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Статті в журналах з теми "N mouse"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Salinger, A. P., and M. J. Justice. "Mouse Mutagenesis Using N-Ethyl-N-Nitrosourea (ENU)." Cold Spring Harbor Protocols 2008, no. 5 (April 1, 2008): pdb.prot4985. http://dx.doi.org/10.1101/pdb.prot4985.

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2

Yan, Lan, Diane M. Otterness, Timothy L. Craddock, and Richard M. Weinshilboum. "Mouse Liver Nicotinamide N-Methyltransferase:." Biochemical Pharmacology 54, no. 10 (November 1997): 1139–49. http://dx.doi.org/10.1016/s0006-2952(97)00325-0.

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3

Cordes, Sabine P. "N-Ethyl-N-Nitrosourea Mutagenesis: Boarding the Mouse Mutant Express." Microbiology and Molecular Biology Reviews 69, no. 3 (September 2005): 426–39. http://dx.doi.org/10.1128/mmbr.69.3.426-439.2005.

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SUMMARY In the mouse, random mutagenesis with N-ethyl-N-nitrosourea (ENU) has been used since the 1970s in forward mutagenesis screens. However, only in the last decade has ENU mutagenesis been harnessed to generate a myriad of new mouse mutations in large-scale genetic screens and focused, smaller efforts. The development of additional genetic tools, such as balancer chromosomes, refinements in genetic mapping strategies, and evolution of specialized assays, has allowed these screens to achieve new levels of sophistication. The impressive productivity of these screens has led to a deluge of mouse mutants that wait to be harnessed. Here the basic large- and small-scale strategies are described, as are the basics of screen design. Finally, and importantly, this review describes the mechanisms by which such mutants may be accessed now and in the future. Thus, this review should serve both as an overview of the power of forward mutagenesis in the mouse and as a resource for those interested in developing their own screens, adding onto existing efforts, or obtaining specific mouse mutants that have already been generated.

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4

Tanaka, M., A. Fukuhara, and I. Shimomura. "N-Linked Glycosylation of Mouse Adiponectin." Hormone and Metabolic Research 43, no. 08 (July 2011): 545–50. http://dx.doi.org/10.1055/s-0031-1280782.

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5

Tinwell, H., J. Yendle, and J. Ashby. "Mutagenicity to the mouse bone marrow by the mouse germ cell mutagen N-propyl-N-nitrosourea." Mutation Research/Genetic Toxicology 370, no. 3-4 (October 1996): 141–43. http://dx.doi.org/10.1016/s0165-1218(96)00047-x.

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6

Shibuya, T., T. Murota, T. Tokiwa, H. Matsumoto, N. Horiya, and T. Hara. "N-Propyl-N-nitrosourea-induced recessive mutations in mouse spermatogonia." Mutation Research/Environmental Mutagenesis and Related Subjects 203, no. 5 (October 1988): 387–88. http://dx.doi.org/10.1016/0165-1161(88)90080-5.

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7

Lu, Shajia, Diane E. Borst, and Robert Horowits. "N-RAP expression during mouse heart development." Developmental Dynamics 233, no. 1 (2005): 201–12. http://dx.doi.org/10.1002/dvdy.20314.

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8

Château, Marie-Thérèse, Herisoa Rabesandratana, and René Caravano. "Suspended mouse peritoneal macrophages." Journal of Immunological Methods 143, no. 1 (September 1991): 103–9. http://dx.doi.org/10.1016/0022-1759(91)90278-n.

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9

Noveroske, J. K., J. S. Weber, and M. J. Justice. "The mutagenic action of N-ethyl-N-nitrosourea in the mouse." Mammalian Genome 11, no. 7 (July 2000): 478–83. http://dx.doi.org/10.1007/s003350010093.

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10

Grosse, Johannes, Patrick Tarnow, Holger Römpler, Boris Schneider, Reinhard Sedlmeier, Ulrike Huffstadt, Dirk Korthaus, et al. "N-ethyl-N-nitrosourea-based generation of mouse models for mutant G protein-coupled receptors." Physiological Genomics 26, no. 3 (August 2006): 209–17. http://dx.doi.org/10.1152/physiolgenomics.00289.2005.

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Анотація:

Chemical random mutagenesis techniques with the germ line supermutagen N-ethyl- N-nitrosourea (ENU) have been established to provide comprehensive collections of mouse models, which were then mined and analyzed in phenotype-driven studies. Here, we applied ENU mutagenesis in a high-throughput fashion for a gene-driven identification of new mutations. Selected members of the large superfamily of G protein-coupled receptors (GPCR), melanocortin type 3 (Mc3r) and type 4 (Mc4r) receptors, and the orphan chemoattractant receptor GPR33, were used as model targets to prove the feasibility of this approach. Parallel archives of DNA and sperm from mice mutagenized with ENU were screened for mutations in these GPCR, and in vitro assays served as a preselection step before in vitro fertilization was performed to generate the appropriate mouse model. For example, mouse models for inherited obesity were established by selecting fully or partially inactivating mutations in Mc4r. Our technology described herein has the potential to provide mouse models for a GPCR dysfunction of choice within <4 mo and can be extended to other gene classes of interest.

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11

Zahn, Laura M. "Identifying single-cell types in the mouse brain." Science 360, no. 6385 (April 12, 2018): 166.14–168. http://dx.doi.org/10.1126/science.360.6385.166-n.

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12

Abraham, S. K., and H. Stopper. "Anti-genotoxicity of coffee against N-methyl-N-nitro-N-nitrosoguanidine in mouse lymphoma cells." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 561, no. 1-2 (July 2004): 23–33. http://dx.doi.org/10.1016/j.mrgentox.2004.03.010.

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13

Supko, J. G., and L. Malspeis. "Dose-dependent pharmacokinetics of rapamycin-28-N,N- dimethylglycinate in the mouse." Cancer Chemotherapy and Pharmacology 33, no. 4 (January 1, 1994): 325–30. http://dx.doi.org/10.1007/s002800050061.

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14

Supko, J. G., and L. Malspeis. "Dose-dependent pharmacokinetics of rapamycin-28-N,N-dimethylglycinate in the mouse." Cancer Chemotherapy and Pharmacology 33, no. 4 (1994): 325–30. http://dx.doi.org/10.1007/bf00685908.

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15

Grigoryev, Sergei, Albert E. Stewart, Yong Tae Kwon, Stuart M. Arfin, Ralph A. Bradshaw, Nancy A. Jenkins, Neal G. Copeland, and Alexander Varshavsky. "A Mouse Amidase Specific for N-terminal Asparagine." Journal of Biological Chemistry 271, no. 45 (November 8, 1996): 28521–32. http://dx.doi.org/10.1074/jbc.271.45.28521.

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16

Vigeant, P., R. Dubois, and P. Viens. "Trypanosoma musculi infection in the CBA/N mouse." Canadian Journal of Microbiology 32, no. 2 (February 1, 1986): 181–83. http://dx.doi.org/10.1139/m86-036.

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Анотація:

The infection of B-cell deficient CBA/N mice by Trypanosoma musculi resulted in a higher parasitaemia, delayed recovery, and a defective antibody response (IgM and IgG1). CBA/N mice were thus less efficient than CBA/J in controlling the infection. These results indicate that B-cells are involved in the immunological control of this parasite.

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17

KAWAMOTO, Susumu, Hisae ISHIDA, Masataka MORI, and Masamiti TATIBANA. "Regulation of N-Acetylglutamate Synthetase in Mouse Liver." European Journal of Biochemistry 123, no. 3 (March 3, 2005): 637–41. http://dx.doi.org/10.1111/j.1432-1033.1982.tb06579.x.

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18

Radice, Glenn L., Helen Rayburn, Hiroaki Matsunami, Karen A. Knudsen, Masatoshi Takeichi, and Richard O. Hynes. "Developmental Defects in Mouse Embryos Lacking N-Cadherin." Developmental Biology 181, no. 1 (January 1997): 64–78. http://dx.doi.org/10.1006/dbio.1996.8443.

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19

Igarashi, Yasuyuki, and Sen-itiroh Hakomori. "Enzymatic synthesis of N,N-dimethyl-sphingosine: Demonstration of the sphingosine: N-methyltransferase in mouse brain." Biochemical and Biophysical Research Communications 164, no. 3 (November 1989): 1411–16. http://dx.doi.org/10.1016/0006-291x(89)91827-5.

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20

Ravindranath, V., and H. K. Ananda Theertha Varada. "High activity of cytochrome P-450-linked aminopyrine N-demethylase in mouse brain microsomes, and associated sex-related difference." Biochemical Journal 261, no. 3 (August 1, 1989): 769–73. http://dx.doi.org/10.1042/bj2610769.

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The presence of cytochrome P-450 and associated mono-oxygenase activities was examined in brain microsomes from male and female mice. Although the cytochrome P-450 level in male mouse brain was very low as compared with mouse liver, the aminopyrine N-demethylase and morphine N-demethylase specific activities in male mouse brain were much higher than those observed in mouse liver. Ethoxycoumarin O-de-ethylase and aniline hydroxylase activities were, however, not detected in mouse brain. Sex-related differences were observed in both the cytochrome P-450 levels and aminopyrine N-demethylase activity in mouse brain, the levels of both being higher in male mouse brain as compared with female mouse brain. Aminopyrine N-demethylase activity in mouse brain microsomes was dependent on the presence of oxygen and NADPH and could be inhibited by piperonyl butoxide, N-octyl imidazole and carbon monoxide. Antiserum raised to the phenobarbital-inducible form of rat liver cytochrome P-450 [P-450(b+e)] inhibited mouse brain aminopyrine N-demethylase activity by around 80+ mouse brain microsomal protein exhibited cross-reactivity against this antiserum when examined by Ouchterlony double diffusion and immunoblotting. The present results indicate the presence of a phenobarbital-inducible form of cytochrome P-450 (or a form of cytochrome P-450 that is similar immunologically) in mouse brain microsomes, which is associated with a sex-related difference.

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21

Percec, Ivona, Joanne L. Thorvaldsen, Robert M. Plenge, Christopher J. Krapp, Joseph H. Nadeau, Huntington F. Willard, and Marisa S. Bartolomei. "An N-Ethyl-N-Nitrosourea Mutagenesis Screen for Epigenetic Mutations in the Mouse." Genetics 164, no. 4 (August 1, 2003): 1481–94. http://dx.doi.org/10.1093/genetics/164.4.1481.

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Abstract The mammalian epigenetic phenomena of X inactivation and genomic imprinting are incompletely understood. X inactivation equalizes X-linked expression between males and females by silencing genes on one X chromosome during female embryogenesis. Genomic imprinting functionally distinguishes the parental genomes, resulting in parent-specific monoallelic expression of particular genes. N-ethyl-N-nitrosourea (ENU) mutagenesis was used in the mouse to screen for mutations in novel factors involved in X inactivation. Previously, we reported mutant pedigrees identified through this screen that segregate aberrant X-inactivation phenotypes and we mapped the mutation in one pedigree to chromosome 15. We now have mapped two additional mutations to the distal chromosome 5 and the proximal chromosome 10 in a second pedigree and show that each of the mutations is sufficient to induce the mutant phenotype. We further show that the roles of these factors are specific to embryonic X inactivation as neither genomic imprinting of multiple genes nor imprinted X inactivation is perturbed. Finally, we used mice bearing selected X-linked alleles that regulate X chromosome choice to demonstrate that the phenotypes of all three mutations are consistent with models in which the mutations have affected molecules involved specifically in the choice or the initiation of X inactivation.

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22

Hara, Takumi, Koichi Hirano, Noriko Hirano, Hironobu Tamura, Hajime Sui, Tohru Shibuya, Atsushi Hyogo, et al. "Mutation induction by N-propyl-N-nitrosourea in eight Muta™Mouse organs." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 444, no. 2 (August 1999): 297–307. http://dx.doi.org/10.1016/s1383-5718(99)00061-3.

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23

Kawamura, Akane, Isaac Westwood, Larissa Wakefield, Hilary Long, Naixia Zhang, Kylie Walters, Christina Redfield, and Edith Sim. "Mouse N-acetyltransferase type 2, the homologue of human N-acetyltransferase type 1." Biochemical Pharmacology 75, no. 7 (April 2008): 1550–60. http://dx.doi.org/10.1016/j.bcp.2007.12.012.

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24

Hoorn, A. J. W., L. L. Custer, and J. A. Gossen. "Mutagenicity of N-nitroso-N-ethylurea (ENU) in the transgenic Muta®Mouse." Mutation Research/Environmental Mutagenesis and Related Subjects 252, no. 2 (April 1991): 184–85. http://dx.doi.org/10.1016/0165-1161(91)90055-d.

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25

Smith, Brennan K., Graham P. Holloway, Sandra Reza-Lopez, Stanley M. Jeram, Jing X. Kang, and David W. L. Ma. "A decreased n-6/n-3 ratio in the fat-1 mouse is associated with improved glucose tolerance." Applied Physiology, Nutrition, and Metabolism 35, no. 5 (October 2010): 699–706. http://dx.doi.org/10.1139/h10-066.

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A reduction in skeletal muscle fatty acid oxidation (FAO), manifested as a reduction in mitochondrial content and (or) FAO within mitochondria, may contribute to the development of insulin resistance. n-3 polyunsaturated fatty acids (PUFA) have been observed to increase the capacity for FAO and improve insulin sensitivity. We used the fat-1 mouse model, a transgenic animal capable of synthesizing n-3 PUFA from n-6 PUFA, to examine this relationship. Fat-1 mice exhibited a ~20-fold decrease in the n-6/n-3 ratio in skeletal muscle, and plasma glucose and the area under the glucose curve were significantly (p < 0.05) lower in fat-1 mice during a glucose challenge test. The improvement in whole-body glucose tolerance in the fat-1 mouse was associated with a ~21% (p < 0.05) decrease in whole-muscle citrate synthase (CS) activity (in red muscle only), without alterations in CS activity of isolated mitochondria (either red or white muscle; p > 0.05). These data suggest that the fat-1 mouse has decreased skeletal muscle mitochondrial content. However, the intrinsic ability of mitochondria to oxidize fatty acids was not altered in the fat-1 mouse, as rates of palmitate oxidation in isolated mitochondria from both red and white muscle were unchanged. Overall, this study demonstrates that a decrease in the n-6/n-3 ratio can enhance glucose tolerance in healthy animals, independent of changes in mitochondrial content.

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26

Kusakiewicz-Dawid, Anna, Marta Bugaj, Jolanta M. Dzik, Barbara Gołos, Patrycja Wińska, Krzysztof Pawełczak, Barbara Rzeszotarska, and Wojciech Rode. "Synthesis and biological activity of N(alpha)-[4-[N-[(3,4-dihydro-2-methyl-4-oxo-6-quinazolinyl)methyl]-N-propargylamino]phenylacetyl]-L-glutamic acid." Acta Biochimica Polonica 49, no. 1 (March 31, 2002): 197–203. http://dx.doi.org/10.18388/abp.2002_3836.

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2-Deamino-2-methyl-N10-propargyl-5,8-dideazafolic acid (ICI 198583) is a potent inhibitor of thymidylate synthase. Its analogue, N(alpha)-[4-[N-[(3,4-dihydro-2-methyl-4-oxo-6-quinazolinyl)methyl]-N-propargylamino]phenylacetyl]-L-glutamic acid, containing p-aminophenylacetic acid residue substituting p-aminobenzoic acid residue, was synthesized. The new analogue exhibited a moderately potent thymidylate synthase inhibition, of linear mixed type vs. the cofactor, N(5,10)-methylenetetrahydrofolate. The Ki value of 0.34 microM, determined with a purified recombinant rat hepatoma enzyme, was about 30-fold higher than that reported for inhibition of thymidylate synthase from mouse leukemia L1210 cells by ICI 198583 (Hughes et al., 1990, J. Med. Chem. 33, 3060). Growth of mouse leukemia L5178Y cells was inhibited by the analogue (IC50 = 1.26 mM) 180-fold weaker than by ICI 198583 (IC50 = 6.9 microM).

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27

Fujita, Yoshihiro, Tetsuro Yamane, Masumi Tanaka, Katsuya Kuwata, Junichi Okuzumi, Toshio Takahashi, Hirota Fujiki, and Takuo Okuda. "Inhibitory Effect of (-)-Epigallocatechin Gallate on Carcinogenesis with N-Ethyl-N′-nitro-N-nitrosoguanidine in Mouse Duodenum." Japanese Journal of Cancer Research 80, no. 6 (June 1989): 503–5. http://dx.doi.org/10.1111/j.1349-7006.1989.tb01666.x.

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28

Masahiro, Kuramochi, Seki Hiroshi, Tazawa Tadashi, Sakai Sayuri, and Sakai Yoshiki. "The micronucleus test with mouse peripheral blood on N-methyl-N'-nitro-N-nitrosoguanidine and mitomycin C." Mutation Research/Genetic Toxicology 278, no. 2-3 (February 1992): 121–25. http://dx.doi.org/10.1016/0165-1218(92)90221-k.

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29

Stanley, L. A., A. J. Copp, J. Pope, S. Rolls, V. Smelt, V. H. Perry, and E. Sim. "Immunochemical detection of arylamine N-acetyltransferase during mouse embryonic development and in adult mouse brain." Teratology 58, no. 5 (November 1998): 174–82. http://dx.doi.org/10.1002/(sici)1096-9926(199811)58:5<174::aid-tera3>3.0.co;2-q.

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30

Yang, Shao H., Anuraag Shrivastav, Cynthia Kosinski, Rajendra K. Sharma, Miao-Hsueh Chen, Luc G. Berthiaume, Luanne L. Peters, Pao-Tien Chuang, Stephen G. Young, and Martin O. Bergo. "N-Myristoyltransferase 1 Is Essential in Early Mouse Development." Journal of Biological Chemistry 280, no. 19 (March 7, 2005): 18990–95. http://dx.doi.org/10.1074/jbc.m412917200.

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31

Kadowaki, Masakazu, Shoko Nakamura, Ondrej Machon, Stefan Krauss, Glenn L. Radice, and Masatoshi Takeichi. "N-cadherin mediates cortical organization in the mouse brain." Developmental Biology 304, no. 1 (April 2007): 22–33. http://dx.doi.org/10.1016/j.ydbio.2006.12.014.

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32

Pieralisi, A., C. Martini, D. Soto, M. C. Vila, J. C. Calvo, and L. N. Guerra. "N-acetylcysteine inhibits lipid accumulation in mouse embryonic adipocytes." Redox Biology 9 (October 2016): 39–44. http://dx.doi.org/10.1016/j.redox.2016.05.006.

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33

Hamanoue, Makoto, Yoshitaka Ikeda, and Ken Takamatsu. "Analysis of N-acetylglucosaminyltransferase in mouse neural stem cells." Neuroscience Research 71 (September 2011): e238-e239. http://dx.doi.org/10.1016/j.neures.2011.07.1043.

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34

Konttila, J., S. Auriola, P. Pellinen, M. Pasanen, and R. O. Juvonen. "Norcocaine N-hydroxylation in human and mouse liver microsomes." Toxicology Letters 95 (July 1998): 93. http://dx.doi.org/10.1016/s0378-4274(98)80372-x.

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35

Schmid, Patricia C., Toyoyasu Kuwae, Randy J. Krebsbach, and Harald H. O. Schmid. "Anandamide and other N-acylethanolamines in mouse peritoneal macrophages." Chemistry and Physics of Lipids 87, no. 2 (July 1997): 103–10. http://dx.doi.org/10.1016/s0009-3084(97)00032-7.

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36

Baxter, C. Stuart, and Marian L. Miller. "Mechanism of mouse skin tumor promotion by n-dodecane." Carcinogenesis 8, no. 12 (1987): 1787–90. http://dx.doi.org/10.1093/carcin/8.12.1787.

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37

Sun, Bingyun, Li Ma, Xiaowei Yan, Denis Lee, Vinita Alexander, Laura J. Hohmann, Cynthia Lorang, Lalangi Chandrasena, Qiang Tian, and Leroy Hood. "N-Glycoproteome of E14.Tg2a Mouse Embryonic Stem Cells." PLoS ONE 8, no. 2 (February 6, 2013): e55722. http://dx.doi.org/10.1371/journal.pone.0055722.

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38

Schulze, Johannes. "Presystemic Intestinal Metabolism of N-Nitrosodimethylamine in Mouse Intestine." Cancer Detection Prevention 23, no. 2 (February 1999): 107–15. http://dx.doi.org/10.1046/j.1525-1500.1999.09913.x.

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39

Rahilly, Maeve A., Kay Samuel, J. D. Ansell, H. S. Micklem, and S. Fleming. "Polycystic kidney disease in the CBA/N immunodeficient mouse." Journal of Pathology 168, no. 3 (November 1992): 335–42. http://dx.doi.org/10.1002/path.1711680315.

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40

Armant, D. Randall, Howard A. Kaplan, and William J. Lennarz. "N-linked glycoprotein biosynthesis in the developing mouse embryo." Developmental Biology 113, no. 1 (January 1986): 228–37. http://dx.doi.org/10.1016/0012-1606(86)90125-9.

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41

Jun, Ji Hae, Sun-Hwan Lee, Han Bok Kwak, Zang Hee Lee, Sang-Beum Seo, Kyung Mi Woo, Hyun-Mo Ryoo, Gwan-Shik Kim, and Jeong-Hwa Baek. "N-acetylcysteine stimulates osteoblastic differentiation of mouse calvarial cells." Journal of Cellular Biochemistry 103, no. 4 (2008): 1246–55. http://dx.doi.org/10.1002/jcb.21508.

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42

Bates, Carlton M., Sadeq Kharzai, Trent Erwin, Janet Rossant, and Luis F. Parada. "Role of N-myc in the Developing Mouse Kidney." Developmental Biology 222, no. 2 (June 2000): 317–25. http://dx.doi.org/10.1006/dbio.2000.9716.

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43

Pugh, Perdita L., Sharlin F. Ahmed, Martin I. Smith, Neil Upton, and A. Jacqueline Hunter. "A behavioural characterisation of the FVB/N mouse strain." Behavioural Brain Research 155, no. 2 (December 2004): 283–89. http://dx.doi.org/10.1016/j.bbr.2004.04.021.

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44

Bai, Haitao, and Fang Dong. "N-MYC INDUCES VARIOUS TYPES OF MOUSE ACUTE LEUKEMIA." Experimental Hematology 76 (August 2019): S57—S58. http://dx.doi.org/10.1016/j.exphem.2019.06.327.

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45

Dellafazia, M. A., T. Beccari, G. Servillo, M. P. Violamagni та A. Orlacchio. "Different Expression of β-N-Acetylhexosaminidase in Mouse Tissues". Biochemical and Biophysical Research Communications 199, № 3 (березень 1994): 1341–46. http://dx.doi.org/10.1006/bbrc.1994.1378.

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46

Miyamoto, S., S. Sukumar, R. C. Guzman, R. C. Osborn, and S. Nandi. "Transforming c-Ki-ras mutation is a preneoplastic event in mouse mammary carcinogenesis induced in vitro by N-methyl-N-nitrosourea." Molecular and Cellular Biology 10, no. 4 (April 1990): 1593–99. http://dx.doi.org/10.1128/mcb.10.4.1593-1599.1990.

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Анотація:

Mouse mammary epithelial cells can be transformed in primary cultures to preneoplastic and neoplastic states when treated with N-methyl-N-nitrosourea (MNU). Mammary carcinomas arising from MNU-induced hyperplastic alveolar nodules (a type of mouse mammary preneoplastic lesion) contained transforming c-Ki-ras genes when examined by the NIH 3T3 focus assay. Hybridization of allele-specific oligonucleotides to c-Ki-ras sequences amplified by the polymerase chain reaction demonstrated the presence of a specific G-35----A-35 point mutation in codon 12 in each of the NIH 3T3 foci as well as the mammary carcinomas. This mutation resulted in the substitution of the normal glycine with an aspartic acid. Furthermore, this mutation in the c-Ki-ras proto-oncogenes was also detected in 9 of 10 hyperplastic alveolar nodules. These results demonstrate that the specific c-Ki-ras mutation is a preneoplastic event in MNU-induced mouse mammary carcinogenesis.

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47

Miyamoto, S., S. Sukumar, R. C. Guzman, R. C. Osborn, and S. Nandi. "Transforming c-Ki-ras mutation is a preneoplastic event in mouse mammary carcinogenesis induced in vitro by N-methyl-N-nitrosourea." Molecular and Cellular Biology 10, no. 4 (April 1990): 1593–99. http://dx.doi.org/10.1128/mcb.10.4.1593.

Повний текст джерела

Анотація:

Mouse mammary epithelial cells can be transformed in primary cultures to preneoplastic and neoplastic states when treated with N-methyl-N-nitrosourea (MNU). Mammary carcinomas arising from MNU-induced hyperplastic alveolar nodules (a type of mouse mammary preneoplastic lesion) contained transforming c-Ki-ras genes when examined by the NIH 3T3 focus assay. Hybridization of allele-specific oligonucleotides to c-Ki-ras sequences amplified by the polymerase chain reaction demonstrated the presence of a specific G-35----A-35 point mutation in codon 12 in each of the NIH 3T3 foci as well as the mammary carcinomas. This mutation resulted in the substitution of the normal glycine with an aspartic acid. Furthermore, this mutation in the c-Ki-ras proto-oncogenes was also detected in 9 of 10 hyperplastic alveolar nodules. These results demonstrate that the specific c-Ki-ras mutation is a preneoplastic event in MNU-induced mouse mammary carcinogenesis.

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48

SHIMIZU, K., and K. YOSHIZATO. "Organ-specific proteins in mouse dermal fibroblasts." Cell Biology International Reports 14 (September 1990): 256. http://dx.doi.org/10.1016/0309-1651(90)91125-n.

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49

Londei, Tiziano, and Vincenzo G. Leone. "Mouse pups discriminate food gnawed by conspecifics." Behavioural Processes 34, no. 2 (July 1995): 105–12. http://dx.doi.org/10.1016/0376-6357(94)00057-n.

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50

Zhang, Qian-Kun, Kyu-Hyuk Cho, Jae-Woo Cho, Dal-Sun Cha, Han-Jin Park, Seok-Joo Yoon, ShouFa Zhang, and Chang-Woo Song. "Studies on the Small Body Size Mouse Developed by Mutagen N-Ethyl-N-nitrosourea." Toxicological Research 24, no. 1 (March 31, 2008): 69–78. http://dx.doi.org/10.5487/tr.2008.24.1.069.

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