Relevant bibliographies by topics / Mice – Genetics

Academic literature on the topic 'Mice – Genetics'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Mice – Genetics"

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Nilsson, Annika I., Elisabeth Kugelberg, Otto G. Berg, and Dan I. Andersson. "Experimental Adaptation ofSalmonella typhimuriumto Mice." Genetics 168, no. 3 (November 2004): 1119–30. http://dx.doi.org/10.1534/genetics.104.030304.

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Cook, Donald N., Gregory S. Whitehead, Lauranell H. Burch, Katherine G. Berman, Zareen Kapadia, Christine Wohlford-Lenane, and David A. Schwartz. "Spontaneous Mutations in Recombinant Inbred Mice: Mutant Toll-like Receptor 4 (Tlr4) in BXD29 Mice." Genetics 172, no. 3 (December 1, 2005): 1751–55. http://dx.doi.org/10.1534/genetics.105.042820.

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Jasny, B. "MOLECULAR GENETICS: Making Mito-Mice." Science 290, no. 5492 (October 27, 2000): 673a—673. http://dx.doi.org/10.1126/science.290.5492.673a.

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Kono, Dwight H., and Argyrios N. Theofilopoulos. "Genetics of SLE in mice." Springer Seminars in Immunopathology 28, no. 2 (September 14, 2006): 83–96. http://dx.doi.org/10.1007/s00281-006-0030-7.

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Landel, C. P., S. Chen, and G. A. Evans. "Reverse Genetics Using Transgenic Mice." Annual Review of Physiology 52, no. 1 (October 1990): 841–51. http://dx.doi.org/10.1146/annurev.ph.52.030190.004205.

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Legarra, Andrés, Christèle Robert-Granié, Eduardo Manfredi, and Jean-Michel Elsen. "Performance of Genomic Selection in Mice." Genetics 180, no. 1 (August 30, 2008): 611–18. http://dx.doi.org/10.1534/genetics.108.088575.

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Clarke, Angus. "Genetic imprinting in clinical genetics." Development 108, Supplement (April 1, 1990): 131–39. http://dx.doi.org/10.1242/dev.108.supplement.131.

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Genetic, and indeed genomic, imprinting does occur in humans. This is manifest at the level of the genome, the individual chromosome, subchromosomal region or fragile site, or the single locus. The best evidence at the single gene level comes from a consideration of familial tumour syndromes. Chromosomal imprinting effects are revealed when uniparental disomy occurs, as in the Prader-Willi syndrome and doubtless other sporadic, congenital anomaly syndromes. Genomic imprinting is manifest in the developmental defects of hydatidiform mole, teratoma and triploidy. Fragile (X) mental retardation shows an unusual pattern of inheritance, and imprinting can account for these effects. Future work in clinical genetics may identify congenital anomalies and growth disorders caused by imprinting: the identification of imprinting effects for specific chromosomal regions in mice will allow the examination of the homologous chromosomal region in humans.
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Lee, G. H., L. M. Bennett, R. A. Carabeo, and N. R. Drinkwater. "Identification of hepatocarcinogen-resistance genes in DBA/2 mice." Genetics 139, no. 1 (January 1, 1995): 387–95. http://dx.doi.org/10.1093/genetics/139.1.387.

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Abstract Male DBA/2J mice are approximately 20-fold more susceptible than male C57BL/6J mice to hepatocarcinogenesis induced by perinatal treatment with N,N-diethylnitrosamine (DEN). In order to elucidate the genetic control of hepatocarcinogenesis in DBA/2J mice, male BXD recombinant inbred, D2B6F1 x B6 backcross, and D2B6F2 intercross mice were treated at 12 days of age with DEN and liver tumors were enumerated at 32 weeks. Interestingly, the distribution of mean tumor multiplicities among BXD recombinant inbred strains indicated that hepatocarcinogen-sensitive DBA/2 mice carry multiple genes with opposing effects on the susceptibility to liver tumor induction. By analyzing D2B6F1 x B6 backcross and D2B6F2 intercross mice for their liver tumor multiplicity phenotypes and for their genotypes at simple sequence repeat marker loci, we mapped two resistance genes carried by DBA/2J mice, designated Hcr1 and -2, to chromosomes 4 and 10, respectively. Hcr1 and Hcr2 resolved the genetic variance in the backcross population well, indicating that these resistance loci are the major determinants of the variance in the backcross population. Although our collection of 100 simple sequence repeat markers allowed linkage analysis for approximately 95% of the genome, we failed to map any sensitivity alleles for DBA/2J mice. Thus, it is likely that the susceptibility of DBA/2J mice is the consequence of the combined effects of multiple sensitivity loci.
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Gelman, R., A. Watson, E. Yunis, and R. M. Williams. "Genetics of survival in mice: subregions of the major histocompatibility complex." Genetics 125, no. 1 (May 1, 1990): 167–74. http://dx.doi.org/10.1093/genetics/125.1.167.

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Abstract In this study of murine survival, 422 F1 hybrids between DBA/2J (D2) female mice and C57BL/10 (B10) background H-2 congenic male mice (11 strains), 88 F1 hybrids between B10 female mice and B10 background H-2 congenic male mice (3 strains), and 532 control mice from the 11 parental B10 background H-2 congenic mice were bred over a period of 2 yr. Toward the end of the breeding period there was documentation of Sendai infection in the mouse rooms. All analyses were done separately for the two sexes. Although it did not appear that an unusually high number of mice died during the time the colony was infected with Sendai, there was a highly significant tendency for mice who were younger at the time of the Sendai infection to have shorter survival than mice who were older at that time point. The effect of birth date on survival was approximately as significant as the effect of strain on survival. Hence all analyses of genetic effects on survival were either done within subsets of mice born in the same quarter of a particular year or else included date of birth variables in survival models. Of the 18 possible comparisons of pairs of strains which overlapped in birth dates and differed only in the D end of H-2, five were associated with highly significant survival differences. Of the 11 pairs of strains which overlapped in birth date and differed only in the K end of H-2, none was associated with significant survival differences.(ABSTRACT TRUNCATED AT 250 WORDS)
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Roper, Randall J., Heidi K. St. John, Jessica Philip, Ann Lawler, and Roger H. Reeves. "Perinatal Loss of Ts65Dn Down Syndrome Mice." Genetics 172, no. 1 (September 19, 2005): 437–43. http://dx.doi.org/10.1534/genetics.105.050898.

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Dissertations / Theses on the topic "Mice – Genetics"

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McGowan, Kelly Ann. "Genetics of skin color in mice /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Bhanji, Tania. "Elastin in zebrafish and mice." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111938.

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The extracellular matrix is a vital component of the cardiovascular system, in that, it not only provides structural support but also plays a critical role in the maintenance of cellular stability. One of the major components of the vascular matrix is elastin, which confers vessels with the specialized property of stretch and recoil. Elastin deficiency has been implicated in many vascular diseases and determined experimentally to be a negative regulator of smooth muscle cell proliferation. In zebrafish, two elastin genes have been identified, which are actively expressed during development. Based on this finding, protein production and spatial localization for the two elastin proteins was studied by immunohistochemistry with specific antibodies. Results revealed a global distribution for elastin 1 in the ventral aorta and swim bladder, whereas elastin 2 was preferentially localized to the bulbus arteriosus indicating a possible specialized function of elastin 2 in this structure. This observation, and the unique physiological property of this structure, suggests a possible reason for the preservation of both elastin genes during evolution.
In the second part of this study, elastin-null mice were studied to uncover the impact of the loss of elastin on the expression of other elastic fiber-associated proteins. The expression of fibrillin-1, the major component of microfibrils, was not altered in the absence of elastin, implying that elastin is not necessary for the formation of microfibrils. On the other hand, both fibulin-2 and -5 were upregulated in the absence of elastin, suggesting that expression of these genes are controlled by elastin. Overall, this study highlights the importance of elastin in evolution, as well as its potential role in the regulation of expression of other matrix molecules.
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Byers, Shannon L. "Use of Inbred Strains of Mice to Study the Genetics and Biology of Sperm Function." Fogler Library, University of Maine, 2006. http://www.library.umaine.edu/theses/pdf/ByersSL2006.pdf.

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Gini, Beatrice. "The genetics of family interactions in mice." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/the-genetics-of-family-interactions-in-mice(afdad740-ef76-403c-b4fc-738a3470cffe).html.

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Parents and offspring engage in conflict over the amount of resources provisioned by parents, because parents wish to distribute resources equally between all offspring, while each offspring attempts to secure a greater than average share of resources for itself. Parents are responsible for the act of provisioning, yet they need to be sensitive to signals of hunger from their offspring (begging) and therefore they can be manipulated by cheating offspring into provisioning more than the parental optimum. Both parents and offspring evolve strategies to cope with this conflict and, because the payoff of each strategy depends on the behaviour of the interacting party, parents and offspring co-evolve pairs of compatible strategies. While these dynamics have been studied in detail from a game-theoretical and phenotypic perspective, little is known about the genetics underlying parental and offspring strategies. In this study, I used a panel of recombinant inbred mouse lines to investigate the genetics of provisioning and begging. The results clearly show that some areas of the genome are associated with particular strategies in each individual, and also that the genome of offspring can be linked to maternal behaviour through indirect genetic effects. They also show that provisioning and growth are co-adapted in these mice, and that linkage disequilibrium is the mechanism maintaining co-adaptation in this case. Importantly, the genotype of mothers interacts with the environment created by pups in highly significant and complex ways. Finally, I describe an area of the genome associated with sex ratio, and find that a male-biased sex ratio causes mothers to intensify provisioning. All findings are discussed with regards to their implications for evolutionary models.
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Bell, Cindy Lea. "Transport studies in primary cultures of mouse renal epithelial cells." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75363.

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The Hyp (hypophosphatemic) mouse, a murine homologue of X-linked hypophosphatemia (XLH) in man, is a Mendelian disorder of phosphate (Pi) homeostasis. The mutant genotype is characterized by abnormal Pi transport at the brush border membrane (BBM) of the proximal tubule and a defect in renal metabolism of vitamin D$ sb3$. The exact nature of these defects has not been elucidated.
In order to determine if the defect is intrinsic to the renal cell or dependent upon an extrinsic humoral factor, I established primary cultures of renal epithelial cells from normal and Hyp mouse kidney. The cultures demonstrated several differentiated properties of epithelial cells of the renal proximal tubule, the site of the Pi transport defect in the Hyp mouse.
Primary cultures initiated from Hyp mice had decreased Pi transport (expressed as an uptake ratio, Pi/$ alpha$-MG), and increased production of 24,25 dihydroxyvitamin D$ sb3$. These results provide evidence for the intrinsic nature of the primary defect in the Hyp mouse.
This appears to be the first time that expression of a mutant transport gene has been demonstrated in cultured renal cells.
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Chau, Hien Nguyet 1977. "Renal calcification in Npt2 knockout mice." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78338.

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Mice homozygous for the disrupted renal type 11a sodium/phosphate (Na/Pi) cotransporter gene, Npt2, (Npt2 KO) exhibit renal Pi wasting and hypercalciuria, predisposing factors for renal stone formation. We observed that Npt2 KO mice, but not wild-type littermates form renal stones. The renal stones were evident in newborn, weanling and adult mice and composed of calcium (Ca) and Pi. The presence of renal calcification correlated with the absence of Npt2 gene expression and the presence of genes responsible for the synthesis (1alpha-hydroxylase) and catabolism (24-hydroxylase) of 1,25-dihydroxyvitamin D, whose elevated levels contribute to the hypercalciuria and renal calcification in Npt2 KO mice. The renal calcification was associated with increased osteopontin (OPN) mRNA expression and colocalized with OPN, the latter associates with renal stones in vivo and inhibits Ca mineralization in vitro). These data demonstrate that hyperphosphaturia and hypercalciuria, secondary to Npt2 gene disruption, are sufficient for the development of renal calcification.
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邱大安 and Tai-on Yau. "Regulation of the mouse hoxb-3 gene in the neural expression domains during embryogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31242601.

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Husbands, Sandra D. "Tolerance and immunity in transgenic mice." Thesis, University College London (University of London), 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303680.

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Devine, Jill Christine. "POPULATION GENETICS OF GOLDEN MICE (OCHROTOMYS NUTTALLI) AND WHITE-FOOTED MICE (PEROMYSCUS LEUCOPUS)." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/theses/943.

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Golden mice (Ochrotomys nuttalli) are generally an elusive and rare species throughout their geographic range in the southeastern United States. They are considered to be habitat specialists that prefer dense understory consisting of shrubs and vines. Golden mice are less vagile, and likely disperse shorter distances than other sympatric species such as the white-footed mouse (Peromyscus leucopus). Conversely, white-footed mice are considered habitat generalists that inhabit a variety of habitat types, are more vagile, and disperse farther than golden mice. Because of this it is likely that golden mice have a lower genetic diversity and are more genetically subdivided than white-footed mice. In southern Illinois, golden mice are on the periphery of their range, which is one of the reasons they are on the state-threatened list in Illinois. It has been hypothesized that populations on the periphery of a species range will have more population structure and lower genetic diversity than populations in the core of the range. Tissue samples for golden mice and white-footed mice were collected from 24 sites throughout southern Illinois and 24 sites throughout the golden mouse core range. I analyzed 13 and 10 microsatellite markers as well as 594 and 624 base pairs of the mitochondrial control region for golden mice and white-footed mice, respectively, to characterize and compare the genetic diversity and population structure of both species. Overall haplotype diversity (0.76) and nucleotide diversity (0.20%) was lower in golden mice compared to white footed mice (0.99 and 1.97%). Results of an AMOVA using the mitochondrial control region revealed more subdivision among the 3 populations of golden mice (Φst = 0.099, P < 0.001) than among the 3 populations of white-footed mice (Φst = 0.058, P < 0.001). Microsatellite loci showed a similar trend with overall FST values of 0.027 (P < 0.001) for golden mice and 0.004 (P = 0.137) for white-footed mice. I intended to compare golden mouse individuals from southern Illinois and the core of the range, but too few individuals were collected from the core. More samples need to be collected throughout the core of the range to better understand the population genetics of golden mice in the core of the range compared to the periphery.
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Shek, Kim Fung. "Identification of cis-regulatory elements in mouse Mab21l2 gene by comparative genomics /." View abstract or full-text, 2010. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202010%20SHEK.

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Books on the topic "Mice – Genetics"

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Silver, Lee M. Mouse genetics: Concepts and applications. New York: Oxford University Press, 1995.

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Singh, Shree Ram, and Vincenzo Coppola. Mouse genetics: Methods and protocols. New York: Humana Press, 2014.

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M, Brown Stephen D., Lyon Mary F, Rastan Sohaila, and International Committee on Standardized Genetic Nomenclature for Mice., eds. Genetic variants and strains of the laboratory mouse. 3rd ed. Oxford: Oxford University Press, 1996.

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R, Capecchi Mario, and Cold Spring Harbor Laboratory, eds. Molecular genetics of early Drosophila and mouse development. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 1989.

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Auwrex, Johan. Current protocols in mouse biology. Hoboken, N.J: Wiley, 2011.

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A, Goffinet, ed. The reeler mouse as a model of brain development. Berlin: Springer, 1998.

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Martin, Hrabé de Angelis, Chambon Pierre, and Brown Stephen D. M, eds. Standards of mouse model phenotyping. Weinheim: Wiley-VCH, 2006.

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Egorov, I. K. Transgenic Mice and Mutants in MHC Research. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990.

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Lamoreux, M. Lynn. The colors of mice: A model genetic network. Chichester, West Sussex: Wiley-Blackwell, 2010.

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Lynn, Lamoreux M., ed. The colors of mice: A model genetic network. Chichester, West Sussex: Wiley-Blackwell, 2010.

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Book chapters on the topic "Mice – Genetics"

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Gaudilliere, Jean-Paul. "Circulating Mice and Viruses." In The Practices of Human Genetics, 89–124. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4718-7_4.

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Leder, P. "Transgenic Mice in the Study of Human Disease." In Human Genetics, 377. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_47.

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Yunis, E. J., and M. Salazar. "Genetics of life span in mice." In Genetics and Evolution of Aging, 243–55. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-017-1671-0_21.

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Maxson, Stephen C. "The Genetics of Offensive Aggression in Mice." In Handbook of Behavior Genetics, 301–16. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-76727-7_21.

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Anderson, Lucy M., Marek A. Sipowicz, Wei Yu, Bhalchandra A. Diwan, Lisa Birely, Diana C. Haines, Charles W. Riggs, and Kazimierz S. Kasprzak. "Chromium(III) as a Male Preconception Carcinogen in Mice." In Metals and Genetics, 171–82. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4723-5_12.

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Kono, D. H., and A. N. Theofilopoulos. "Genetic Susceptibility to Spontaneous Lupus in Mice." In Genes and Genetics of Autoimmunity, 72–98. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000060497.

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D’Hoostelaere, L., K. Huppi, B. Mock, C. Mallett, D. Gibson, J. Hilgers, and M. Potter. "The Organization of the Immunoglobulin Kappa Locus in Mice." In Genetics of Immunological Diseases, 116–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-50059-6_18.

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Ukai, Hideki, Koji L. Ode, and Hiroki R. Ueda. "Next-Generation Mice Genetics for Circadian Studies." In Circadian Clocks, 359–76. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2577-4_17.

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Guénet, Jean-Louis, Fernando Benavides, Jean-Jacques Panthier, and Xavier Montagutelli. "The Different Categories of Genetically Standardized Populations of Laboratory Mice." In Genetics of the Mouse, 319–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44287-6_9.

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Gardner, Murray B. "Genetic control of retroviral disease in aging wild mice." In Genetics and Evolution of Aging, 232–42. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-017-1671-0_20.

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Conference papers on the topic "Mice – Genetics"

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Turner, Charles H., and Alexander G. Robling. "Genetic Effects on Skeletal Mechanosensitivity in Mice." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32596.

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The accumulation of bone mass during growth can be enhanced by environmental factors such as mechanical loading (exercise) or calcium intake, but 60–70% of the variance in adult bone mineral density (BMD) is explained by heredity. Consequently, understanding the signaling pathways targeted by the genes governing bone accumulation holds perhaps the greatest potential in reducing fracture incidence later in life. Rodent models are particularly useful for studying the genetics of skeletal traits. Of the available inbred mouse strains, three in particular have been studied extensively in skeletal genetics: C57BL/6, DBA/2, and C3H/He. The C57BL/6 strain is characterized by low BMD and large total cross-sectional area (CSA) in the midshaft femur; the C3H/He strain exhibits very high femoral BMD and a smaller femoral CSA than the C57BL/6 mice; and DBA/2 mice have moderately high femoral BMD and a very small midshaft femur CSA. Mechanical loading of the skeleton during growth can substantially enhance periosteal bone apposition, and ultimately produce a diaphyseal cross section with enlarged area. Therefore we hypothesized that the mouse strain with greater femoral cross-sectional area (C57BL/6) might have a genetic predisposition for greater mechanosensitivity than mice with smaller cross sections (C3H/He and DBA/2).
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Turner, Charles H. "How Microimaging Technology Is Transforming the Field of Skeletal Genetics." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33057.

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Microcomputed tomography (microCT) is emerging as the technique of choice for skeletal genetics research. The goal of these studies is to identify genes that modulate bone strength and skeletal biomechanics. Many studies use animal models, namely rats and mice. To fully characterize the skeletal phenotype, one must determine the size, shape, and microstructure of the bones preferably in three dimensions. In what follows are three examples of how μCT has been used to illuminate genetic effects on bone structure.
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Perez, B. C., A. Savchuk, P. Duenk, M. P. L. Calus, and M. C. A. M. Bink. "293. Using convolutional neural networks for image-based genomic prediction in mice." In World Congress on Genetics Applied to Livestock Production. The Netherlands: Wageningen Academic Publishers, 2022. http://dx.doi.org/10.3920/978-90-8686-940-4_293.

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Gutiérrez, J. P., N. Formoso-Rafferty, C. Ojeda-Marín, L. El-Ouazizi El-Kahia, K. D. Arias, and I. Cervantes. "476. Selection for birth weight environmental variability in mice as a model to improve animal welfare in livestock species." In World Congress on Genetics Applied to Livestock Production. The Netherlands: Wageningen Academic Publishers, 2022. http://dx.doi.org/10.3920/978-90-8686-940-4_476.

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"The effect of "early"protein of papillomavirus HPV16 E2 made in plant expression system on the base of tomato fruit on tumor formation in mice infected with cancer HeLa cells." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Novosibirsk ICG SB RAS 2021, 2021. http://dx.doi.org/10.18699/plantgen2021-168.

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Kulik, M. J., D. S. Shenoda, and C. R. Forest. "A Low-Cost, Two-Axis, Precision Robot for Automated Fluorescence In-Situ Hybridization Assays." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-13272.

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Genetics research often relies on experiments that require repetitive, time-consuming handling of small volumes of liquid (1 mL) and biomass (10–20 μL) such as fluorescence in-situ hybridization (FISH), β-galactosidase staining, immunohisto chemistry, skeletal and tunel assays. Often manual, these experiments are time intensive and error-prone. We report on the design, fabrication, and testing of a low-cost, two-axis, precision robot for FISH assays on whole mice embryos. The robot can complete 20 successive embryo immersions in unique isothermal solutions in minutes for 6 samples. Repeatability of the orthogonal axes is 66 and 214 μm, near the measurement uncertainty limit and sufficient for operation. Accuracy is achieved by systematic error compensation. Low-cost and precision are obtained using design and manufacturing techniques and processes, resulting in a cost of 15% of comparable instruments (e.g., InsituStain, Intavis Bioanalytical Instruments). This design demonstrates a simple, automated platform to perform a typically manual experimental genetics technique.
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Ratnadiwakara, Madara, Rohan B. Williams, and Anneke C. Blackburn. "Abstract A117: Vitamin D, parathyroid hormone,Cyp2r1, and breast cancer susceptibility in mice." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-a117.

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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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Kim, K., BL Scott, MJ Tuvim, Z. Ammar-Aouchiche, CG Clement, and BF Dickey. "Genetic Dissection of Airway Mucin Secretion in Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6295.

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Piccotti, Lucia, Kyubo Kim, Zoulikha Ammar-Aouchiche, Michael J. Tuvim, and Burton F. Dickey. "Genetic Dissection Of Airway Mucin Secretion In Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6424.

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Reports on the topic "Mice – Genetics"

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Blank, Robert D. Genetics of Bone Mineralization and Morphology in Inbred Mice: Analysis of the HcB/Dem Recombinant Congenic Strains. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada400522.

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Takahashi, Joseph S. Genetic Analysis of Daily Activity in Humans and Mice. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada387128.

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Turek, Fred W., and Martha H. Vitatema. Uncovering the Genetic Basis of Sleep: Use of Clock Mutant Mice. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada396387.

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Robins, Diane M. Humanized Androgen Receptor Mice: A Genetic Model for Differential Response to Prostate Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada582175.

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Robins, Diane. Humanized Androgen Receptor Mice: A Genetic Model for Differential Response to Prostate Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada547343.

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Nelson, Brad H. Eliciting Autoimmunity to Ovarian Tumors in Mice by Genetic Disruption of T Cell Tolerance Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada409619.

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Raber, Jacob, and Tessa Marzulla. Effects of Pharmacologic and Genetic Inhibition of Alk on Cognitive Impairments in NF1 Mutant Mice. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada606392.

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Nelson, Brad H. Eliciting Autoimmunity to Ovarian Tumors in Mice by Genetic Disruption of T Cell Tolerance Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada462679.

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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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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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