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Thematische Bibliographien / Transgenic Mice / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Transgenic Mice“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

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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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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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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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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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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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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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Painter, Meghan, and Moses Rodriguez. "Intrinsic upregulation of critical innate immune effectors in a novel transgenic mouse model confers viral resistance (P1389)." Journal of Immunology 190, no. 1_Supplement (2013): 57.6. http://dx.doi.org/10.4049/jimmunol.190.supp.57.6.

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Abstract Our laboratory generated a transgenic mouse that ubiquitously expresses 3D, a picorno viral RNA-dependent RNA polymerase. 3D transgenic mice display an extreme antiviral phenotype when challenged with viruses from distinct families. To probe this protective molecular mechanism, we assayed differential gene expression in tissues of uninfected 3D transgenic mice. Microarray analysis revealed increased levels of 78 genes &gt;4-fold, including a distinct upregulation of critical innate antiviral effectors across tissues. RT-PCR analysis of liver, lung, kidney, CNS and heart tissue fro

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Sigurdardottir, D., J. Sohn, J. Kass, and E. Selsing. "Regulatory regions 3' of the immunoglobulin heavy chain intronic enhancer differentially affect expression of a heavy chain transgene in resting and activated B cells." Journal of Immunology 154, no. 5 (1995): 2217–25. http://dx.doi.org/10.4049/jimmunol.154.5.2217.

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Abstract We have compared the expression patterns of three Ig heavy chain transgenes. The three constructs differ only by deletion of J-C intron sequences located downstream of the Emu enhancer region. When stably transfected into a myeloma cell line, all three constructs are expressed at comparable levels. However, transgenic mice carrying each construct show dramatic differences in transgene expression. Our results indicate that, in addition to the Emu enhancer, at least two regions, RegA and RegS, within the J-C intron influence transgene expression. RegA, located directly downstream of the

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Kwan, H., V. Pecenka, A. Tsukamoto, et al. "Transgenes expressing the Wnt-1 and int-2 proto-oncogenes cooperate during mammary carcinogenesis in doubly transgenic mice." Molecular and Cellular Biology 12, no. 1 (1992): 147–54. http://dx.doi.org/10.1128/mcb.12.1.147-154.1992.

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The Wnt-1 and int-2 proto-oncogenes are transcriptionally activated by mouse mammary tumor virus insertion mutations in virus-induced tumors and encode secretory glycoproteins. To determine whether these two genes can cooperate during carcinogenesis, we have crossed two previously characterized lines of transgenic mice to obtain bitransgenic animals carrying both Wnt-1 and int-2 transgenes under the control of the mouse mammary tumor virus long terminal repeat. Mammary carcinomas appear earlier and with higher frequency in the bitransgenic animals, especially the males, than in either parental

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Kwan, H., V. Pecenka, A. Tsukamoto, et al. "Transgenes expressing the Wnt-1 and int-2 proto-oncogenes cooperate during mammary carcinogenesis in doubly transgenic mice." Molecular and Cellular Biology 12, no. 1 (1992): 147–54. http://dx.doi.org/10.1128/mcb.12.1.147.

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The Wnt-1 and int-2 proto-oncogenes are transcriptionally activated by mouse mammary tumor virus insertion mutations in virus-induced tumors and encode secretory glycoproteins. To determine whether these two genes can cooperate during carcinogenesis, we have crossed two previously characterized lines of transgenic mice to obtain bitransgenic animals carrying both Wnt-1 and int-2 transgenes under the control of the mouse mammary tumor virus long terminal repeat. Mammary carcinomas appear earlier and with higher frequency in the bitransgenic animals, especially the males, than in either parental

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Plopper, C. G., C. Helton, A. J. Weir, J. A. Whitsett та T. R. Korfhagen. "Quantitative Microscopic Comparison of the Organization of the Lung in Transgenic Mice Expressing Transforming Growth Factor-α (TGF-α)". Proceedings, annual meeting, Electron Microscopy Society of America 54 (11 серпня 1996): 14–15. http://dx.doi.org/10.1017/s0424820100162533.

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A wide variety of growth factors are thought to be involved in the regulation of pre- and postnatal lung maturation, including factors which bind to the epidermal growth factor receptor. Marked pulmonary fibrosis and enlarged alveolar air spaces have been observed in lungs of transgenic mice expressing human TGF-α under control of the 3.7 KB human SP-C promoter. To test whether TGF-α alters lung morphogenesis and cellular differentiation, we examined morphometrically the lungs of adult (6-10 months) mice derived from line 28, which expresses the highest level of human TGF-α transcripts among t

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Tsao, B. P., K. Ohnishi, H. Cheroutre, et al. "Failed self-tolerance and autoimmunity in IgG anti-DNA transgenic mice." Journal of Immunology 149, no. 1 (1992): 350–58. http://dx.doi.org/10.4049/jimmunol.149.1.350.

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Abstract Transgenic mice were generated that express both the H and L chain genes derived from a hybridoma secreting an IgG2a mAb specific for ds- and ssDNA. This hybridoma is derived from a lupus mouse and can accelerate nephritis in young NZB x NZW F1 female mice and induce clinical nephritis in BALB/c mice. Some transgenic B cells did not exhibit allelic exclusion; they expressed both transgene-derived IgG and endogenous IgM intracellularly. Most of the B cells in transgenic mice expressed endogenous IgM, some of them expressed low levels of IgG on cell membranes. The transgenic mice, creat

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Yang, Jianqi, Alison N. DeVore, Daniel A. Fu, et al. "Rapid and precise genotyping of transgene zygosity in mice using an allele-specific method." Life Science Alliance 6, no. 6 (2023): e202201729. http://dx.doi.org/10.26508/lsa.202201729.

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Precise determination of transgene zygosity is essential for use of transgenic mice in research. Because integration loci of transgenes are usually unknown due to their random insertion, assessment of transgene zygosity remains a challenge. Current zygosity genotyping methods (progeny testing, qPCR, and NGS-computational biology analysis) are time consuming, prone to error or technically challenging. Here, we developed a novel method to determine transgene zygosity requiring no knowledge of transgene insertion loci. This method applies allele-specific restriction enzyme digestion of PCR produc

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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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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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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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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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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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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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Faerman, A., I. Barash, R. Puzis, M. Nathan, D. R. Hurwitz, and M. Shani. "Dramatic heterogeneity of transgene expression in the mammary gland of lactating mice: a model system to study the synthetic activity of mammary epithelial cells." Journal of Histochemistry & Cytochemistry 43, no. 5 (1995): 461–70. http://dx.doi.org/10.1177/43.5.7730585.

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We studied the expression of human serum albumin (HSA) driven by the ovine beta-lactoglobulin promoter in the mammary glands of lactating mice from five independent transgenic strains, by employing combined in situ hybridization and immunostaining techniques. Four strains displayed a heterogeneous pattern of expression: mice of strains 91 and 92 expressed the transgene in only a fraction of the lobules, whereas in strains 69 and 83 all lobules contained cells expressing HSA. In all four strains the patterns of expression within expressing lobules corresponded to the morphology of alveolar cell

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Rath, S., A. Nisonoff, E. Selsing, and J. M. Durdik. "B cell abnormalities induced by a mu Ig transgene extend to L chain isotype usage." Journal of Immunology 146, no. 8 (1991): 2841–46. http://dx.doi.org/10.4049/jimmunol.146.8.2841.

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Abstract We have analyzed the phenotype of B cell populations from mice transgenic for a rearranged Ig mu H chain gene. We find a decrease in the number of B cells in the spleens of these mice. Transgenic B cells have decreased surface levels of both IgM and IgD. The circulating IgM in these mice is 3- to 10-fold enriched in lambda L chains, compared with that in non-transgenic mice. Analysis of IgM-producing hybridomas, from transgenic mice that express the transgene at high levels, demonstrates that this higher lambda frequency is observed in transgene-nonexpressing as well as transgene-expr

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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 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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Imanishi-Kari, T., C. A. Huang, J. Iacomini, and N. Yannoutsos. "Endogenous Ig production in mu transgenic mice. II. Anti-Ig reactivity and apparent double allotype expression." Journal of Immunology 150, no. 8 (1993): 3327–46. http://dx.doi.org/10.4049/jimmunol.150.8.3327.

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Abstract In 17.2.25 mu transgenic mice (M54, M95), many of the expressed Ig, whether encoded by the transgene or endogenous H chain genes, react with Ig. IgM antibodies encoded by the 17.2.25 mu transgene transfected into J558L myeloma cells are also Ig reactive. In addition, anti-Ig reactivity was manifested by antibodies of the IgM, IgG, and IgA isotypes from the transgenic mice, suggesting that this characteristic reactivity is associated with VH and VL domains of these antibodies. These antibodies bind the (Fab')2 fragment of mouse IgG1 mAb known to be directed against C mu allotypic deter

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Rudin, C. M., J. Hackett, and U. Storb. "Precursors of both conventional and Ly-1 B cells can escape feedback inhibition of Ig gene rearrangement." Journal of Immunology 146, no. 9 (1991): 3205–10. http://dx.doi.org/10.4049/jimmunol.146.9.3205.

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Abstract Experiments with transgenic mice carrying rearranged Ig transgenes have shown that membrane bound Ig molecules cause feedback inhibition of endogenous Ig gene rearrangement. However, this inhibition is never complete. It has been postulated that escape from feedback may be a property of the Ly-1 B cell subset, whereas rearrangement of endogenous Ig genes may be completely inhibited in conventional B cells. This possibility was investigated in transgenic mice carrying a lambda transgene under the control of the H chain enhancer. It was found that kappa producing B cells in these lambda

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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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Rimm, I. J., T. Ghayur, D. L. Gasser, et al. "Alloreactive lymphocytes from T cell receptor (beta-chain) transgenic mice do not mediate a graft-versus-host reaction." Journal of Immunology 146, no. 4 (1991): 1130–33. http://dx.doi.org/10.4049/jimmunol.146.4.1130.

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Abstract The injection of mature T cells into a tolerant or immunocompromised allogeneic host animal produces a graft versus host response (GVHR) that can result in splenomegaly, immunosuppression and death of the host animal. We demonstrate here that lymphocytes from T cell receptor beta-chain (TCR-beta) transgenic mice, in which the expression of the transgene inhibits endogenous beta- and gamma-gene rearrangements and thus causes abnormal T cell development, are unable to mediate a GVHR. The GVHR was measured after the injection of lymphocytes from transgenic mice into normal F1 mice and al

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Robbiani, Davide F., Kaity Colon, Kruti Naik, et al. "Enforced BCL6 Expression Inhibits B Cell Development in Vivo." Blood 104, no. 11 (2004): 1535. http://dx.doi.org/10.1182/blood.v104.11.1535.1535.

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Abstract The B-Cell Lymphoma 6 (BCL6) gene encodes for a zinc finger motifs containing transcriptional repressor that is frequently dysregulated by chromosomal translocations in germinal center lymphomas. A putative protooncogene, its transforming ability in vivo was reported in I-mu-HA-BCL6 knock-in mice by Cattoretti et al last year. We also tested this assumption in transgenic mice expressing BCL6 in B cells under the control of kappa light chain regulatory elements. We replaced the murine C-kappa locus with the 16kb human BCL6 genomic locus in a construct containing the murine kappa light

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Brooks, A. R., B. P. Nagy, S. Taylor, W. S. Simonet, J. M. Taylor, and B. Levy-Wilson. "Sequences containing the second-intron enhancer are essential for transcription of the human apolipoprotein B gene in the livers of transgenic mice." Molecular and Cellular Biology 14, no. 4 (1994): 2243–56. http://dx.doi.org/10.1128/mcb.14.4.2243-2256.1994.

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To identify DNA sequence elements from the human apolipoprotein B (apoB) gene required for high-level, correct tissue-specific expression in transgenic mice, we made several constructs that included one or more of the key regulatory elements that were previously characterized with cultured liver-derived and intestine-derived cell lines. Our data show that the apoB promoter alone (-898 to +121) is not sufficient to direct transcription in transgenic mice. An enhancer located in the second intron is absolutely required to specify transcription by the homologous apoB promoter in the livers of tra

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Brooks, A. R., B. P. Nagy, S. Taylor, W. S. Simonet, J. M. Taylor, and B. Levy-Wilson. "Sequences containing the second-intron enhancer are essential for transcription of the human apolipoprotein B gene in the livers of transgenic mice." Molecular and Cellular Biology 14, no. 4 (1994): 2243–56. http://dx.doi.org/10.1128/mcb.14.4.2243.

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To identify DNA sequence elements from the human apolipoprotein B (apoB) gene required for high-level, correct tissue-specific expression in transgenic mice, we made several constructs that included one or more of the key regulatory elements that were previously characterized with cultured liver-derived and intestine-derived cell lines. Our data show that the apoB promoter alone (-898 to +121) is not sufficient to direct transcription in transgenic mice. An enhancer located in the second intron is absolutely required to specify transcription by the homologous apoB promoter in the livers of tra

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Seery, John P., Eddie C. Y. Wang, Victoria Cattell, Joseph M. Carroll, Michael J. Owen та Fiona M. Watt. "A Central Role for αβ T Cells in the Pathogenesis of Murine Lupus". Journal of Immunology 162, № 12 (1999): 7241–48. http://dx.doi.org/10.4049/jimmunol.162.12.7241.

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Abstract We have previously shown that female transgenic mice expressing IFN-γ in the epidermis, under the control of the involucrin promoter, develop inflammatory skin disease and a form of murine lupus. To investigate the pathogenesis of this syndrome, we generated female IFN-γ transgenic mice congenitally deficient in either αβ or γδ T cells. TCRδ−/− transgenics continued to produce antinuclear autoantibodies and to develop severe kidney lesions. In contrast, TCRβ−/− IFN-γ transgenic mice failed to produce antinucleosome, anti-dsDNA, or antihistone autoantibodies, and kidney disease was abo

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Clutter, A. C., D. Pomp, and J. D. Murray. "Quantitative Genetics of Transgenic Mice: Components of Phenotypic Variation in Body Weights and Weight Gains." Genetics 143, no. 4 (1996): 1753–60. http://dx.doi.org/10.1093/genetics/143.4.1753.

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Abstract Transgenic mice possessing an ovine growth hormone gene were used to study the effects of elevated growth hormone on quantitative genetic variation. Males hemizygous for the transgene were mated to wild-type females to produce half- and full-sib families in which approximately half the progeny were transgenic and half were wild type. Analyses of body weights at 3–10 weeks, and weight gains from 3 to 6, and 6 to 10 weeks produced estimates of the proportion of total variance due to additive genetic effects (h2) and common litter effects (c2), and the genetic correlation between transge

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Tsika, G. L., J. L. Wiedenman, L. Gao, et al. "Induction of beta-MHC transgene in overloaded skeletal muscle is not eliminated by mutation of conserved elements." American Journal of Physiology-Cell Physiology 271, no. 2 (1996): C690—C699. http://dx.doi.org/10.1152/ajpcell.1996.271.2.c690.

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Mechanical overload leads to hypertrophy, increased type I fiber composition, and beta-myosin heavy chain (beta-MHC) induction in the fast-twitch plantaris muscle. To better understand the mechanism(s) involved in beta-MHC induction, we have examined inducible expression of transgenes carrying the simultaneous mutation of three DNA regulatory subregions [muscle CAT (MCAT), C-rich, and beta e3] in the context of either 5,600-base pair (bp; beta 5.6mut3) or 600-bp (beta 0.6mut3) beta-MHC promoter in overloaded plantaris muscles of transgenic mice. Protein extract from mechanically overloaded pla

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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 uni

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

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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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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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Doglio, Lynn, Joo Yeun Kim, Grazyna Bozek та Ursula Storb. "Expression ofλand K Genes Can Occur in all B Cells and is Initiated Around the Same Pre-B-Cell Developmental Stage". Developmental Immunology 4, № 1 (1994): 13–26. http://dx.doi.org/10.1155/1994/87352.

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Transgenic mice that carry a λ2 transgene under the control of the Vλ2 promoter and the Eλ2-4 enhancer (λ2Eλ mice) are described. A high proportion of B cells in the spleen and the bone marrow express the λ transgene on the cell membrane. λ2 protein is synthesized by all λ2Eλ-derived spleen B-cell hybridomas that have retained the transgene, suggesting that all B cells have the ability to express λ genes. Feedback inhibition of endogenous K-gene rearrangement is significant, but not complete. The results are similar to those with transgenic mice expressing the same λ2 transgene under the contr

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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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Heath, W. R., and J. F. Miller. "Expression of two alpha chains on the surface of T cells in T cell receptor transgenic mice." Journal of Experimental Medicine 178, no. 5 (1993): 1807–11. http://dx.doi.org/10.1084/jem.178.5.1807.

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CD8+ T cells taken directly from mice expressing a Kb-specific T cell receptor (TCR) transgene expressed the transgenic TCR in a bimodal profile as detected by flow cytometric analysis using a clonotype-specific monoclonal antibody. Those cells expressing the lower density of the transgenic TCR expressed the transgenic beta chain and two different alpha chains on their surface. One alpha chain was the product of the alpha transgene, whereas the other was derived by endogenous rearrangement. This report provides the first demonstration that T cells isolated directly from mice may express two di

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