Relevant bibliographies by topics / Genetic, Gene

Contents

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

Academic literature on the topic 'Genetic, Gene'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Genetic, Gene"

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Isobe, N., V. Damotte, V. Lo Re, M. Ban, D. Pappas, L. Guillot-Noel, I. Rebeix, et al. "Genetic burden in multiple sclerosis families." Genes & Immunity 14, no. 7 (August 1, 2013): 434–40. http://dx.doi.org/10.1038/gene.2013.37.

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Robinson, P. C., P. J. Leo, J. J. Pointon, J. Harris, K. Cremin, L. A. Bradbury, S. Stebbings, et al. "The genetic associations of acute anterior uveitis and their overlap with the genetics of ankylosing spondylitis." Genes & Immunity 17, no. 1 (November 26, 2015): 46–51. http://dx.doi.org/10.1038/gene.2015.49.

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A, Shahin. "The Role of Genetic Mutations in Gene MTHFR in Anencephaly Syndrome." Journal of Embryology & Stem Cell Research 3, no. 1 (2019): 1–5. http://dx.doi.org/10.23880/jes-16000117.

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McGEE, GLENN. "Gene Patents Can Be Ethical." Cambridge Quarterly of Healthcare Ethics 7, no. 4 (October 1998): 417–21. http://dx.doi.org/10.1017/s0963180198004125.

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When one examines the emerging debate about genetic patenting, it becomes clear that those who oppose so-called “gene patents” misunderstand genetics or apply inappropriate moral and jurisprudential theory. In this brief essay I examine some arguments against gene patents of the “methods for detection” variety, and conclude that patents on methods for detecting the presence of a genetic correlation with disease-related (and other) phenotypes can be appropriate, and that with several precautions the U.S. Patent and Trademark Office should continue granting patent protection to investigators who generate genetic disease diagnostic innovations.
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Berghout, J., S. Higgins, C. Loucoubar, A. Sakuntabhai, K. C. Kain, and P. Gros. "Genetic diversity in human erythrocyte pyruvate kinase." Genes & Immunity 13, no. 1 (August 11, 2011): 98–102. http://dx.doi.org/10.1038/gene.2011.54.

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Sabbagh, A., P. Luisi, E. C. Castelli, L. Gineau, D. Courtin, J. Milet, J. D. Massaro, et al. "Worldwide genetic variation at the 3′ untranslated region of the HLA-G gene: balancing selection influencing genetic diversity." Genes & Immunity 15, no. 2 (December 19, 2013): 95–106. http://dx.doi.org/10.1038/gene.2013.67.

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Fang, Fang, Zhe Xu, Yue Suo, Hui Wang, Si Cheng, Hao Li, Wei Li, and Yongjun Wang. "Gene panel for Mendelian strokes." Stroke and Vascular Neurology 5, no. 4 (April 26, 2020): 416–21. http://dx.doi.org/10.1136/svn-2020-000352.

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BackgroundMendelian stroke causes nearly 7% of ischaemic strokes and is also an important aetiology of cryptogenic stroke. Identifying the genetic abnormalities in Mendelian strokes is important as it would facilitate therapeutic management and genetic counselling. Next-generation sequencing makes large-scale sequencing and genetic testing possible.MethodsA systematic literature search was conducted to identify causal genes of Mendelian strokes, which were used to construct a hybridization-based gene capture panel. Genetic variants for target genes were detected using Illumina HiSeq X10 and the Novaseq platform. The sensitivity and specificity were evaluated by comparing the results with Sanger sequencing.Results53 suspected patients of Mendelian strokes were analysed using the panel of 181 causal genes. According to the American College of Medical Genetics and Genomics standard, 16 likely pathogenic/variants of uncertain significance genetic variants were identified. Diagnostic testing was conducted by comparing the consistency between the results of panel and Sanger sequencing. Both the sensitivity and specificity were 100% for the panel.ConclusionThis panel provides an economical, time-saving and labour-saving method to detect causal mutations of Mendelian strokes.
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Kalefetoğlu Macar1, Tuğçe, Oksal Macar, Emine Yalçın, and Kültiğin Çavuşoğlu. "Gene Technology and Plant Genetic Transformation Methods." Afyon Kocatepe University Journal of Sciences and Engineering 17, no. 2 (August 1, 2017): 377–92. http://dx.doi.org/10.5578/fmbd.58669.

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Pekmezović, Tatjana. "Gene-Environment Interaction: A Genetic-Epidemiological Approach." Journal of Medical Biochemistry 29, no. 3 (July 1, 2010): 131–34. http://dx.doi.org/10.2478/v10011-010-0021-z.

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Gene-Environment Interaction: A Genetic-Epidemiological ApproachClassical epidemiology addresses the distribution and determinants of diseases in populations, and the factors associated with disease causation, with the aim of preventing disease. Both genetic and environmental factors may contribute to susceptibility, and it is still unclear how these factors interact in their influence on risk. Genetic epidemiology is the field which incorporates concepts and methods from different disciplines including epidemiology, genetics, biostatistics, clinical and molecular medicine, and their interaction is crucial to understanding the role of genetic and environmental factors in disease processes. The study of gene-environment interaction is central in the field of genetic epidemiology. Gene-environment interaction is defined as »a different effect of an environmental exposure on disease risk in persons with different genotypes,« or, alternatively, »a different effect of a genotype on disease risk in persons with different environmental exposures.« Five biologically plausible models are described for the relations between genotypes and environmental exposures, in terms of their effects on disease risk. Therefore, the study of gene-environment interaction is important for improving accuracy and precision in the assessment of both genetic and environmental factors, especially in disorders of less defined etiology. Genetic epidemiology is also applied at the various levels of disease prevention.
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Lu, R., G. S. Vidal, J. A. Kelly, A. M. Delgado-Vega, X. K. Howard, S. R. Macwana, N. Dominguez, et al. "Genetic associations of LYN with systemic lupus erythematosus." Genes & Immunity 10, no. 5 (April 16, 2009): 397–403. http://dx.doi.org/10.1038/gene.2009.19.

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Dissertations / Theses on the topic "Genetic, Gene"

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Button, Eric A. "Regulation of T-DNA gene 7." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26177.

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The purpose of this study was two-fold. The first objective was to determine if Saccharomyces cerevisiae is a useful system for investigating the expression of T-DNA (it takes several months to obtain sufficient bacteria-free transformed plant tissue to investigate T-DNA transcription). A short fragment of T-DNA carrying T-DNA gene 7 was cloned into a yeast plasmid in an attempt to investigate the expression of gene 7 in yeast. The second objective was to determine the significance of a heat shock related sequence identified in the 5¹ region of T-DNA gene 7. Primer extension analysis, SI nuclease mapping, and Northern hybridizations indicate that transcription of T-DNA gene 7 in yeast is different from that of transcription of gene 7 in crown gall tumors. Transcription is different because the distance between the TATA box and the transcription initiation sites must be at least 40 nucleotides in yeast. Therefore, Saccharomyces cerevisiae does not appear to be a useful system for investigating the expression of T-DNA. Crown gall tumors were subjected to a number of stress agents, including heat shock, to determine the significance of the heat shock related sequence identified in gene 7. Primer extension analyses indicate that only cadmium and mercury have a significant effect on the expression of T-DNA gene 7. Although gene 7 responds to cadmium and mercury, the increase in transcription does not appear to be heat shock or metallothionein related, indicating that another mechanism is involved in the enhanced transcription of T-DNA gene 7 in crown gall tumors.
Medicine, Faculty of
Medical Genetics, Department of
Graduate
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Heilbronn, Leonie Kaye. "Gene/environment interactions in human obesity." Title page, table of contents and summary only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phh466.pdf.

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Sturm, Richard Alan. "Control mechanisms of higher eukaryotic gene transcription--divergent histone genes /." Title page, contents and abstract only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phs936.pdf.

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Purohit, Shri Kant. "Analysis of nodulin-44 gene of soybean." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66088.

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Lonie, Andrew. "Cloning and characterisation of the Polycomblike gene, a transacting repressor of homeotic gene expression in Drosophila." Title page, contents and summary only, 1994. http://hdl.handle.net/2440/21504.

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Includes bibliographies.
{59} leaves : ill. ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
The Polycomblike gene of Drosophila melanogaster is required for the correct spatial expression of the homeotic genes of Antenapaedia and Bithorax Complexes. This thesis describes the isolation and molecular characterization of the Polycomblike gene.
Thesis (Ph.D.)--University of Adelaide, Dept. of Biochemistry, 1995
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Nicholls, Felicity K. M. "Genetic analysis of the gene Additional sex combs and interacting loci." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29644.

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In order to recover new mutant alleles of the Polycomb group gene Additional sex combs (Asx), mutagenized chromosomes were screened over the putative Asx allele XT129. Thirteen new mutant strains that fail to complement XT129 were recovered. Unexpectedly, the thirteen strains sorted into four complementation groups. Recombination mapping suggests that each complementation group represents a separate locus. The largest group fails to complement a deletion of Asx and maps in the vicinity of 2-72, the published location of Asx. All new mutant strains enhance the phenotype of Polycomb mutant flies and are not allelic to any previously discovered second chromosome Polycomb group genes. Therefore, the new mutants may be considered putative new members of the Polycomb group. This study suggests that Asx belongs to a sub-group of genes displaying intergenic non-complementation.
Science, Faculty of
Zoology, Department of
Graduate
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Greenberg, Norman Michael. "Cellulase gene transcription in Cellulomonas fimi and an Agrobacterium." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28836.

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Transcriptional analysis was used to investigate the molecular mechanisms which effect cellulase gene expression in the gram-positive bacterium Cellulomonas fimi strain ATCC 484 and the gram-negative bacterium Agrobacterium sp. strain ATCC 21400. The cenA, cex and cenB genes of C. fimi encoding the extracellular β-1,4-endoglucanase, EngA (EC 3.2.1.4; Mr 48,700), the extracellular β-1, 4-exoglucanase, Exg (EC 3.2.1.91; Mr 47,300) and the extracellular β-1,4-endoglucanase EngB (EC 3.2.1.4; Mr 110,000) respectively, were characterised. By northern blot analysis, cenA mRNA was detected in C. fimi RNA prepared from glycerol- and carboxymethylcellulose (CMC)-grown cells but not in RNA from glucose-grown cells. The cex mRNA was found only in RNA from CMC-grown cells. The cenB mRNA was found in all three preparations of RNA. Therefore, the expression of these genes is subject to regulation by the carbon source provided to C. fimi. High resolution nuclease SI protection studies with unique 5'-labeled DNA probes and C. fimi RNA isolated in vivo, were used to map the 5' termini of cenA and cex mRNAs. Two cenA mRNA 5' ends, 11 bases apart, mapped 51 and 62 bases upstream of the cenA start codon, suggesting that in vivo, cenA transcription was directed from two promoters in tandem. The cex mRNA 5' end was found to map 28 bases upstream of the cex start codon. Using SI mapping with unlabeled DNA probes and C. fimi RNA which had been isolatedin vivo but which had been 5'-labeled in vitro with vaccinia virus capping enzyme confirmed that true transcription initiation sites for cenA and cex mRNA had been identified. The SI mapping revealed mRNA 3' termini 1,438, 1,449, and 1, 464 bases from the major cenA start site, and one 3' terminus 1,564 bases from the major cex mRNA start site, in good agreement with the northern blot data. High resolution SI studies were also used to show that abundant mRNA 5' ends mapped upstream of the cenB start codon in RNA prepared from CMC-grown cells, while less-abundant species mapped 52 bases closer to the ATG codon in RNA prepared from C. fimi grown on any one of the three substrates. These results seem to indicate a tandem promoter arrangement with an ATG-proximal promoter directing low-level constitutive cenB transcription and a more distal promoter directing higher levels of cenB transcription as a result of C. fimi growth on cellulosic substrate. Steady- state levels were determined for cenA, cex and cenB mRNAs with RNA prepared from glycerol-, glucose-, and CMC-grown cultures of C. fimi in slot-blot hybridisations with radiolabeled oligodeoxyribonucleotide probes. A cex-linked gene (clg) was identified by sequence inspection and SI mapping. Transcripts of the abg gene encoding the β-glucosidase (Abg, EC 3.2.2.21/ Mr 50,000) of Agrobacterium sp. strain ATCC 21400 were also characterised. Northern blot analysis of Agrobacterium RNA revealed the size of the in vivo abgmRNA was approximately 1,500 bases in length. High resolution SI mapping determined abg mRNA 5' ends 22 bases upstream of the abg ATG codon and 3' ends 71 bases downstream of the abg stop codon.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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Melville, Scott Andrew Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Disease gene mapping in border collie dogs." Awarded by:University of New South Wales. School of Biotechnology and Biomolecular Sciences, 2006. http://handle.unsw.edu.au/1959.4/25511.

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Pedigree dog breeds are genetically isolated and inbred populations with characteristics specific to each breed. Some breeds carry genetic diseases which affect the health of the animals, but may also serve as a valuable model to identify genes involved in human disease. In the Border Collie breed in Australia, the identification of two disease genes would enable breeders to DNA test their animals and prevent future cases. Over 530 samples were collected to identify the genes responsible for these diseases through linkage mapping and candidate gene approaches. Collie Eye Anomaly (CEA) defines a group of symptoms that cause the incorrect development of different regions within the eye, and may also result in the detachment of the retina. The presence of the disease in different breeds of collies suggests that the disease originated before the differentiation of the collie breeds. The CEA gene was mapped to a region of CFA37, but the disease gene was identified by another research group. Neuronal Ceroid Lipofuscinosis (NCL) is a fatal neurodegenerative disorder that affects Border Collie dogs from approximately 16 months of age. The disease is inherited in an autosomal recessive manner and affected animals display a range of physiological and behavioural symptoms that include loss of muscular control, nervousness and sometimes aggression. Due to the debilitating nature of the disease, dogs rarely survive beyond 28 months of age. Microsatellite markers were used to exclude the Border Collie NCL gene from the region of the English Setter NCL gene (homolog of human NCL gene CLN8). Further work mapped the disease gene to CFA22, in a region containing the homolog for CLN5, one of the identified human disease genes for NCL. Subsequent sequencing of canine CLN5 revealed a nonsense mutation (c.619C>T, Q206X) that co-segregated with NCL in Border Collie pedigrees. This truncation mutation resulted in a protein product of similar size to some mutations identified in human CLN5 and therefore the Border Collie may make a good model for future NCL studies. With DNA testing now available, breeders of Border Collies can now ensure that no animal will die of NCL.
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Ganesan, Savita Ayre Brian Gordon. "FLP-mediated conditional loss of an essential gene to facilitate complementation assays." [Denton, Tex.] : University of North Texas, 2007. http://digital.library.unt.edu/permalink/meta-dc-5180.

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Dibbens, Justin Andrew. "Studies on the control of late gene transcription in coliphage 186 /." Title page, contents and summary only, 1990. http://web4.library.adelaide.edu.au/theses/09PH/09phd543.pdf.

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Books on the topic "Genetic, Gene"

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Genes and gene regulation. London: Edward Arnold, 1989.

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W, Bennett J., Lasure Linda L, American Society for Microbiology, Miles Laboratories, and Conference on Gene Manipulations in Fungi (1983 : South Bend, Ind.), eds. Gene manipulations in fungi. Orlando: Academic Press, 1985.

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The century of the gene. Cambridge, Mass: Harvard University Press, 2000.

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Raju, Kucherlapati, ed. Gene transfer. New York: Plenum Press, 1986.

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Maurizio, Federico, ed. Lentivirus gene engineering protocols. Totowa, N.J: Humana Press, 2003.

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Gene control. New York: Garland Science, 2010.

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Dr, Cooper David N., and Lemoine Nicholas R, eds. Gene therapy. Oxford, UK: Bios Scientific Publishers, 1996.

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A, Veitia Reiner, ed. The biology of genetic dominance. Georgetown, Tex: Landes Bioscience, 2005.

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F, Millot, and Francis J. L. 1952-, eds. Genetic biochemistry: From gene to protein. Chichester: Ellis Horwood, 1988.

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Gene defense: A fictional genetic thriller. [Bloomington, IN]: Xlibris Corporation, 2010.

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Book chapters on the topic "Genetic, Gene"

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Zheng, Gang, Yaning Yang, Xiaofeng Zhu, and Robert C. Elston. "Gene-Gene Interactions." In Analysis of Genetic Association Studies, 235–56. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2245-7_8.

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Cornetta, Kenneth. "Gene Therapy." In Molecular Genetic Pathology, 717–29. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-405-6_29.

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Jefferson, Richard A. "Plant Reporter Genes: The Gus Gene Fusion System." In Genetic Engineering, 247–63. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-7081-3_13.

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Kmiec, Eric B., Allyson Cole-Strauss, Michael C. Rice, and Pamela Havre. "Genetic Correction for Gene Therapy." In Gene Therapy, 111–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72160-1_12.

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Lai, Chen-Ching, and Wen-Hwa Lee. "Human Retinoblastoma Susceptibility Gene." In Genetic Engineering, 21–35. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0641-2_2.

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Kolesar, Jill M., and John G. Kuhn. "Capillary Electrophoresis for Quantitative Genetic Analysis." In Gene Quantification, 79–96. Boston, MA: Birkhäuser Boston, 1998. http://dx.doi.org/10.1007/978-1-4612-4164-5_5.

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Wynshaw-Boris, Anthony, Carrolee Barlow, Amy Chen, Michael Gambello, Lisa Garrett, Theresa Hernandez, Shinji Hirotsune, et al. "Modeling Genetic Diseases in the Mouse." In Gene Therapy, 37–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72160-1_3.

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Horser, Cathryn, David Abbott, Varsha Wesley, Neil Smith, and Peter Waterhouse. "Gene Silencing - Principles And Application." In Genetic Engineering, 239–56. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0721-5_11.

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Moseley, A. B., and C. T. Caskey. "Prospects for Human Gene Therapy." In Genetic Engineering, 213–23. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4899-1666-2_10.

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Kado, Clarence I. "Agrobacterium-Mediated Horizontal Gene Transfer." In Genetic Engineering, 1–24. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-1739-3_1.

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Conference papers on the topic "Genetic, Gene"

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Sharma, Jai, and Vidhyacharan Bhaskar. "An Rna Sequencing Analysis of Glaucoma Genesis in Mice." In 12th International Conference on Artificial Intelligence, Soft Computing and Applications. Academy and Industry Research Collaboration Center (AIRCC), 2022. http://dx.doi.org/10.5121/csit.2022.122306.

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Glaucoma is the leading cause of irreversible blindness in people over the age of 60, accounting for 6.6 to 8% of all blindness in 2010, but there is still much to be learned about the genetic origins of the eye disease. With the modern development of Next-Generation Sequencing (NGS) technologies, scientists are starting to learn more about the genetic origins of Glaucoma. This research uses differential expression (DE) and gene ontology (GO) analyses to study the genetic differences between mice with severe Glaucoma and multiple control groups. Optical nerve head (ONH) and retina data samples of genome-wide RNA expression from NCBI (NIH) are used for pairwise comparison experimentation. In addition, principal component analysis (PCA) and dispersion visualization methods are employed to perform quality control tests of the sequenced data. Genes with skewed gene counts are also identified, as they may be marker genes for a particular severity of Glaucoma. The gene ontologies found in this experiment support existing knowledge of Glaucoma genesis, providing confidence that the results were valid. Future researchers can thoroughly study the gene lists generated by the DE and GO analyses to find potential activator or protector genes for Glaucoma in mice to develop drug treatments or gene therapies to slow or stop the progression of the disease. The overall goal is that in the future, such treatments can be made for humans as well to improve the quality of life for human patients with Glaucoma and reduce Glaucoma blindness rates.
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Fabri, Júlia Campos, Maria Julia Filgueiras Granato, Maria Clara Lopes Rezende, Maria Luiza Franco de Oliveira, and Leandro de Souza Cruz. "The impact of genetic polymorphism in pain mechanisms." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.708.

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Background:Variations in genes codifying target structures in the nociceptive pathway can result in pain attenuation or increase.Objective:Investigate the genetic polymorphism influence in the individual pain threshold. Methods: Search on PubMed with the terms “genetic”, “pain” and its synonyms published in the last 10 years. Results:The subjective and individual mechanisms of pain aren’t completely understood, but genetic susceptibility is one of the hypothesis to explain these differences.The KCNK18 gene influences the synaptic transmission by producing potassium channel protein that equalizes resting membrane potential, calcineurin activated and inhibited by arachidonic acid. This gene was found more frequently in migraine individuals. The COMT gene increase the sensibility to pain by met-enkephalins reduction and/or catecholamine elevation. Its activity’s reduced in fibromyalgia patients. However, the OPRM1 gene, an opioid receptor, was found in individuals with a higher pain threshold.Furthermore, studies with human cell culture shows the analgesic role of the gene A118G, by its greater binding affinity for β-endorphin.It is associated with more effective endorphinergic endogenous pain inhibition. Conclusion:Researches indicates a striking participation of genetic polymorphism in pain mechanisms. The knowledge about genetic variables on pain perception can contribute to the development of individualized analgesic protocols and therapeutic strategies, accordantly to the patient genetic profile. This evolution becomes fundamental in a population that tend to the indiscriminate use of analgesics.
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Lutze, Margaret, Curtis R. Brandt, Vivianne C. Smith, Joel Pokorny, and Ron G. Gregg. "Genetic studies of normal color vision." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1989. http://dx.doi.org/10.1364/oam.1989.fa3.

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We have studied the familial transmissions of Rayleigh match midpoints and photometric matches (667-551 nm) in observers with normal color vision to assess genetic bases for these two color vision traits (Lutze et al., in press). We first employed segregation analysis to evaluate whether each trait was consistent with determination by allelic variation of a single gene, by multiple genes (polygenic), or by environmental factors. We found that each trait was consistent with determination by a single gene. Blood samples were obtained from the majority of family members tested and DNA was isolated for use in molecular genetic analysis. We are using Southern blot analysis to determine whether the visual pigment genes on the X-chromosome may be responsible for the variation observed in the two color vision traits. To begin this evaluation, we chose to use a highly polymeric, established X-chromosome marker (St14) that is located very close to the visual pigment genes in a linkage analysis.
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Wilson, Mary E., Lina M. González, Warren C. Ruder, and Philip R. LeDuc. "Engineering Magnetic Nanomaterial Production in Magnetotactic Bacteria Through Gene Regulation." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80446.

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Magnetotactic bacteria endogenously synthesize intracellular magnetic nanoparticles (magnetosomes); however, little is known regarding the genetic regulatory networks that control magnetosome production. In this paper, we explore the genetic response of Magnetospirillum magneticum strain AMB-1 to an applied electromagnetic field as a means to identify genes activated by magnetic stimulation. The expression of magnetosome island, flagellar and cytoskeletal genes was found to be differentially altered by magnetic stimulation at short and long times points. These results indicate previously uncharacterized endogenous gene network modules that could be exploited to engineer magnetic bacteria as magnetic nanomaterial producing-machines through gene regulation.
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SOMOGYI, ROLAND, and HIROAKI KITANO. "GENE EXPRESSION AND GENETIC NETWORKS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 1998. http://dx.doi.org/10.1142/9789814447300_0001.

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Jimenez, Ray Duenas, David Correa Martins, and Carlos Silva Santos. "Gene Networks Inference through One Genetic Algorithm Per Gene." In 2014 14th IEEE International Conference on Bioinformatics and Bioengineering (BIBE). IEEE, 2014. http://dx.doi.org/10.1109/bibe.2014.9.

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Cussat-Blanc, Sylvain, and Wolfgang Banzhaf. "Introduction to Gene Regulatory Networks." In GECCO '15: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2739482.2756586.

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Cussat-Blanc, Sylvain, and Wolfgang Banzhaf. "Introduction to gene regulatory networks." In GECCO '17: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3067695.3067728.

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Vesnina, Anna. "INFLUENCE OF GENETIC FEATURES ON THE DEVELOPMENT OF ATHEROSCLEROSIS." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-22.

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In the course of the work, it was found that a large number of genetic features affect the development of atherosclerosis (gene SNPs, telomere length, epigenetic factors, circadian rhythms). Studies of SNP genes, in particular those affecting lipid metabolism, predominate. Relatively new is the study of the relationship between chrononutrition and the development of metabolic diseases.
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Atkinson, Timothy, Detlef Plump, and Susan Stepney. "Evolving graphs with horizontal gene transfer." In GECCO '19: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3321707.3321788.

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Reports on the topic "Genetic, Gene"

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Zephyr, Yvelande, and Susan Walsh. Exploring Genetic Variation in a Caffeine Amplification Gene. Genetics Society of America Peer-Reviewed Education Portal (GSA PREP), March 2015. http://dx.doi.org/10.1534/gsaprep.2015.001.

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Michelmore, Richard, Eviatar Nevo, Abraham Korol, and Tzion Fahima. Genetic Diversity at Resistance Gene Clusters in Wild Populations of Lactuca. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7573075.bard.

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Genetic resistance is often the least expensive, most effective, and ecologically-sound method of disease control. It is becoming apparent that plant genomes contain large numbers of disease resistance genes. However, the numbers of different resistance specificities within a genepool and the genetic mechanisms generating diversity are poorly understood. Our objectives were to characterize diversity in clusters of resistance genes in wild progenitors of cultivated lettuce in Israel and California in comparison to diversity within cultivated lettuce, and to determine the extent of gene flow, recombination, and genetic instability in generating variation within clusters of resistance genes. Genetic diversity of resistance genes was analyzed in wild and cultivated germplasm using molecular markers derived from lettuce resistance gene sequences of the NBS-LRR type that mapped to the major cluster if resistance genes in lettuce (Sicard et al. 1999). Three molecular markers, one microsatellite marker and two SCAR markers that amplified LRR- encoding regions, were developed from sequences of resistance gene homologs at the Dm3 cluster (RGC2s) in lettuce. Variation for these markers was assessed in germplasm including 74 genotypes of cultivated lettuce, L. saliva and 71 accessions of the three wild Lactuca spp., L. serriola, L. saligna and L. virosa that represent the major species in the sexually accessible genepool for lettuce. Diversity was also studied within and between natural populations of L. serriola from Israel and California. Large numbers of haplotypes were detected indicating the presence of numerous resistance genes in wild species. We documented a variety of genetic events occurring at clusters of resistance genes for the second objective (Sicard et al., 1999; Woo el al., in prep; Kuang et al., in prepb). The diversity of resistance genes in haplotypes provided evidence for gene duplication and unequal crossing over during the evolution of this cluster of resistance genes. Comparison of nine resistance genes in cv. Diana identified 22 gene conversion and five intergenic recombinations. We cloned and sequenced a 700 bp region from the middle of RGC2 genes from six genotypes, two each from L. saliva, L. serriola, and L. saligna . We have identified over 60 unique RGC2 sequences. Phylogenetic analysis surprisingly demonstrated much greater similarity between than within genotypes. This led to the realization that resistance genes are evolving much slower than had previously been assumed and to a new model as to how resistance genes are evolving (Michelmore and Meyers, 1998). The genetic structure of L. serriola was studied using 319 AFLP markers (Kuang et al., in prepa). Forty-one populations from Turkey, Armenia, Israel, and California as well as seven European countries were examined. AFLP marker data showed that the Turkish and Armenian populations were the most polymorphic populations and the European populations were the least. The Davis, CA population, a recent post-Columbian colonization, showed medium genetic diversity and was genetically close to the Turkish populations. Our results suggest that Turkey - Armenia may be the center of origin and diversity of L. serriola and may therefore have the greatest diversity of resistance genes. Our characterization of the diversity of resistance genes and the genetic mechanisms generating it will allow informed exploration, in situ and ex situ conservation, and utilization of germplasm resources for disease control. The results of this project provide the basis for our future research work, which will lead to a detailed understanding of the evolution of resistance genes in plants.
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Reichardt, Juergen K. Genetic Variation in the HSD3B2 Gene and Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada427886.

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Knoll, Kenneth M. Genetic Methods for Rapid Gene Localization in Hyperthermophilic Eubacteria. Fort Belvoir, VA: Defense Technical Information Center, August 1993. http://dx.doi.org/10.21236/ada276062.

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Reichardt, Juergen. Genetic Variation in the HSD3B2 Gene and Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada419804.

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Fluhr, Robert, and Volker Brendel. Harnessing the genetic diversity engendered by alternative gene splicing. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7696517.bard.

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Our original objectives were to assess the unexplored dimension of alternative splicing as a source of genetic variation. In particular, we sought to initially establish an alternative splicing database for Arabidopsis, the only plant for which a near-complete genome has been assembled. Our goal was to then use the database, in part, to advance plant gene prediction programs that are currently a limiting factor in annotating genomic sequence data and thus will facilitate the exploitation of the ever increasing quantity of raw genomic data accumulating for plants. Additionally, the database was to be used to generate probes for establishing high-throughput alternative transcriptome analysis in the form of a splicing-specific oligonucleotide microarray. We achieved the first goal and established a database and web site termed Alternative Splicing In Plants (ASIP, http://www.plantgdb.org/ASIP/). We also thoroughly reviewed the extent of alternative splicing in plants (Arabidopsis and rice) and proposed mechanisms for transcript processing. We noted that the repertoire of plant alternative splicing differs from that encountered in animals. For example, intron retention turned out to be the major type. This surprising development was proven by direct RNA isolation techniques. We further analyzed EST databases available from many plants and developed a process to assess their alternative splicing rate. Our results show that the lager genome-sized plant species have enhanced rates of alternative splicing. We did advance gene prediction accuracy in plants by incorporating scoring for non-canonical introns. Our data and programs are now being used in the continuing annotation of plant genomes of agronomic importance, including corn, soybean, and tomato. Based on the gene annotation data developed in the early part of the project, it turned out that specific probes for different exons could not be scaled up to a large array because no uniform hybridization conditions could be found. Therefore, we modified our original objective to design and produce an oligonucleotide microarray for probing alternative splicing and realized that it may be reasonable to investigate the extent of alternative splicing using novel commercial whole genome arrays. This possibility was directly examined by establishing algorithms for the analysis of such arrays. The predictive value of the algorithms was then shown by isolation and verification of alternative splicing predictions from the published whole genome array databases. The BARD-funded work provides a significant advance in understanding the extent and possible roles of alternative splicing in plants as well as a foundation for advances in computational gene prediction.
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Shani, Moshe, and C. P. Emerson. Genetic Manipulation of the Adipose Tissue via Transgenesis. United States Department of Agriculture, April 1995. http://dx.doi.org/10.32747/1995.7604929.bard.

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The long term goal of this study was to reduce caloric and fat content of beef and other red meats by means of genetic modification of the animal such that fat would not be accumulated. This was attempted by introducing into the germ line myogenic regulatory genes that would convert fat tissue to skeletal muscle. We first determined the consequences of ectopic expression of the myogenic regulatory gene MyoD1. It was found that deregulation of MyoD1 did not result in ectopic skeletal muscle formation but rather led to embryonic lethalities, probably due to its role in the control of the cell cycle. This indicated that MyoD1 should be placed under stringent control to allow survival. Embryonic lethalities were also observed when the regulatory elements of the adipose-specific gene adipsin directed the expression of MyoD1 or myogenin cDNAs, suggesting that these sequences are probably not strong enough to confer tissue specificity. To determine the specificity of the control elements of another fat specific gene (adipocyte protein 2-aP2), we fused them to the bacterial b-galactosidase reporter gene and established stable transgenic strains. The expression of the reporter gene in none of the strains was adipose specific. Each strain displayed a unique pattern of expression in various cell lineages. Most exciting results were obtained in a transgenic strain in which cells migrating from the ventro-lateral edge of the dermomyotome of developing somites to populate the limb buds with myoblasts were specifically stained for lacZ. Since the control sequences of the adipsin or aP2 genes did not confer fat specificity in transgenic mice we have taken both molecular and genetic approaches as an initial effort to identify genes important in the conversion of a multipotential cell such as C3H10T1/2 cell to adipoblast. Several novel adipocyte cell lines have been established that differ in the expression of transcription factors of the C/EBP family known to be markers for adipocyte differentiation. These studies revealed that one of the genetic programming changes which occur during 10T1/2 conversion from multipotential cell to a committed adipoblast is the ability to linduce C/EBPa gene expression. It is expected that further analysis of this gene would identify elements which regulate this lineage-specific expression. Such elements might be good candidates in future attempts to convert adipoblasts to skeletal muscle cells in vivo.
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Mohan, Subburaman. Molecular Genetic and Gene Therapy Studies of the Musculoskeletal System. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada512941.

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Mohan, Subburaman. Molecular Genetic and Gene Therapy Studies of the Musculoskeletal System. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada469196.

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Mohan, Subburaman. Molecular Genetic and Gene Therapy Studies of the Musculoskeletal System. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada469369.

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