recombinants constructed between the two virus isolates determined that the HC-Pro protein of LMV-E causes the severe stunting and necrotic mosaic induced by this isolate in susceptible cultivars. In contrast, the ability to overcome mo1 resistance and induce symptoms in the resistant-tolerant cultivars was mapped to the 3′ half of the LMV-E genome. These results indicate that the ability to induce severe symptoms and to overcome the protection afforded by the recessive genes mo11 or mo12 are independent phenomena.
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Parish, Joanna L., Anna Kowalczyk, Hsin-Tien Chen, Geraldine E. Roeder, Richard Sessions, Malcolm Buckle, and Kevin Gaston. "E2 Proteins from High- and Low-Risk Human Papillomavirus Types Differ in Their Ability To Bind p53 and Induce Apoptotic Cell Death." Journal of Virology 80, no. 9 (May 1, 2006): 4580–90. http://dx.doi.org/10.1128/jvi.80.9.4580-4590.2006.

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ABSTRACT The E2 proteins from oncogenic (high-risk) human papillomaviruses (HPVs) can induce apoptotic cell death in both HPV-transformed and non-HPV-transformed cells. Here we show that the E2 proteins from HPV type 6 (HPV6) and HPV11, two nononcogenic (low-risk) HPV types, fail to induce apoptosis. Unlike the high-risk HPV16 E2 protein, these low-risk E2 proteins fail to bind p53 and fail to induce p53-dependent transcription activation. Interestingly, neither the ability of p53 to activate transcription nor the ability of p53 to bind DNA, are required for HPV16 E2-induced apoptosis in non-HPV-transformed cells. However, mutations that reduce the binding of the HPV16 E2 protein to p53 inhibit E2-induced apoptosis in non-HPV-transformed cells. In contrast, the interaction between HPV16 E2 and p53 is not required for this E2 protein to induce apoptosis in HPV-transformed cells. Thus, our data suggest that this high-risk HPV E2 protein induces apoptosis via two pathways. One pathway involves the binding of E2 to p53 and can operate in both HPV-transformed and non-HPV-transformed cells. The second pathway requires the binding of E2 to the viral genome and can only operate in HPV-transformed cells.
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Efimova, Olga A., Alla S. Koltsova, Mikhail I. Krapivin, Andrei V. Tikhonov, and Anna A. Pendina. "Environmental Epigenetics and Genome Flexibility: Focus on 5-Hydroxymethylcytosine." International Journal of Molecular Sciences 21, no. 9 (May 2, 2020): 3223. http://dx.doi.org/10.3390/ijms21093223.

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Convincing evidence accumulated over the last decades demonstrates the crucial role of epigenetic modifications for mammalian genome regulation and its flexibility. DNA methylation and demethylation is a key mechanism of genome programming and reprogramming. During ontogenesis, the DNA methylome undergoes both programmed changes and those induced by environmental and endogenous factors. The former enable accurate activation of developmental programs; the latter drive epigenetic responses to factors that directly or indirectly affect epigenetic biochemistry leading to alterations in genome regulation and mediating organism response to environmental transformations. Adverse environmental exposure can induce aberrant DNA methylation changes conducive to genetic dysfunction and, eventually, various pathologies. In recent years, evidence was derived that apart from 5-methylcytosine, the DNA methylation/demethylation cycle includes three other oxidative derivatives of cytosine—5-hydroxymethylcytosine (5hmC), 5-formylcytosine, and 5-carboxylcytosine. 5hmC is a predominantly stable form and serves as both an intermediate product of active DNA demethylation and an essential hallmark of epigenetic gene regulation. This makes 5hmC a potential contributor to epigenetically mediated responses to environmental factors. In this state-of-the-art review, we consolidate the latest findings on environmentally induced adverse effects on 5hmC patterns in mammalian genomes. Types of environmental exposure under consideration include hypnotic drugs and medicines (i.e., phenobarbital, diethylstilbestrol, cocaine, methamphetamine, ethanol, dimethyl sulfoxide), as well as anthropogenic pollutants (i.e., heavy metals, particulate air pollution, bisphenol A, hydroquinone, and pentachlorophenol metabolites). We put a special focus on the discussion of molecular mechanisms underlying environmentally induced alterations in DNA hydroxymethylation patterns and their impact on genetic dysfunction. We conclude that DNA hydroxymethylation is a sensitive biosensor for many harmful environmental factors each of which specifically targets 5hmC in different organs, cell types, and DNA sequences and induces its changes through a specific metabolic pathway. The associated transcriptional changes suggest that environmentally induced 5hmC alterations play a role in epigenetically mediated genome flexibility. We believe that knowledge accumulated in this review together with further studies will provide a solid basis for new approaches to epigenetic therapy and chemoprevention of environmentally induced epigenetic toxicity involving 5hmC patterns.
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Sanchez, David Jesse, Daniel Miranda, Vaithilingaraja Arumugaswami, Seungmin Hwang, Adam E. Singer, Ashkon Senaati, Arash Shahangian, Moon Jung Song, Ren Sun, and Genhong Cheng. "A Repetitive Region of Gammaherpesvirus Genomic DNA Is a Ligand for Induction of Type I Interferon." Journal of Virology 82, no. 5 (December 12, 2007): 2208–17. http://dx.doi.org/10.1128/jvi.01718-07.

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ABSTRACT Innate immune responses against viral infection, especially the induction of type I interferon, are critical for limiting the replication of the virus. Although it has been shown that DNA can induce type I interferon, to date no natural DNA ligand of a virus that induces type I interferon has been described. Here we screened the genome of murine gammaherpesvirus 68 with mutations at various genomic locations to map the region of DNA that induces type I interferon. A repetitive region termed the 100-base-pair repeat region is a ligand that is both necessary and sufficient for the viral genomic DNA to induce type I interferon. A region colinear with this ligand in the genome of Kaposi's sarcoma-associated herpesvirus also induces type I interferon. We have thus defined a repetitive region of the genomes of gammaherpesviruses as the first natural DNA virus ligand that induces type I interferon.
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Holthusen, Kirsten, Pooja Talaty, and David N. Everly. "Regulation of Latent Membrane Protein 1 Signaling through Interaction with Cytoskeletal Proteins." Journal of Virology 89, no. 14 (May 6, 2015): 7277–90. http://dx.doi.org/10.1128/jvi.00321-15.

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ABSTRACTLatent membrane protein 1 (LMP1) of Epstein-Barr virus (EBV) induces constitutive signaling in EBV-infected cells to ensure the survival of the latently infected cells. LMP1 is localized to lipid raft domains to induce signaling. In the present study, a genome-wide screen based on bimolecular fluorescence complementation (BiFC) was performed to identify LMP1-binding proteins. Several actin cytoskeleton-associated proteins were identified in the screen. Overexpression of these proteins affected LMP1-induced signaling. BiFC between the identified proteins and LMP1 was localized to lipid raft domains and was dependent on LMP1-induced signaling. Proximity biotinylation assays with LMP1 induced biotinylation of the actin-associated proteins, which were shifted in molecular mass. Together, the findings of this study suggest that the association of LMP1 with lipid rafts is mediated at least in part through interactions with the actin cytoskeleton.IMPORTANCELMP1 signaling requires oligomerization, lipid raft partitioning, and binding to cellular adaptors. The current study utilized a genome-wide screen to identify several actin-associated proteins as candidate LMP1-binding proteins. The interaction between LMP1 and these proteins was localized to lipid rafts and dependent on LMP1 signaling. This suggests that the association of LMP1 with lipid rafts is mediated through interactions with actin-associated proteins.
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Wei, Taiyun, Tyng-Shyan Huang, Jamie McNeil, Jean-François Laliberté, Jian Hong, Richard S. Nelson, and Aiming Wang. "Sequential Recruitment of the Endoplasmic Reticulum and Chloroplasts for Plant Potyvirus Replication." Journal of Virology 84, no. 2 (November 11, 2009): 799–809. http://dx.doi.org/10.1128/jvi.01824-09.

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ABSTRACT The replication of positive-strand RNA viruses occurs in cytoplasmic membrane-bound virus replication complexes (VRCs). Depending on the virus, distinct cellular organelles such as the endoplasmic reticulum (ER), chloroplast, mitochondrion, endosome, and peroxisome are recruited for the formation of VRC-associated membranous structures. Previously, the 6,000-molecular-weight protein (6K) of plant potyviruses was shown to be an integral membrane protein that induces the formation of 6K-containing membranous vesicles at endoplasmic reticulum (ER) exit sites for potyvirus genome replication. Here, we present evidence that the 6K-induced vesicles predominantly target chloroplasts, where they amalgamate and induce chloroplast membrane invaginations. The vesicular transport pathway and actomyosin motility system are involved in the trafficking of the 6K vesicles from the ER to chloroplasts. Viral RNA, double-stranded RNA, and viral replicase components are concentrated at the 6K vesicles that associate with chloroplasts in infected cells, suggesting that these chloroplast-bound 6K vesicles are the site for potyvirus replication. Taken together, these results suggest that plant potyviruses sequentially recruit the ER and chloroplasts for their genome replication.
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Durant, Stephen T., Kimberly S. Paffett, Meena Shrivastav, Graham S. Timmins, William F. Morgan, and Jac A. Nickoloff. "UV Radiation Induces Delayed Hyperrecombination Associated with Hypermutation in Human Cells." Molecular and Cellular Biology 26, no. 16 (August 15, 2006): 6047–55. http://dx.doi.org/10.1128/mcb.00444-06.

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ABSTRACT Ionizing radiation induces delayed genomic instability in human cells, including chromosomal abnormalities and hyperrecombination. Here, we investigate delayed genome instability of cells exposed to UV radiation. We examined homologous recombination-mediated reactivation of a green fluorescent protein (GFP) gene in p53-proficient human cells. We observed an ∼5-fold enhancement of delayed hyperrecombination (DHR) among cells surviving a low dose of UV-C (5 J/m2), revealed as mixed GFP+/− colonies. UV-B did not induce DHR at an equitoxic (75 J/m2) dose or a higher dose (150 J/m2). UV is known to induce delayed hypermutation associated with increased oxidative stress. We found that hypoxanthine phosphoribosyltransferase (HPRT) mutation frequencies were ∼5-fold higher in strains derived from GFP+/− (DHR) colonies than in strains in which recombination was directly induced by UV (GFP+ colonies). To determine whether hypermutation was directly caused by hyperrecombination, we analyzed hprt mutation spectra. Large-scale alterations reflecting large deletions and insertions were observed in 25% of GFP+ strains, and most mutants had a single change in HPRT. In striking contrast, all mutations arising in the hypermutable GFP+/− strains were small (1- to 2-base) changes, including substitutions, deletions, and insertions (reminiscent of mutagenesis from oxidative damage), and the majority were compound, with an average of four hprt mutations per mutant. The absence of large hprt deletions in DHR strains indicates that DHR does not cause hypermutation. We propose that UV-induced DHR and hypermutation result from a common source, namely, increased oxidative stress. These two forms of delayed genome instability may collaborate in skin cancer initiation and progression.
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Dissertations / Theses on the topic "Genová indukce"

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Link, Emma. "Genome-wide association of statin-induced myopathy." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:ca675486-d678-4200-8bb4-988a923e9c4c.

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Lowering LDL-cholesterol with statin therapy produces substantial reductions in cardiovascular events, and larger cholesterol reductions may produce larger benefits. Rarely, myopathy occurs with statins, especially at higher doses and in combination with certain medications. Similarly strong associations might exist between myopathy with high-dose statin regimens and genetic variants, especially those affecting blood statin levels. This study aimed to find genetic variants associated with statin-induced myopathy. A feasibility study was completed to assess whether plausible effect sizes of 5 to10-fold higher risks per genetic variants could be detected among 50-100 cases with statin-induced myopathy and to consider the best study design. A genome-wide association study was then carried out using approximately 300,000 genetic markers (and additional fine-mapping) in 85 people with definite or incipient myopathy and 90 controls, who were all taking 80mg simvastatin daily in a 12,000 participant trial of 80mg vs 20mg simvastatin daily. The cases were also compared to 2,300 additional controls who had not been exposed to intensive-dose statin therapy. Replication of the myopathy result and lipid-lowering associations were tested in a 20,000 participant trial of 40mg simvastatin daily versus placebo. The genome-wide scan yielded a single strong association (p = 4x10-9) of myopathy with the rs4363657 single nucleotide polymorphism (SNP) located within the SLCO1B1 gene on chromosome 12. This non-coding SNP was in nearly complete linkage disequilibrium (r2=0.97) with the non-synonymous rs4149056 SNP. The population prevalence of the rs4149056 C allele was 15%, and the odds ratio for myopathy was 4.5 (95% confidence interval 2.6 to 7.7) for each copy of the C allele and 16.9 (4.7 to 61.1) for CC vs TT homozygotes. Over 60% of these myopathy cases could be attributed to the C variant. The SLCO1B1 gene encodes the organic anion transport polypeptide OATP1B1, which has been shown to regulate hepatic uptake of statins. In literature reports, rs4149056 reduced statin transport and was associated with 37% (31% to 44%) higher systemic statin acid levels per C allele. The association of rs4149056 with myopathy was replicated in the trial of 40mg simvastatin daily, which also showed that it was associated with the cholesterol-lowering effects of simvastatin. No SNPs in any other region were clearly associated with myopathy (although comparison of the myopathy cases with the 2,300 controls identified a region of chromosome 1p12 that warrants further study). This study identified common variants in SLCO1B1 that influence the risks of statin-induced myopathy substantially. Genotyping these variants may be useful for tailoring both the statin dose and safety monitoring. More generally, such studies of the genetic determinants of serious adverse reactions with other drug classes may help to improve the balance between treatment efficacy and safety.
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Johansson, Caroline. "Genome-wide association study of drug-induced angioedema." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-373135.

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Alrumaihi, Faris Abdulrahman I. "Assessment of UVR-induced DNA damage and repair in nuclear genome versus mitochondrial genome." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37614.

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DNA is a key molecular-target for the deleterious effects of ultraviolet radiation (UVR). Cells contain two types of DNA: nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) and UVR induces various types of damage in the both DNAs, notably CPDs and 8-oxodG. The aim of this thesis is to examine UVR induced DNA damage formation and repair in nDNA and mtDNA and to determine which is the most important genomic target with respect to cell killing in vitro using HaCaT calls as models of human skin. The cell viability data showed that UVB induces significant cell death, which increased over 48 h. SSR-exposure also showed significant levels of cell death after 24 h but with evidence of significant survival after 48 h. Alkaline modified comet assay data showed that CPDs and 8-oxodG were significantly produced in HaCaT cells exposed to UVB and SSR, with CPDs being formed in a greater yields and there being no significant repair of CPDs over 48 h post-exposure to UVB. However, HaCaT cells irradiated with SSR showed significant repair of both CPD and 8-oxodG over 48 h. QPCR data showed that UVB and SSR induced similar profiles of damage in both nDNA and mtDNA; despite the induced damage levels being higher with UVB. The data also showed that nDNA is the main target for UVR in HaCaT cells exposed to UVB and SSR. The UVB-induced QPCR-detectable DNA damage in nDNA and mtDNA was not fully repaired, with a significant level of DNA damage remaining at 48 h, however, there was significant repair of the induced-damage in nDNA post-exposure to SSR (correlating with survival/re-growth), whereas the damage to mtDNA was not fully repaired. The greater lethality of UVB is probably due to more the damage induced and poorer repair (notably of CPD) in nuclear DNA following UVB exposure. Whereas the proficient repair of SSR-induced CPD in nDNA probably dictates survival following SSR exposure – as there was still a notable level of residual damage in mtDNA post-SSR exposure. However, nDNA is the main target for UVR causing DNA damage and may lead to mutations, which increase the risk of skin cancer development.
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Kim, Hyun-Min. "Genome instability induced by triplex forming mirror repeats in S.cerevisiae." Diss., Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/33874.

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The main goal of this research is to understand molecular mechanisms of GAA/TTC-associated genetic instability in a model eukaryotic organism, S. cerevisiae. We demonstrate that expanded GAA/TTC repeats represent a threat to eukaryotic genome integrity by triggering double-strand breaks and gross chromosomal rearrangements. The fragility potential strongly depends on the length of the tracts and orientation of the repeats relative to the replication origin and to block replication fork progression. MutSbeta complex and endonuclease activity of MutLalpha play an important role in facilitation of fragility. In addition to GAA/TTC triplex forming repeats, non-GAA polypurine polypyrimidine mirror repeats that are prone to the formation of similar structures were found to be hotspots for rearrangements in humans and other model organisms. These include H-DNA forming sequences located in the major breakpoint cluster region at BCL2, intron 21 of PKD1, and promoter region of C-MYC. Lastly, we have investigated the effect of the triplex-binding small molecules, azacyanines, on GAA-mediated fragility using the chromosomal arm loss assay. We have found that in vivo, azacyanines stimulate (GAA/TTC)-mediated arm loss in a dose dependent manner in actively dividing cells. Azacyanines treatment enhances the GAA-induced replication arrest. We discovered that also, azacyanines at concentrations that induce fragility also inhibit cell growth. Over 60% of yeast cells are arrested at G2/M stage of the cell cycle. This implies an activation of DNA-damage checkpoint response.
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Yu, Chuanhe. "Genome rearrangement induced by Ac/Ds transposable element in plants." [Ames, Iowa : Iowa State University], 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3389166.

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Schalbetter, Stephanie. "Genome instability induced by structured DNA and replication fork restart." Thesis, University of Sussex, 2012. http://sro.sussex.ac.uk/id/eprint/38853/.

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DNA replication is a central mechanism to all forms of life. Errors occurring during DNA replication can result in mutagenesis and genome rearrangements, which can cause various diseases. In this work I have investigated the stability of direct tandem repeats (TRs) in the context of replication and replication-associated repair mechanisms. During DNA replication the replication fork encounters many obstacles, such as DNA-protein barriers, secondary DNA structures and DNA lesions. How and if replication resumes or restarts in these circumstances in order to complete genome replication is not well understood and the fidelity of replication in response to such obstacles remains unclear. I have developed TR assays to assess replication errors in the context of replication fork restart and secondary structures. The results suggest that structured DNA (G4) can cause instability of TRs in the context of normal replication and that restarted replication can be intrinsically error-prone. Surprisingly, the mutagenic effect of G4-DNA on TR stability was not elevated in the context of replication fork restart. Therefore, deletions of TRs containing G4-DNA are not more susceptible to the compromised fidelity of a restarted replication fork. Structures such as stalled replication forks can induce checkpoint responses to maintain genome stability. The stabilisation of replication forks is central in the response to replication stress. These protective mechanisms include the regulation of enzymatic activities. Mus81-Eme1 is a structure-specific endonuclease which is regulated by the DNA replication checkpoint, but has also been shown to be required for replication fork restart in certain circumstances. In collaboration with Professor Neil McDonald I analysed a novel domain identified in Mus81-Eme1. Mutagenesis of key residues deduced from the protein structure and comparison of their genetic analysis to known phenotypes of Mus81-Eme1 suggests distinct requirements for this domain.
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Li, Xiang. "STRESS-INDUCED GENETIC CHANGE IN FLAX REVEALS GENOME VARIATION MECHANISM." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1565964370435691.

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Johnson, James. "Large scale simulations of genome organisation in living cells." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31206.

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Within every human cell, approximately two meters of DNA must be compacted into a nucleus with a diameter of around ten micrometers. Alongside this daunting storage problem, the 3D organisation of the genome also helps determine which genes are up- or down-regulated, which in turn effects the functionality of the cell itself. While the organisational structure of the genome can be revealed using experimental techniques such as chromosome conformation capture and its high-throughput variant Hi-C, the mechanisms driving this organisation are still unclear. The first two results chapters of this thesis use molecular dynamics simulations to investigate the effect of a potential organisational mechanisms for DNA known as the "bridging-induced attraction". This mechanism involves multivalent DNA-binding proteins bridging genomically distant regions of DNA, which in turn promotes further binding of proteins and compaction of the DNA. In chapter 2 (the first results chapter) we look at a model where proteins can bind non-specifically to DNA, leading to cluster formation for suitable protein-DNA interaction strengths. We also show the effects of protein concentration on the DNA, with a collapse from a swollen to a globular phase observed for suitably high protein concentrations. Chapter 3 develops this model further, using genomic data from the ENCODE project to simulate the "specific binding" of proteins to either active (euchromatin) or inactive (heterochromatin) regions. We were then able to compare contact maps for specific simulated chromosomes with the experimental Hi-C data, with our model reproducing well the topologically associated domains (TADs) seen in Hi-C contact maps. In chapter 4 of the thesis we use numerical methods to study a model for the coupling between DNA topology (in particular, supercoiling in DNA and chromatin) and transcription in a genome. We present details of this model, where supercoiling flux is induced by gene transcription, and can diffuse along the DNA. The probability of transcription is also related to supercoiling, as regions of DNA which are negatively supercoiled have a greater likelihood of being transcribed. By changing the magnitude of supercoiling flux, we see a transition between a regime where transcription is random and a regime where transcription is highly correlated. We also find that divergent gene pairs show increased transcriptional activity, along with transcriptional waves and bursts in the highly correlated regime { all these features are associated with genomes of living organisms.
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Novoa, Carolina. "RecQ-like helicase SGS1 counteracts DNA : RNA hybrid induced genome instability." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/60964.

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Dividing cells are constantly under threat from both endogenous and exogenous DNA damaging stresses that can lead to mutations and structural variations in DNA. One contributor to genome instability is three-stranded DNA:RNA hybrid structures called R-loops. Though R-loops are known to induce DNA damage and DNA replication stress, it is unclear whether they are recognized and processed by an established DNA repair pathway prior to inducing DNA breaks. Canonically, DNA repair proteins work downstream of R-loop-induced DNA damage to stimulate repair and suppress genome instability. Recently, the possibility that some DNA repair pathways actively destabilize R-loops, thus preventing unscheduled DNA damage has emerged. Here we identify the helicase SGS1 as a suppressor of R-loop stability. Our data reveals that SGS1 depleted cells accumulate R-loops. In addition, we define a role for transcription in genome instability of cells lacking SGS1, which is consistent with an R-loop based mechanism. Hyper-recombination in SGS1 mutants is dependent on transcript length, transcription rate, and active DNA replication. Also, rDNA instability in sgs1Δ can be suppressed by ectopic expression of RNaseH1, a protein that degrades DNA:RNA hybrids. Interestingly, R-loops are known to form at rDNA loci. We favour a model in which SGS1 contributes to the stabilization of stalled replication forks associated with transcription complexes, and unresolved DNA:RNA hybrids. Finally, we showed that knockdown of the human Sgs1 orthologue BLM in HCT116 cells also led to the accumulation of more R-loops than control HCT116 cells. In summary, our data supports the idea that some DNA repair proteins involved in replication fork stabilization might also prevent and process R-loops.
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Lee, Jong Wook. "A genome-wide association study of cisplatin-induced hearing loss in children." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/48487.

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Cisplatin is an effective chemotherapeutic agent used for a variety of solid organ malignancies in children and adults. However, its clinical use is limited by the high incidence of cisplatin-induced ototoxicity (CIO), which can affect up to 40-60% of children treated. To date, the genetic basis for CIO has been studied with only focused candidate-gene approaches. Here we report the findings of the first genome-wide association study (GWAS) of cisplatin-induced ototoxicity in children. We examined 738,432 genetics markers in a discovery cohort of 282 Canadian paediatric patients treated with cisplatin, followed by a replication study in an independent Canadian cohort of 82 children. In addition, clinical, therapeutic, and demographic characteristics of cases and controls were analysed to identify clinical factors that may also contribute to the susceptibility to CIO. The genome-wide analyses identified a significant association within the toll-like receptor 4 (TLR4) gene on chromosome 9. The most highly associated single nucleotide polymorphism (SNP) rs960312 conferred a highly protective effect against cisplatin-induced hearing loss (P = 1.19x10-⁸ , odds ratio = 0.22). This variant was subsequently replicated in an independent paediatric cohort (P = 0.018, odds ratio = 0.25). This variant is a tag SNP for a TLR4 promoter haplotype reported to have significantly altered transcriptional efficiency of TLR4. In both cohorts, CIO is significantly associated with younger age (P = 3.41x10-⁶), concomitant vincristine use (P = 2.03x10-¹²), and germ-cell tumour type (P = 4.50x10-⁶). After correcting for these clinical factors, TLR4 rs960312 remains highly associated (Uncorrected P = 1.16x10-⁹ ; Corrected P = 1.01x10-⁹). Several lines of evidence from in vitro and in vivo studies have implicated TLR4 in cisplatin-induced cochlear toxicity and hearing loss. Here we provide the first evidence linking TLR4 and CIO in human patients treated for cancer, leading to new insights into the mechanism underlying this pervasive and clinically limiting adverse drug reaction. The identification of additional markers that contribute to the susceptibility of CIO can be used to develop individualized patient treatments, which can potentially improve safety and treatment outcome of cisplatin.
Medicine, Faculty of
Medical Genetics, Department of
Graduate
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Books on the topic "Genová indukce"

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Levitan, Irwin B., and Leonard K. Kaczmarek. The Neuron. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.001.0001.

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The Fourth Edition of The Neuron provides a comprehensive first course in the cell and molecular biology of nerve cells. It begins with properties of the many newly discovered ion channels that have emerged through mapping of the genome and which shape the way a single neuron generates varied patterns of electrical activity. It also covers the molecular mechanisms that convert electrical activity into the secretion of neurotransmitter hormones at synaptic junctions between neurons. It discusses the biochemical pathways that are linked to the action of neurotransmitters and that can alter the cellular properties of neurons or sensory cells that transduce information from the outside world into the electrical code used by neurons, and the rapidly expanding knowledge of the molecular factors that induce an undifferentiated cell to become a neuron, and then guide it to form appropriate synaptic connections with its partners. Also addressed is the role of ongoing experience and activity in shaping these connections, and the mechanisms thought to underlie the phenomena of learning and memory.
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Казачинская, Е. И. ВИРУС ДЕНГЕ. Академическое изд-во «Гео», 2021. http://dx.doi.org/10.21782/b978-5-6043022-6-2.

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The review is devoted to the analysis of literature data on the history research of dengue fever, the discovery of the etiological infectious agent of this disease-dengue virus and its serotypes. A taxonomic overview of the }lavivirus family, genome organization, structure and function of viral proteins, mosquito species-viral vectors and virus transmission cycles, theories of its origin are presented. As well as the evolution, characteristics and epidemiology of viral serotypes, cellular receptors for dengue virus penetration, pathogenicity for human and factors for the development of severe disease, induced immunity, applied methods and markers for diagnosis, principles of disease treatment and drug development (more information about monoclonal antibodies-potential therapeutic drugs), vaccine options and their effectiveness are considered. The book is intended for students, graduate students, employees of research institutions and universities, as well as doctors involved in the study of }laviviruses and the problem of differential diagnosis of flavivirus infections.
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Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.
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Book chapters on the topic "Genová indukce"

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Woltjen, Knut, Fabian Oceguera-Yanez, Harunobu Kagawa, and Shin-Il Kim. "At the Conflux of Human Genome Engineering and Induced Pluripotency." In Genome Editing, 45–64. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34148-4_3.

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Allen, Christopher P., Akira Fujimori, Ryuichi Okayasu, and Jac A. Nickoloff. "Radiation-Induced Delayed Genome Instability and Hypermutation in Mammalian Cells." In Stress-Induced Mutagenesis, 183–98. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6280-4_9.

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Lu, Xiangyi, Luan Wang, Vincent E. Sollars, Mark D. Garfinkel, and Douglas M. Ruden. "Hsp90 as a Capacitor of Both Genetic and Epigenetic Changes in the Genome During Cancer Progression and Evolution." In Stress-Induced Mutagenesis, 79–101. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6280-4_5.

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Klein, George. "Virus-Induced, Tumour-Associated Antigens." In Ciba Foundation Symposium - Strategy of the Viral Genome, 295–315. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719824.ch17.

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El-Heliebi, Amin, Shukun Chen, and Thomas Kroneis. "Heat-Induced Fragmentation and Adapter-Assisted Whole Genome Amplification Using GenomePlex® Single-Cell Whole Genome Amplification Kit (WGA4)." In Whole Genome Amplification, 101–9. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2990-0_7.

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Golubov, Andrey. "Environmentally Induced Genome Instability and its Inheritance." In Somatic Genome Variation in Animals, Plants, and Microorganisms, 91–101. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118647110.ch5.

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Liu, Juntao, Dawei Liang, Li Yao, Ya Zhang, Chunxia Liu, Yubo Liu, Yanli Wang, et al. "Rice Haploid Inducer Development by Genome Editing." In Methods in Molecular Biology, 221–30. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1068-8_14.

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Sharma, Sharu Paul, and Thomas Peterson. "Rapid Detection of Transposon-Induced Genome Rearrangements." In Methods in Molecular Biology, 131–39. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1134-0_13.

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Sattar, Muhammad Naeem, Zafar Iqbal, Muhammad Nadir Naqqash, S. Mohan Jain, and Jameel M. Al-Khayri. "Induced Mutagenesis in Date Palm (Phoenix dactylifera L.) Breeding." In The Date Palm Genome, Vol. 2, 121–54. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73750-4_7.

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Cullis, Christopher A. "Mechanisms of Induced Inheritable Genome Variation in Flax." In Somatic Genome Variation in Animals, Plants, and Microorganisms, 77–89. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118647110.ch4.

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Conference papers on the topic "Genová indukce"

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Sato, Takumi, Blair Thornton, Tomoko Takahashi, Tetsuo Sakka, Toshihiko Ohki, and Koichi Ohki. "Towards real-time quantification of seawater composition using laser-induced breakdown spectroscopy." In OCEANS 2015 - Genova. IEEE, 2015. http://dx.doi.org/10.1109/oceans-genova.2015.7271743.

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Yang, Yiing Jang, Ching-Sang Chiu, Jeff Chih-Hao Wu, Wen-Der Liang, Steven R. Ramp, D. Benjamin Reeder, and Chi-Fang Chen. "Observations of ambient noises induced by the internal solitary waves on the continental slope of the northern South China Sea:: Ambient noises by ISW in SCS." In OCEANS 2015 - Genova. IEEE, 2015. http://dx.doi.org/10.1109/oceans-genova.2015.7271579.

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Kemna, Stephanie, David A. Caron, and Gaurav S. Sukhatme. "Constraint-induced formation switching for adaptive environmental sampling." In OCEANS 2015. IEEE, 2015. http://dx.doi.org/10.1109/oceans-genova.2015.7271361.

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"Cytokines as markers of oncogenesis and therapy efficiency in chemically induced breast cancer." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-308.

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Zhang, Liping, and Jian S. Dai. "Genome Reconfiguration of Metamorphic Manipulators Based on Lie Group Theory." In ASME 2008 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/detc2008-49906.

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This paper investigates reconfiguration which was induced by topology change as a typical character of metamorphic mechanisms in a way analogous to the concept of genome varation in biological study. Genome is the full complement of genetic information that an organism inherits from its parents, espercially the set of genes they carry. Genome variation is to study the change and variation of this complement with genetic information and genes connectivity and is analogous to mechanisms reconfiguration of metamorphic mechanisms. Metamorphic mechanisms with reconfigurable topology are usually changing their configurations and varying mobility in accordance with different sub-working phase functions. The built-in spatial biological modules are for the first time compiled and introduced in this paper based on metamorphic building blocks in the form of metamorphic cells and associated inside break-down parts as the metamorphic genes for metamorphic bio-modeling as genome. The gene sequencing labels the genetic structure composition principle of the metamorphic manipulators. The bio-inspired mechanism configuration evolution is further introduced in this paper motivated by biological concept to metamorphic characteristics as different sub-phase working mechanisms gradually change and develop into different forms in a particular situation and over a period of time, as an evolutionary process of topological change that takes place over several motion phases during which a taxonomic group of organisms showing the change of their physical characteristics. Moreover, the proposed genetic structure composition principle in metamorphic manipulators leads to the development of module evolution and genetic operations based on the displacement subgroup algebraic properties of the Lie group theory. The topology transformations can further be simulated for configuration evolution and depicted with the genetic growth and degeneration in the living nature. Genome sequential reconfiguration for metamorphic manipulators promises to be mapped from degenerating the source generator to multiple sub-phase configurations. Evolution design illustrations are given to demonstrate the concept and principles.
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Sun, M., B. Rethi, V. Joshua, A. Krishnamurthy, A. Hensvold, SB Catrina, C. Ospelt, et al. "O007 ACPA-induced mobility of primed synovial fibroblasts: the missing link between ACPA-induced bone loss and synovial changes." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.7.

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Wang, L., S. Wang, V. Taneja, and R. Vassallo. "P103 Pro-fibrotic responses induced by thymic stromal lymphopoetin." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.119.

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Matsuda, Koichi, Vinod Kumar, and Yusuke Nakamura. "Abstract 3753: Genome wide association study of HCV-induced hepatocellular carcinoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3753.

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Green, Abby M., Sebastien Landry, James P. Evans, Sophia Shalhout, Ashok S. Bhagwat, and Matthew D. Weitzman. "Abstract 3016: APOBEC3 enzymes induce damage to the cellular genome during DNA replication." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3016.

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"Correlations between lymph concentrations of cytokine and cell morphometric parameters of mesenteric lymph nodes in rats with chemically induced breast cance." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-280.

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