Relevant bibliographies by topics / Mice Transgenic mice

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

Academic literature on the topic 'Mice Transgenic mice'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Mice 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 transgenic (IGF-1R/GHR) mice were produced by the mating between nine pairs of IGF-1R and GHR hemizygous transgenic F1 mice. The transmission patterns in the 78 F2 pups produced from these matings were 20 with no transgene (25.6%), 17 with the IGF-1R gene (21.8%), 25 with the GHR gene (32.1%), and 16 with both GHR and IGF-1R genes (20.5%). The mRNA expression of transgenes using RT-PCR with the specific primers for IGF-IR and GHR genes was checked in tissues of transgenic mice. Double transgenic mice with IGF-IR and GHR genes expressed more mRNAs of transgenes than non-transgenic or single transgenic mice. Growth of double transgenic mice was fastest compared with single transgenic mice containing IGF-1R or GHR genes. And GHR transgenic mice grew faster than IGF-1R transgenic mice. When body weights of 15 transgenic mice for each transgenic line were measured at 4, 10, and 14 weeks after birth, double transgenic mice were significantly heavier compared with non-transgenic control mice at each stage (24 to 30% heavier in double transgenic mice; 15 to 20% heavier in single transgenic mice, P < 0.05). These results suggest that overexpression of growth-related receptor genes could promote the growth of transgenic animals with an additive effect.
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Babinet, C., D. Morello, and J. P. Renard. "Transgenic mice." Genome 31, no. 2 (1989): 938–49. http://dx.doi.org/10.1139/g89-165.

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Stable integration into the mouse genome of exogenous genetic information has become, over the past few years, a very potent approach for different aspects of biology. It is a common feature that the integrated exogenous gene (the transgene) is expressed properly both spatially and temporally. Constructing different lines of transgenic mice carrying various versions of a gene, therefore, permits cis acting DNA sequences involved in the specificity of expression to be defined, in the context of the developing animal. This in turn opens the way to a variety of experiments in which a given gene product is targeted to one or another cell type, thus offering some insight into the physiological role of this product. Such a strategy has been used, for example, to address the questions of the role of oncogenes in malignant transformation. The insertion of foreign DNA per se may disrupt the function of endogenous genes, thus creating an insertional mutation. The corresponding affected genes may subsequently be cloned, using the transgene as a tag. Finally, the ability to perform homologous recombination, recently demonstrated with embryonic stem cells that can colonize the germ line of a foreign embryo, should constitute in the near future a unique way to analyse in detail the functioning of the mammalian genome.Key words: transgenic mice, oncogenes, insertional mutagenesis, cis-acting sequences, homologous recombination.
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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 pronuclear microinjection method as the most accepted way of gene transfer into the mouse genome.
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Hickman-Davis, Judy M., and Ian C. Davis. "Transgenic mice." Paediatric Respiratory Reviews 7, no. 1 (2006): 49–53. http://dx.doi.org/10.1016/j.prrv.2005.09.005.

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PALMITER, R., and R. BRINSTER. "Transgenic mice." Cell 41, no. 2 (1985): 343–45. http://dx.doi.org/10.1016/s0092-8674(85)80004-0.

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Friedman, Rick A., and Allen F. Ryan. "Transgenic Mice." Otolaryngologic Clinics of North America 25, no. 5 (1992): 1017–26. http://dx.doi.org/10.1016/s0030-6665(20)30922-1.

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Westphal, Heiner. "Transgenic mice." BioEssays 6, no. 2 (1987): 73–76. http://dx.doi.org/10.1002/bies.950060208.

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BABINET, CHARLES. "Transgenic Mice." Journal of the American Society of Nephrology 11, suppl 2 (2000): S88—S94. http://dx.doi.org/10.1681/asn.v11suppl_2s88.

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Abstract. Stable integration into the mouse genome of exogenous genetic information, i.e., the creation of transgenic mice, has become a privileged way of analyzing gene function in normal development and pathology. Both gene addition and gene replacement may be performed. This has allowed, in particular, the creation of mice in which precise mutations are introduced into a given gene. Furthermore, in recent years, strategies that induce the expression of a mutation in a given type of cell and/or at a given time in development have been developed. Thus, the transgenic methodology affords a unique and irreplaceable tool for the study of mammalian development and biology and for the creation of animal models for human genetic diseases.
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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 apart from splenomegaly. Eosinophils were at least 65- and 265-fold higher in blood from transgenics, relative to normal littermates, and approximately two- or sevenfold more numerous relative to blood from mice infected with the helminth Mesocestoides corti. Much more modest increases in blood neutrophil, lymphocyte, and monocyte numbers were noted in transgenics, relative to normal littermates (less than threefold). Thus IL-5 in vivo is relatively specific for the eosinophil lineage. Large numbers of eosinophils were present in spleen, bone marrow, and peritoneal exudate, and were highest in the line with the greatest transgene copy number. Eosinophilia was also noted in histological sections of transgenic lungs, Peyer's patches, mesenteric lymph nodes, and gut lamina propria but not in other tissues examined. IL-5 was detected in the sera of transgenics at levels comparable to those seen in sera from parasite-infected animals. IL-3 and granulocyte/macrophage colony-stimulating factor (GM-CSF) were not found. IL-5 mRNA was detected in transgenic thymus, Peyer's patches, and superficial lymph nodes, but not in heart, liver, brain, or skeletal muscle or in any tissues from nontransgenics. Bone marrow from transgenic mice was rich in IL-5-dependent eosinophil precursors. These data indicate that induction of the IL-5 gene is sufficient for production of eosinophilia, and that IL-5 can induce the full pathway of eosinophil differentiation. IL-5 may therefore not be restricted in action to the later stages of eosinophil differentiation, as suggested by earlier in vitro studies.
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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. However, there was no significant difference in conscious mean arterial pressure between transgenic and non-transgenic mice. The levels of renal renin mRNA in transgenics and nontransgenic littermates were compared throughout ontogeny and were found to be equal in newborns, elevated 3- to 5-fold in 1-wk-old transgenics, and yet decreased 10-fold by 6 wk of age in transgenic mice. Expression of the transgene in the kidney exhibited the proper developmental pattern and was properly restricted to juxtaglomerular cells in neonatal mice. Nevertheless, in adult mice, T-antigen-containing cells were found throughout the entire renal arterial tree. The observed ability of renal vascular cells to be recruited to express both renin and T-antigen suggests a mechanism that can explain the development of the renal pathology in these mice.
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Dissertations / Theses on the topic "Mice 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 nephritis, segmental glomerulosclerosis), lung (lymphocytic interstitial pneumonitis) and heart disease. In addition, these Tg mice fail to mount a class-switched antibody response after immunization with ovalbumin, produce anti-DNA autoantibodies and some of them develop P. Carinii lung infection. These CD4C/SHIV-nefSIV Tg mice develop an AIDS-like disease very similar to that of CD4C/HIV Tg mice, except that the kidney and cardiac diseases were more severe, and that a thymic developmental defect was observed. Heart enlargement was very severe in CD4C/SIV Tg mice during early breeding on the C3H background. Histopathological lesions in the heart of these mice were also multifocal and were similar to those found in CD4C/HIV Tg mice. Data from echocardiography analysis are not yet available for these Tg mice. The low number of peripheral CD8+ and CD4 + T cells likely reflects a thymic defect and may be similar to the DiGeorge-like "thymic defect" immunophenotype described in a subgroup of HIV-1 infected children. Ontogeny studies show that the Tg mice were born with a smaller thymus and that this phenotype is not progressive in nature. As young as embryonic day 17, the thymic absolute cell numbers are lower in the Tg mice when compared to their non-Tg controls and there is a defect in thymocyte maturation in the transition between DN3 and DN4, with a failure to generate normal numbers of DP cells. Fetal liver transplantation studies have ruled out a significant impairment of the thymic epithelium and have suggested that this defect is likely a direct consequence of abnormal T cell progenitors in the thymus.<br>Therefore, it appears that SIV Nef alone expressed in mice, in appropriate cell types and at sufficient levels, can elicit many of the phenotypes of simian and human AIDS. These Tg mice should be instrumental in studying the pathogenesis of SIV Nef-induced phenotypes.
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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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Oghumu, Steve Onyeka. "Generation and Characterization of CXCR3 Bicistronic Reporter Mice and CXCR3 Transgenic Mice." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274927351.

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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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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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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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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 medium triggering a bystander effect was observed. This prodrug system was also assessed <i>in vivo</i>, for which transgenic mice were generated expressing NTR specifically in adipose tissue under the control of the aP2 promoter. Upon CB1954 treatment, transgenic mice showed extensive cell depletion in different fat deposits, which was directly correlated to both the dose of prodrug and the levels of NTR expressed. The present model provides a new inducible approach to manipulate the number of adipocytes at different stages of the mouse development and provides a new system for the study of fat metabolism especially in abnormal conditions such as obesity and its modulation through the manipulation of the target cell population. Also reported are preliminary experiments to assess a novel system of ablation mediated by the murine adapter molecule RAIDD. Stable cell lines were generated to overexpress RAIDD after differentiation. A range of phenotypes was observed with these clones from a complete blockage of the differentiation to the killing of cells that escape the blockage. The present results suggest for first time a new developmental role for this gene and strongly encourage further experimentation to confirm this effect in an experimental animal model.
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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 of age, Tg+ mice were pre-tested in the radial arm water maze (RAWM) task of working memory and found to be unimpaired. At 4.5 months of age, half of the Tg+ mice received the first of 3 equally-spaced hyperoxia sessions (3 hrs each) given over the ensuing 3 months. The other half of the Tg+ mice were exposed to compressed air during these 3 sessions. RAWM testing performed immediately following the final gas session at 7.5 months of age revealed significant working memory impairment in Tg+ mice exposed to hyperoxia. The Tg+ group that was exposed to placebo treatment showed a trend towards impairment, however, was not significantly different from the non-transgenic group. Hyperoxia-induced memory impairment in Tg+ mice did not involve changes in brain A[beta] deposition, degenerative cell numbers in hippocampus, neocortical lipid peroxidation, or hippocampal levels of APP, ApoE, COX-2, or GFAP. The combination of excess A[beta] and hyperoxia could have induced greater oxidative stress and cerebral vasoconstriction than either one alone, resulting in a pathologic cerebral hypoperfusion that triggered subsequent cognitive impairment.
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Derrett-Smith, E. C. "Systemic sclerosis vasculopathy : exploration in transgenic mice." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1383812/.

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Vascular disease in systemic sclerosis (SSc) leads to significant morbidity and mortality. No robust animal model of vasculopathy in SSc has been described. The hypothesis underpinning work described in this thesis is that a primary defect in TGFβ signalling is sufficient to generate the fibrotic, vascular and inflammatory phenotype of this condition. This is explored using a novel transgenic mouse model of SSc (TβRIIΔk-fib). The transgenic mouse strain TβRIIΔk-fib carries a kinase-deficient type II TGFβ receptor which is expressed under the control of a fibroblast specific promoter leading to balanced ligand-dependent upregulation of TGFβ signalling. Consequent increased TGFβ ligand in the peri-fibroblast microenvironment modulates other cell types. The phenotype is one of ubiquitous skin and gut fibrosis and increased susceptibility to severe and persistent fibrosis in response to epithelial lung injury. In this thesis, a cardiovascular phenotype is characterised for the first time, with adventitial fibrosis and medial attenuation within the large elastic arteries of the systemic circulation resulting in systemic hypertension with cardiac fibrosis. Within the pulmonary arterial circulation, there is ubiquitous medial hypertrophy, perivascular inflammation and mild pulmonary hypertension. In both circulations, the phenotype can be exaggerated additional vascular stress: NO synthase inhibition results hypertensive renal stress and VEGFR2 inhibition results in obliterative vascular changes representative of pulmonary arterial hypertension. This thesis demonstrates a unique phenotype that is strikingly relevant to that of human SSc vasculopathy, providing compelling evidence for the role of altered TGFβ signaling in systemic and pulmonary vasculopathy and for the role of altered cell interactions and responses to injury in the development of vascular consequences. A paradigm in which a background TGFβ dependent vasculopathy renders mice susceptible to injury leading to hallmark features of SSc vasculopathy is suggested. This model provides mechanistic insight and a potential platform for preclinical interventional studies in these important complications of SSc.
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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 "Mice Transgenic mice"

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

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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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Transgenic mouse methods and protocols. 2nd ed. Humana Press, 2011.

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

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Haddad, George E. Expression of HLA class II genes in transgenic mice. National Library of Canada, 1994.

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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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Ferrick, David A. Transgenic mice as a in vivo model for self reactivity. R.G. Landes Co., 1994.

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What's wrong with my mouse?: Behavioral phenotyping of transgenic and knockout mice. 2nd ed. Wiley-Interscience, 2007.

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Gingrich, Jeffrey R. Characterization of a neural-specific inducible genetic system in transgenic mice. National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Book chapters on the topic "Mice 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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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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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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Lee, Myung-Shik, and Nora Sarvetnick. "IL-10 Transgenic Mice." In Interleukin-10. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22038-2_15.

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Hanahan, Douglas. "Oncogenesis in Transgenic Mice." In Oncogenes and Growth Control. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-73325-3_48.

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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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Götz, Jürgen, Markus Tolnay, Robi Barmettler, et al. "Human Tau Transgenic Mice." In Advances in Experimental Medicine and Biology. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1249-3_6.

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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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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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Feng, Guoping, Jing Lu, and Jimmy Gross. "Generation of Transgenic Mice." In Pain Research. Humana Press, 2004. http://dx.doi.org/10.1385/1-59259-770-x:155.

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Conference papers on the topic "Mice Transgenic mice"

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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 TGFβ2- and TGFβ3-deficient mice exacerbated cardiovascular aneurysms in TGFβ2/TGFβ3-doubly deficient embryos. In vitro cell culture experiments demonstrated an impaired ability of TGFβ2-deficient mouse embryonic fibroblasts to reorganize collagen. Previous data indicate reduced levels of TGFβ2 leading to a higher susceptibility to aortic aneurysm. We present here the macroscopic biomechanical characterization of the aorta of a transgenic mouse line showing this susceptibility and compare it to wild-type mice. We also present results comparing the microstructure between mouse lines.
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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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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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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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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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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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Gibson, Katelin A., Merit L. Goodman, and Christy R. Hagan. "Abstract 5228: Mammary gland tumors in progesterone receptor transgenic mice." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5228.

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10

Ooi, Chen Yen, and Naomi C. Chesler. "The Role of Collagen in Pulmonary Hypertension-Induced Large Artery Stiffening." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192951.

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Abstract:
Hypoxic pulmonary hypertension (HPH) leads to stiffening of large pulmonary arteries, which affects right ventricular afterload. We hypothesized that vascular collagen accumulation is the major cause of large pulmonary artery (PA) stiffening in HPH. We tested this hypothesis with transgenic mice that produce collagen type I resistant to degradation (Col1a1R/R) and wild type littermate controls (Col1a1+/+) exposed to hypoxia and allowed to recover. Pressure-diameter testing on left PAs demonstrated that stiffness in control mice increased with hypoxia and decreased with recovery (p &lt; 0.05). Preliminary tests in degradation-resistant mice suggest that PA stiffness decreases less with recovery than in controls. Quantitative measurements of vascular collagen content in right PAs are planned to develop statistical correlations between structure and function.
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Reports on the topic "Mice Transgenic mice"

1

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

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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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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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