Academic literature on the topic 'Transgenic Mice'

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Journal articles on the topic "Transgenic Mice"

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Ju Kim, H., K. i. Naruse, W. S. Choi, K. S. Im, C. S. Park, and D. I. Jin. "332 ENHANCEMENT OF GROWTH PERFORMANCE IN DOUBLE TRANSGENIC MICE WITH GROWTH HORMONE RECEPTOR AND IGF-1 RECEPTOR GENES." Reproduction, Fertility and Development 17, no. 2 (2005): 317. http://dx.doi.org/10.1071/rdv17n2ab332.

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The effect of amplifying growth-related receptor signaling, through overexpression of receptors, on growth regulation in animals was examined. Transgenic mice lines were produced by DNA microinjection using the metallothionein promoter ligated to either the growth hormone receptor (GHR) or IGF-1 receptor (IGF-1R) genes (3 GHR founders and 3 IGF-1R founders). Transgenic mouse lines were estimated to contain approximately 4 to 20 copies of transgenes per cell by Southern blot analysis. Founder mice of each transgenic line transmitted transgenes into F1 and F2 pups with Mendelian ratio. Double tr
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Auerbach, Anna B. "Production of functional transgenic mice by DNA pronuclear microinjection." Acta Biochimica Polonica 51, no. 1 (2004): 9–31. http://dx.doi.org/10.18388/abp.2004_3593.

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Successful experiments involving the production of transgenic mice by pronuclear microinjection are currently limited by low efficiency of random transgene integration into the mouse genome. Furthermore, not all transgenic mice express integrated transgenes, or in other words are effective as functional transgenic mice expressing the desired product of the transgene, thus allowing accomplishment of the ultimate experimental goal--in vivo analysis of the function of the gene or gene network. The purpose of this review is to look at the current state of transgenic technology, utilizing a pronucl
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Sigmund, C. D., C. A. Jones, H. J. Jacob, et al. "Pathophysiology of vascular smooth muscle in renin promoter-T-antigen transgenic mice." American Journal of Physiology-Renal Physiology 260, no. 2 (1991): F249—F257. http://dx.doi.org/10.1152/ajprenal.1991.260.2.f249.

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The pathophysiological consequence of targeted production of SV-40 T-antigen to renin-expressing cells in the kidney of transgenic mice is reported. A histopathologic analysis of the kidney from adult transgenic mice (12–16 wk old) revealed the presence of severe vascular lesions manifested by marked atypical hyperplasia of vascular smooth muscle. The levels of plasma renin, kidney renin, and kidney renin mRNA were examined in 6- and 9-wk-old transgenic mice and were found to be significantly lower than their age-matched non-transgenic littermates and were nonresponsive to captopril treatment.
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Kong, Siyuan, Jinxue Ruan, Kaiyi Zhang, et al. "Kill two birds with one stone: making multi-transgenic pre-diabetes mouse models through insulin resistance and pancreatic apoptosis pathogenesis." PeerJ 6 (April 17, 2018): e4542. http://dx.doi.org/10.7717/peerj.4542.

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Background Type 2 diabetes is characterized by insulin resistance accompanied by defective insulin secretion. Transgenic mouse models play an important role in medical research. However, single transgenic mouse models may not mimic the complex phenotypes of most cases of type 2 diabetes. Methods Focusing on genes related to pancreatic islet damage, peripheral insulin resistance and related environmental inducing factors, we generated single-transgenic (C/EBP homology protein, CHOP) mice (CHOP mice), dual-transgenic (human islet amyloid polypeptide, hIAPP; CHOP) mice (hIAPP-CHOP mice) and tripl
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Dent, L. A., M. Strath, A. L. Mellor, and C. J. Sanderson. "Eosinophilia in transgenic mice expressing interleukin 5." Journal of Experimental Medicine 172, no. 5 (1990): 1425–31. http://dx.doi.org/10.1084/jem.172.5.1425.

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Experiments in vitro suggest that although interleukin 5 (IL-5) stimulates the late stages of eosinophil differentiation, other cytokines are required for the generation of eosinophil progenitor cells. In this study transgenic mice constitutively expressing the IL-5 gene were established using a genomic fragment of the IL-5 gene coupled to the dominant control region from the gene encoding human CD2. Four independent eosinophilic transgenic lines have thus far been established, two of which with 8 and 49 transgene copies, are described in detail. These mice appeared macroscopically normal apar
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Heinzelmann, Andy, Subbiah Kumar, Scott Noggle, et al. "Deletion of a Recombined Ig Heavy Chain Transgene in B-Lineage Cells of Transgenic Mice." Journal of Immunology 161, no. 2 (1998): 666–73. http://dx.doi.org/10.4049/jimmunol.161.2.666.

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Abstract Fully recombined transgenes are stable in their transmission in the germline of transgenic mice, in common with the endogenous genetic complement of most mammalian somatic tissues, including the genes for lymphoid Ag receptors somatically generated from germline minigenes. There have, however, been isolated reports of unusual low frequency transgene losses in various transgenic mice. Here we show, using Southern blots and PCR-based assays, that plasmablast hybridomas and B cells from three independently derived founder lines of transgenic mice bearing a recombined heavy chain Ig trans
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Choi, T., M. Huang, C. Gorman, and R. Jaenisch. "A generic intron increases gene expression in transgenic mice." Molecular and Cellular Biology 11, no. 6 (1991): 3070–74. http://dx.doi.org/10.1128/mcb.11.6.3070-3074.1991.

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To investigate the role of splicing in the regulation of gene expression, we have generated transgenic mice carrying the human histone H4 promoter linked to the bacterial gene for chloramphenicol acetyltransferase (CAT), with or without a heterologous intron in the transcription unit. We found that CAT activity is 5- to 300-fold higher when the transgene incorporates a hybrid intron than with an analogous transgene precisely deleted for the intervening sequences. This hybrid intron, consisting of an adenovirus splice donor and an immunoglobulin G splice acceptor, stimulated expression in a bro
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Choi, T., M. Huang, C. Gorman, and R. Jaenisch. "A generic intron increases gene expression in transgenic mice." Molecular and Cellular Biology 11, no. 6 (1991): 3070–74. http://dx.doi.org/10.1128/mcb.11.6.3070.

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To investigate the role of splicing in the regulation of gene expression, we have generated transgenic mice carrying the human histone H4 promoter linked to the bacterial gene for chloramphenicol acetyltransferase (CAT), with or without a heterologous intron in the transcription unit. We found that CAT activity is 5- to 300-fold higher when the transgene incorporates a hybrid intron than with an analogous transgene precisely deleted for the intervening sequences. This hybrid intron, consisting of an adenovirus splice donor and an immunoglobulin G splice acceptor, stimulated expression in a bro
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Xing, Shu, Wanming Zhao, Wanting Tina Ho, and Zhizhuang Joe Zhao. "Transgenic Expression of Wild Type JAK2 Suppresses Myeloproliferative Disorder Phenotypes Induced by Mutant JAK2V617F in Mice." Blood 112, no. 11 (2008): 180. http://dx.doi.org/10.1182/blood.v112.11.180.180.

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Abstract JAK2V617F, a mutant form of tyrosine kinase JAK2, is found in the majority of patients with myeloproliferative disorders (MPDs). It displays increased kinase activity and causes MPD phenotypes in transgenic mice in a transgence dosage-dependent manner. Following our initial generation and characterization of JAK2V617F transgenic mice, we further generated transgenic mice expressing wild type JAK2 by using the same vav promoter employed for JAK2V617F. Three lines of JAK2 transgenic mice were generated. Real time PCR analyses revealed transgene copy numbers of 38, 2, and 1. All these mi
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Picarella, D. E., A. Kratz, C. B. Li, N. H. Ruddle, and R. A. Flavell. "Transgenic tumor necrosis factor (TNF)-alpha production in pancreatic islets leads to insulitis, not diabetes. Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice." Journal of Immunology 150, no. 9 (1993): 4136–50. http://dx.doi.org/10.4049/jimmunol.150.9.4136.

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Abstract To understand the role of TNF in the regulation of inflammation and the development of autoimmune diseases such as insulin-dependent diabetes mellitus, we produced transgenic mice in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter. The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+
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Dissertations / Theses on the topic "Transgenic Mice"

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Simard, Marie-Chantal. "Nef pathogenesis in transgenic mice." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103182.

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In order to study the functions of SIV Nef in vivo, in a small animal model, transgenic (Tg) mice expressing the SIVmac239 nef gene, under the control of the human CD4 gene promoter (CD4C) were generated. The transgene was found to be expressed in the same cells targeted by the virus, in vivo. These CD4C/SHIV-nef SIV Tg mice develop a severe AIDS-like disease, including premature death, failure to thrive/weight loss, wasting, thymic atrophy, exhibit an especially low number of peripheral CD8+ T cells as well as low number of peripheral CD4+ T cells, diarrhea, splenomegaly, kidney (interstitial
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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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Cosentino, Lidia. "A comparison of transgenic and endogenous loci in vivo." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/NQ56223.pdf.

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Malmström, Vivianne. "Arthritis susceptibility and tolerance in collagen transgenic mice." Lund : Dept. of Cell and Molecular Biology, Section for Medical Inflammation Research, Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/38986502.html.

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So, Chi-leung. "Transgenic mouse model of human chondrodysplasia /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19161347.

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Gratao, Ana Angélica. "Impaired fertility in transgenic mice overexpressing betacellulin." [S.l.] : [s.n.], 2007. http://edoc.ub.uni-muenchen.de/archive/00006575.

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Gratao, Ana Angelica. "Impaired Fertility in Transgenic Mice Overexpressing Betacellulin." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-65751.

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Felmer, R. "Genetic manipulation of fat in transgenic mice." Thesis, University of Edinburgh, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.650832.

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The present dissertation describes the use of a novel system to achieve specific cell ablation in fat tissue. The method is based on the use of <i>E.coli</i> nitroreductase (NTR) enzyme that activates certain nitro compounds into cytotoxic DNA interstrand cross-linking agents. This system was assessed first <i>in vitro,</i> in a preadipocyte cell line (3T3L1). Clones of cells that expressed NTR were successfully killed after treatment with CB1954. It was confirmed that the mechanism of cell killing involved is apoptosis and the presence of a cell-permeable metabolite that is released to the me
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Cox, April. "Effects of hyperoxia in alzheimers transgenic mice." Scholar Commons, 2005. http://scholarcommons.usf.edu/etd/2836.

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An association between major surgery in the elderly and precipitation of Alzheimers disease (AD) has been reported. Hyperoxia (100%) oxygen is commonly administered after surgery to increase the oxygen content of blood. However, hyperoxia is a potent cerebral vasoconstrictor and generator of free radicals, as is [beta]amyloid (A[beta];). This study was aimed at examining behavioral, neuropathological, and neurochemical effects of hyperoxia treatments in APPsw transgenic mice (Tg+), which have elevated brain A[beta]; levels by 3-4 months of age but are not yet cognitively-impaired. At 3 months
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Calver, Andrew Robert. "Oligodendrocyte population dynamics : insights from transgenic mice." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322239.

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Books on the topic "Transgenic Mice"

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Tinsley, Jonathon Mark. Human papillomavirus transgenic mice. University of Birmingham, 1991.

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M, Bader, Offermanns Stefan, and Hein Lutz, eds. Transgenic models in pharmacology. Springer, 2004.

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H, Hofker Marten, and Deursen Jan van 1930-, eds. Transgenic mouse methods and protocols. Humana Press, 2003.

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

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Egorov, Igor K., and Chella S. David, eds. Transgenic Mice and Mutants in MHC Research. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75442-5.

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K, Egorov I., and David Chella S, eds. Transgenic mice and mutants in MHC research. Springer-Verlag, 1990.

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M, Matzuk Martin, Brown Chester W, and Kumar T. Rajendra, eds. Transgenics in endocrinology. Humana Press, 2001.

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

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Herrup, Karl. Transgenic and ES cell chimeric mice as tools for the study of the nervous system. Published by Elsevier for the Foundation for the Study of the Nervous System, 1995.

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

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Book chapters on the topic "Transgenic Mice"

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Lo, Lilian H., and Vincent W. Keng. "Transgenic Mice." In Encyclopedia of Gerontology and Population Aging. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_967-1.

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Lo, Lilian H., and Vincent W. Keng. "Transgenic Mice." In Encyclopedia of Gerontology and Population Aging. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_967.

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Diack, Abigail B., Rona Wilson, Enrico Cancellotti, Barry Bradford, Matthew Bishop, and Jean C. Manson. "Transgenic Mice Modelling." In Prions and Diseases. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5338-3_10.

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Chen, X., Y. Matsuura, and J. F. Kearney. "CD5 Transgenic Mice." In Current Topics in Microbiology and Immunology. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_25.

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Rüther, Ulrich. "Insertional Mutagenesis in Transgenic Mice." In Transgenic Animals. CRC Press, 2022. http://dx.doi.org/10.1201/9781003211099-68.

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Lowell, Bradford B. "Genetically Engineered Mice in Obesity Research." In Transgenic Animals. CRC Press, 2022. http://dx.doi.org/10.1201/9781003211099-80.

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Strange, Robert, and Robert D. Cardiff. "Transgenic Mice and Transgenic Mammary Glands." In Breast Cancer: Progress in Biology, Clinical Management and Prevention. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1617-6_1.

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Jaenisch, Rudolf, Douglas Gray, Tetsuo Noda, and Hans Weiher. "Mutations in Transgenic Mice." In Vectors as Tools for the Study of Normal and Abnormal Growth and Differentiation. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74197-5_6.

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Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, et al. "Ataxin-3 Transgenic Mice." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_659.

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Wagner, E. F. "Oncogenes and Transgenic Mice." In Growth Factors, Differentiation Factors, and Cytokines. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74856-1_27.

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Conference papers on the topic "Transgenic Mice"

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Welsh, John P., Josef Turecek, and Eric E. Turner. "Evaluating cerebellar functions using optogenetic transgenic mice." In SPIE BiOS, edited by Samarendra K. Mohanty and Nitish V. Thakor. SPIE, 2013. http://dx.doi.org/10.1117/12.2010204.

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Keyes, Joseph T., Stacy Borowicz, Urs Utzinger, Mohamad Azhar, and Jonathan P. Vande Geest. "Quantification of the Biomechanical Differences in Wild-Type and Heterozygous TGF Beta2 Knockout Mice." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19482.

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The use of transgenic mice is an incredibly powerful tool in understanding the underlying etiology of disease. To understand the usefulness of specific transgenic mice, the systems of interest should be characterized. We have created TGFβ2-deficient mouse fetuses that develop widespread aortic and coronary artery aneurysms [1]. Several studies have pointed to a strong connection between elevated TGFβ signaling and aortic aneurysm [2]. In situ hybridization has shown that Tgfb2 and Tgfb3 are major ligands expressed in the aortic medial wall. Further reduction of TGFβ signaling by combining TGFβ
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Stepanenko, E. A., T. P. Gerasimova, N. E. Bondareva, et al. "THE ROLE OF THE TRIM14 PROTEIN IN THE IMMUNE RESPONSE TO A BACTERIAL INFECTION CAUSED BY PSEUDOMONAS AERUGINOSA IN TRANSGENIC MICE." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-375.

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The study of the molecular mechanisms of interaction between the innate immune system and the bacterial pathogen Pseudomonas aeruginosa may contribute to the development of new approaches to combat bacterial infections. In this work, we showed that overexpression of human TRIM14 led to a decrease in the survival rate of transgenic mice upon P. aeruginosa infection. At the same time, the amount of phosho-STAT3 (p-STAT3) protein in the nuclear fraction in the lungs of transgenic mice increased after infection.
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Luo, Xue-Gang, Ting-Ting Qin, Zhong-Shuai Xin, Dao-Zhu Huangfu, and Tao Xi. "Construction of SMYD3 liver-specific expression transgene for the eestablishment of transgenic mice." In 2010 International Conference on Bioinformatics and Biomedical Technology. IEEE, 2010. http://dx.doi.org/10.1109/icbbt.2010.5478970.

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Kamioka, Yuji, Kenta Sumiyama, Rei Mizuno, and Michiyuki Matsuda. "Live imaging of transgenic mice expressing FRET biosensors." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609453.

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Sakai, Mizu, Tetsuya Kubota, Mayuka Isaka, et al. "Lung Injury Model Using Human MUC1 Transgenic Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5987.

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Laufer, J. G., J. O. Cleary, E. Z. Zhang, M. F. Lythgoe, and P. C. Beard. "Photoacoustic imaging of vascular networks in transgenic mice." In BiOS, edited by Alexander A. Oraevsky and Lihong V. Wang. SPIE, 2010. http://dx.doi.org/10.1117/12.842204.

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Aulova, K. S., and G. S. Nevinsky. "CATALYTIC ANTIBODIES DURING THE SPONTANEOUS DEVELOPMENT OF EXPERIMENTAL ENCEPHALOMYELITIS IN MICE OF 2D2, TH LINES AND FIRST-GENERATION HYBRIDS." In XI МЕЖДУНАРОДНАЯ КОНФЕРЕНЦИЯ МОЛОДЫХ УЧЕНЫХ: БИОИНФОРМАТИКОВ, БИОТЕХНОЛОГОВ, БИОФИЗИКОВ, ВИРУСОЛОГОВ, МОЛЕКУЛЯРНЫХ БИОЛОГОВ И СПЕЦИАЛИСТОВ ФУНДАМЕНТАЛЬНОЙ МЕДИЦИНЫ. IPC NSU, 2024. https://doi.org/10.25205/978-5-4437-1691-6-299.

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The parameters of the spontaneous experimental autoimmune encephalomyelitis development in mice, a model of multiple sclerosis, were investigated in first-generation hybrids obtained by crossing transgenic lines 2D2 and Th. The data were compared with similar parameters for mice of the parental lines 2D2 and Th.
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Liu, C., M. Kronenberg, X. Jiang, D. Rowe, and M. Hadjiargyrou. "Characterization of Mustn1PRO-GFPtpz transgenic mice." In 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413256.

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Irungbam, K., M. Roderfeld, Y. Churin, et al. "Abcb4-knockout reduces hepatic lipid steatosis in HBs transgenic mice." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402182.

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Reports on the topic "Transgenic Mice"

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Segall, Jeffrey E. Analysis of Metastasis in Transgenic Mice. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada403427.

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Segall, Jeffrey. Analysis of Metastasis in Transgenic Mice. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada384861.

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Kast, W. M. Prostate Cancer Immunotherapy Development in Prostate Specific Antigen Transgenic Mice. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada395836.

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Shankar, Deepa. Analysis of Multistep Mammary Tumorigenesis in WNT-1 Transgenic Mice. Defense Technical Information Center, 1995. http://dx.doi.org/10.21236/ada302270.

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Windle, Jolene J. Mechanisms of Ras Control of Mammary Tumor Properties in Transgenic Mice. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada403384.

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Windle, Jolene J. Mechanisms of Ras Control of Mammary Tumor Properties in Transgenic Mice. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada392893.

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Mao, Muling. Development and Characterization of Transgenic Mice with Mammary Gland Specific Expression of the Tumor Suppressor. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada404605.

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Cadieux, Chantal. Mammary Gland Tumor Development in Transgenic Mice Overexpressing Different Isoforms of the CDP/Cux Transcription Factor. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada506317.

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Cadieux, Chantal. Mammary Gland Tumor Development in Transgenic Mice Overexpressing Different Isoforms of the CDP/Cux Transcription Factor. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada469226.

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Cuevas, Bruce. Training Entitled Development and Characterization of Transgenic Mice With Mammary Gland Specific Expression of the Tumor Suppressor. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada390697.

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