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Journal articles on the topic 'Transgenic mice. Mice'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

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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2

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 p

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3

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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4

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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5

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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6

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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7

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

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8

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 uni

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9

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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10

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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11

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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12

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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13

Greten, Florian R., Martin Wagner, Christoph K. Weber, Ulrich Zechner, Guido Adler та Roland M. Schmid. "TGFα transgenic mice". Pancreatology 1, № 4 (2001): 363–68. http://dx.doi.org/10.1159/000055835.

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14

Higuchi, Yasunori, Atsushi Yasui, Keiko Matsuura, and Shunsuke Yamamoto. "CD156 Transgenic Mice." Pathobiology 70, no. 1 (2002): 47–54. http://dx.doi.org/10.1159/000066003.

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15

Brenner, Michael, and Albee Messing. "GFAP Transgenic Mice." Methods 10, no. 3 (1996): 351–64. http://dx.doi.org/10.1006/meth.1996.0113.

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16

Abrams, Irene, and Martine Kaiser. "Licensing Transgenic Mice." Industry and Higher Education 15, no. 4 (2001): 295–302. http://dx.doi.org/10.5367/000000001101295795.

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Transgenic mice are phenomenal research tools that are of interest to both industry and academic researchers. Many technology transfer offices will be faced with the challenge of licensing transgenic mice. In this paper the authors illustrate some of the unique issues that arise in licensing transgenic mice and provide some strategies for successful commercialization. They discuss patent and licensing options and provide examples from their own experience in transgenic mouse licensing at the Massachusetts Institute of Technology.

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17

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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18

Wei, S., Y. Feng, FY Che, et al. "Obesity and diabetes in transgenic mice expressing proSAAS." Journal of Endocrinology 180, no. 3 (2004): 357–68. http://dx.doi.org/10.1677/joe.0.1800357.

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ProSAAS is a neuroendocrine peptide precursor that potently inhibits prohormone convertase 1 in vitro. To explore the function of proSAAS and its derived peptides, transgenic mice were created which express proSAAS using the beta-actin promoter. The body weight of transgenic mice was normal until approximately 10-12 weeks, and then increased 30-50% over wild-type littermates. Adult transgenic mice had a fat mass approximately twice that of wild-type mice, and fasting blood glucose levels were slightly elevated. In the pituitary, the levels of several fully processed peptides in transgenic mice

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19

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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20

Storb, U., C. Pinkert, B. Arp, et al. "Transgenic mice with mu and kappa genes encoding antiphosphorylcholine antibodies." Journal of Experimental Medicine 164, no. 2 (1986): 627–41. http://dx.doi.org/10.1084/jem.164.2.627.

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Transgenic mice were produced that carried in their germlines rearranged kappa and/or mu genes with V kappa and VH regions from the myeloma MOPC-167 kappa and H genes, which encode anti-PC antibody. The mu genes contain either a complete gene, including the membrane terminus (mu genes), or genes in which this terminus is deleted and only the secreted terminus remains (mu delta mem genes). The mu gene without membrane terminus is expressed at as high a level as the mu gene with the complete 3' end, suggesting that this terminus is not required for chromatin activation of the mu locus or for sta

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21

Yukawa, K., H. Kikutani, T. Inomoto, et al. "Strain dependency of B and T lymphoma development in immunoglobulin heavy chain enhancer (E mu)-myc transgenic mice." Journal of Experimental Medicine 170, no. 3 (1989): 711–26. http://dx.doi.org/10.1084/jem.170.3.711.

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The transgenic mice were produced by injecting eggs of B6 and C3H/HeJ mice with the human E mu-myc gene. Preferential development of B lymphomas was observed in the B6 transgenic mice, whereas the C3H/HeJ transgenic mice developed mostly T lymphomas. The phenotypic activation of B lineage cells but not of T lineage cells was detected in the prelymphomatous transgenic mice of both strains. The transgene was similarly expressed in B and T cells of the transgenic mice of both strains. These results suggest that a high incidence of T lymphomas in the C3H/HeJ transgenic mice may not be due to the p

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22

Gillam, E. "Transgenic xenosensors: humanizing mice." Trends in Pharmacological Sciences 21, no. 9 (2000): 330–31. http://dx.doi.org/10.1016/s0165-6147(00)01532-7.

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23

Lem, Janis, and Clint L. Makino. "Phototransduction in transgenic mice." Current Opinion in Neurobiology 6, no. 4 (1996): 453–58. http://dx.doi.org/10.1016/s0959-4388(96)80049-3.

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24

Pomeroy, Kimball O. "Cryopreservation of transgenic mice." Genetic Analysis: Biomolecular Engineering 8, no. 3 (1991): 95–101. http://dx.doi.org/10.1016/1050-3862(91)90043-q.

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25

Mellor, Andrew, Min Zhou, Simon J. Conway, and David Munn. "HLA-G transgenic mice." Journal of Reproductive Immunology 43, no. 2 (1999): 253–61. http://dx.doi.org/10.1016/s0165-0378(99)00027-3.

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26

Elmer, G. I., J. L. Evans, S. R. Goldberg, C. J. Epstein, and J. L. Cadet. "Transgenic superoxide dismutase mice." Behavioural Pharmacology 7, no. 7 (1996): 628???639. http://dx.doi.org/10.1097/00008877-199611000-00008.

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27

Windle, Jolene J., Daniel M. Albert, Joan M. O'Brien, et al. "Retinoblastoma in transgenic mice." Nature 343, no. 6259 (1990): 665–69. http://dx.doi.org/10.1038/343665a0.

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28

Crawley, Jacqueline N., Elliott J. Mufson, John G. Hohmann, et al. "Galanin overexpressing transgenic mice." Neuropeptides 36, no. 2-3 (2002): 145–56. http://dx.doi.org/10.1054/npep.2002.0891.

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29

Richa, Jean. "Production of Transgenic Mice." Molecular Biotechnology 17, no. 3 (2001): 261–68. http://dx.doi.org/10.1385/mb:17:3:261.

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30

Cory, Suzanne, and Jerry M. Adams. "Transgenic Mice and Oncogenesis." Annual Review of Immunology 6, no. 1 (1988): 25–48. http://dx.doi.org/10.1146/annurev.iy.06.040188.000325.

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31

SUZUKI, Misao. "Production of transgenic mice." Folia Pharmacologica Japonica 104, no. 2 (1994): 79–84. http://dx.doi.org/10.1254/fpj.104.79.

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32

Suzuki, Misao. "Production of transgenic mice." Folia Pharmacologica Japonica 129, no. 5 (2007): 325–29. http://dx.doi.org/10.1254/fpj.129.325.

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33

Ji, Guangju, Morris E. Feldman, Ke-Yu Deng, et al. "Ca2+-sensing Transgenic Mice." Journal of Biological Chemistry 279, no. 20 (2004): 21461–68. http://dx.doi.org/10.1074/jbc.m401084200.

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34

Mintz, B. "Melanomas in transgenic mice." Melanoma Research 3, no. 1 (1993): 16. http://dx.doi.org/10.1097/00008390-199303000-00049.

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35

Wadghiri, Youssef Zaim, and Joseph A. Helpern. "MR of transgenic mice." NMR in Biomedicine 20, no. 3 (2007): 151–53. http://dx.doi.org/10.1002/nbm.1178.

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36

URANI, ALEXANDRE, and PETER GASS. "Corticosteroid Receptor Transgenic Mice." Annals of the New York Academy of Sciences 1007, no. 1 (2003): 379–93. http://dx.doi.org/10.1196/annals.1286.037.

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37

Degen, Jay L., Nancy J. Jensen, Cynthia C. Daugherty, Kersten McLain, S. Steven Potter, and Theodore T. Suhl. "Fibrinogen-deficient transgenic mice." Fibrinolysis 8 (January 1994): 102. http://dx.doi.org/10.1016/0268-9499(94)90569-x.

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38

Compere, Sally J., Patricia Baldacci, and Rudolf Jaenisch. "Oncogenes in transgenic mice." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 948, no. 2 (1988): 129–49. http://dx.doi.org/10.1016/0304-419x(88)90008-x.

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39

Altmann, D. M., D. C. Douek, A. J. Frater, C. M. Hetherington, H. Inoko, and J. I. Elliott. "The T cell response of HLA-DR transgenic mice to human myelin basic protein and other antigens in the presence and absence of human CD4." Journal of Experimental Medicine 181, no. 3 (1995): 867–75. http://dx.doi.org/10.1084/jem.181.3.867.

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Analysis of HLA class II transgenic mice has progressed in recent years from analysis of single chain HLA class II transgenes with expression of mixed mouse/human heterodimers to double transgenic mice expressing normal human heterodimers. Previous studies have used either HLA transgenic mice in which there is a species-matched interaction with CD4 or mice which lack this interaction. Since both systems are reported to generate HLA-restricted responses, the matter of the requirement for species-matched CD4 remains unclear. We have generated triple transgenic mice expressing three human transge

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40

Nussenzweig, M. C., A. C. Shaw, E. Sinn, J. Campos-Torres, and P. Leder. "Allelic exclusion in transgenic mice carrying mutant human IgM genes." Journal of Experimental Medicine 167, no. 6 (1988): 1969–74. http://dx.doi.org/10.1084/jem.167.6.1969.

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Expression of the membrane-bound version of the human mu chain in transgenic mice results in the allelic exclusion of endogenous mouse Ig heavy chain genes (6). The secreted version of the human Ig transgene has no such effect. F1 hybrid animals that carry transgenes for both secreted and membrane-bound human mu chains produce both forms of the human heavy chain while strongly suppressing endogenous mouse mu expression. The simultaneous expression of the two rearranged transgenes in primary B cells suggests that allelic exclusion operates before the formation of a second functionally rearrange

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41

Kolb, Andreas F., Lecia Pewe, John Webster, Stanley Perlman, C. Bruce A. Whitelaw, and Stuart G. Siddell. "Virus-Neutralizing Monoclonal Antibody Expressed in Milk of Transgenic Mice Provides Full Protection against Virus-Induced Encephalitis." Journal of Virology 75, no. 6 (2001): 2803–9. http://dx.doi.org/10.1128/jvi.75.6.2803-2809.2001.

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ABSTRACT Neutralizing antibodies represent a major host defense mechanism against viral infections. In mammals, passive immunity is provided by neutralizing antibodies passed to the offspring via the placenta or the milk as immunoglobulin G and secreted immunoglobulin A. With the long-term goal of producing virus-resistant livestock, we have generated mice carrying transgenes that encode the light and heavy chains of an antibody that is able to neutralize the neurotropic JHM strain of murine hepatitis virus (MHV-JHM). MHV-JHM causes acute encephalitis and acute and chronic demyelination in sus

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42

Hazel, Mark, Robert C. Cooksey, Deborah Jones, et al. "Activation of the Hexosamine Signaling Pathway in Adipose Tissue Results in Decreased Serum Adiponectin and Skeletal Muscle Insulin Resistance." Endocrinology 145, no. 5 (2004): 2118–28. http://dx.doi.org/10.1210/en.2003-0812.

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Abstract Overexpression of the rate-limiting enzyme for hexosamine synthesis (glutamine:fructose-6-phosphate amidotransferase) in muscle and adipose tissue of transgenic mice was previously shown to result in insulin resistance and hyperleptinemia. Explanted muscle from transgenic mice was not insulin resistant in vitro, suggesting that muscle insulin resistance could be mediated by soluble factors from fat tissue. To dissect the relative contributions of muscle and fat to hexosamine-induced insulin resistance, we overexpressed glutamine:fructose-6-phosphate amidotransferase 2.5-fold, specific

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43

Browning, Shawn R., Gary L. Mason, Tanya Seward, et al. "Transmission of Prions from Mule Deer and Elk with Chronic Wasting Disease to Transgenic Mice Expressing Cervid PrP." Journal of Virology 78, no. 23 (2004): 13345–50. http://dx.doi.org/10.1128/jvi.78.23.13345-13350.2004.

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ABSTRACT We generated mice expressing cervid prion protein to produce a transgenic system simulating chronic wasting disease (CWD) in deer and elk. While normal mice were resistant to CWD, these transgenic mice uniformly developed signs of neurological dysfunction ∼230 days following intracerebral inoculation with four CWD isolates. Inoculated transgenic mice homozygous for the transgene array developed disease after ∼160 days. The brains of sick transgenic mice exhibited widespread spongiform degeneration and contained abnormal prion protein and abundant amyloid plaques, many of which were fl

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44

Starck, J., R. Sarkar, M. Romana, et al. "Developmental regulation of human gamma- and beta-globin genes in the absence of the locus control region." Blood 84, no. 5 (1994): 1656–65. http://dx.doi.org/10.1182/blood.v84.5.1656.1656.

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Abstract Two lines of transgenic mice carrying a normal 40-kb Kpn I beta-globin cluster transgene lacking the locus control region (LCR) were analyzed for the expression of human gamma- and beta-globin genes during mouse development. After RNase protection assays, the ratios of human G gamma- , A gamma-, or beta-mRNAs relative to endogenous mouse zeta + alpha mRNAs were obtained for each stage of development. The two gamma transgenes were expressed in day-11.5 blood (embryonic stage) and day- 13.5 blood (early fetal stage), but their expression was markedly decreased by day 16.5 of fetal life.

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45

Starck, J., R. Sarkar, M. Romana, et al. "Developmental regulation of human gamma- and beta-globin genes in the absence of the locus control region." Blood 84, no. 5 (1994): 1656–65. http://dx.doi.org/10.1182/blood.v84.5.1656.bloodjournal8451656.

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Two lines of transgenic mice carrying a normal 40-kb Kpn I beta-globin cluster transgene lacking the locus control region (LCR) were analyzed for the expression of human gamma- and beta-globin genes during mouse development. After RNase protection assays, the ratios of human G gamma- , A gamma-, or beta-mRNAs relative to endogenous mouse zeta + alpha mRNAs were obtained for each stage of development. The two gamma transgenes were expressed in day-11.5 blood (embryonic stage) and day- 13.5 blood (early fetal stage), but their expression was markedly decreased by day 16.5 of fetal life. Expressi

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46

Zhou, R., H. Flaswinkel, MR Schneider, et al. "Insulin-like growth factor-binding protein-4 inhibits growth of the thymus in transgenic mice." Journal of Molecular Endocrinology 32, no. 2 (2004): 349–64. http://dx.doi.org/10.1677/jme.0.0320349.

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Numerous in vitro studies have demonstrated that IGF-binding protein (IGFBP)-4 is a consistent inhibitor of IGF actions. In order to investigate the functions of IGFBP-4 in vivo, transgenic mice were generated by microinjection of a transgene, in which the murine Igfbp4 cDNA is driven by the H-2K(b) promoter, and followed by a splicing cassette and polyadenylation signal of the human beta-globin gene. Transgene mRNA was expressed ubiquitously, and elevated IGFBP-4 protein was detected in the spleen, thymus, kidney and lung of transgenic mice. The activities of serum IGFBPs were not changed in

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47

Roth, P. E., L. Doglio, J. T. Manz, J. Y. Kim, D. Lo, and U. Storb. "Immunoglobulin gamma 2b transgenes inhibit heavy chain gene rearrangement, but cannot promote B cell development." Journal of Experimental Medicine 178, no. 6 (1993): 2007–21. http://dx.doi.org/10.1084/jem.178.6.2007.

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Transgenic mice with a gamma 2b transgene were produced to investigate whether gamma 2b can replace mu in the development of B lymphocytes. Transgenic gamma 2b is present on the surface of B cells. Young transgenic mice have a dramatic decrease in B cell numbers, however, older mice have almost normal B cell numbers. Strikingly, all gamma 2b-expressing B cells in the spleen also express mu. The same is true for mice with a hybrid transgene in which the mu transmembrane and intracytoplasmic sequences replace those of gamma 2b (gamma 2b-mumem). The B cell defect is not due to toxicity of gamma 2

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48

HIRIPI, LÁSZLÓ, MÁRIA BARANYI, LÁSZLÓ SZABÓ та ін. "Effect of rabbit κ-casein expression on the properties of milk from transgenic mice". Journal of Dairy Research 67, № 4 (2000): 541–50. http://dx.doi.org/10.1017/s0022029900004386.

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Transgenic mice were produced carrying the coding region of the rabbit κ-casein gene linked to the upstream region of the rabbit whey acidic protein gene. Mice from the highest-expressing line produced 2·5 mg rabbit κ-casein/ml in their milk. The foreign protein was associated with the casein micelles and altered micelle size, though in the high-expressing line rabbit κ-casein also segregated into the whey fraction obtained after centrifuging the milk samples. Milk from transgenic mice had the same overall protein content as that from non-transgenic mice, except for the transgene product. Howe

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49

Nguyen, Xinh-Xinh, Matthew Sanderson, Kristi Helke, and Carol Feghali-Bostwick. "Phenotypic Characterization of Transgenic Mice Expressing Human IGFBP-5." International Journal of Molecular Sciences 22, no. 1 (2020): 335. http://dx.doi.org/10.3390/ijms22010335.

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Pulmonary fibrosis is one of the important causes of morbidity and mortality in fibroproliferative disorders such as systemic sclerosis (SSc) and idiopathic pulmonary fibrosis (IPF). Insulin-like growth factor binding protein-5 (IGFBP-5) is a conserved member of the IGFBP family of proteins that is overexpressed in SSc and IPF lung tissues. In this study, we investigated the functional role of IGFBP-5 in the development of fibrosis in vivo using a transgenic model. We generated transgenic mice ubiquitously expressing human IGFBP-5 using CRISPR/Cas9 knock-in. Our data show that the heterozygous

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Loiacono, Christie M., Robert Myers, and William J. Mitchell. "Neurons Differentially Activate the Herpes Simplex Virus Type 1 Immediate-Early Gene ICP0 and ICP27 Promoters in Transgenic Mice." Journal of Virology 76, no. 5 (2002): 2449–59. http://dx.doi.org/10.1128/jvi.76.5.2449-2459.2002.

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Abstract:

ABSTRACT Herpes simplex virus type 1 (HSV-1) immediate-early (IE) proteins are required for the expression of viral early and late proteins. It has been hypothesized that host neuronal proteins regulate expression of HSV-1 IE genes that in turn control viral latency and reactivation. We investigated the ability of neuronal proteins in vivo to activate HSV-1 IE gene promoters (ICP0 and ICP27) and a late gene promoter (gC). Transgenic mice containing IE (ICP0 and ICP27) and late (gC) gene promoters of HSV-1 fused to the Escherichia coli β-galactosidase coding sequence were generated. Expression

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