Готові списки джерел за темами / Transgenic Mice

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Добірка наукової літератури з теми "Transgenic Mice"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 31 липня 2024

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Статті в журналах з теми "Transgenic Mice"

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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Auerbach, Anna B. "Production of functional transgenic mice by DNA pronuclear microinjection." Acta Biochimica Polonica 51, no. 1 (March 31, 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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Sigmund, C. D., C. A. Jones, H. J. Jacob, J. Ingelfinger, U. Kim, D. Gamble, V. J. Dzau, and K. W. Gross. "Pathophysiology of vascular smooth muscle in renin promoter-T-antigen transgenic mice." American Journal of Physiology-Renal Physiology 260, no. 2 (February 1, 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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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 (November 1, 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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Kong, Siyuan, Jinxue Ruan, Kaiyi Zhang, Bingjun Hu, Yuzhu Cheng, Yubo Zhang, Shulin Yang, and Kui Li. "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 triple-transgenic (11β-hydroxysteroid dehydrogenase type 1, 11β-HSD1; hIAPP; CHOP) mice (11β-HSD1-hIAPP- CHOP mice). The latter two types of transgenic (Tg) animals were induced with high-fat high-sucrose diets (HFHSD). We analyzed the diabetes-related symptoms and histology features of the transgenic animals. Results Comparing symptoms on the spot-checked points, we determined that the triple-transgene mice were more suitable for systematic study. The results of intraperitoneal glucose tolerance tests (IPGTT) of triple-transgene animals began to change 60 days after induction (p < 0.001). After 190 days of induction, the body weights (p < 0.01) and plasma glucose of the animals in Tg were higher than those of the animals in Negative Control (Nc). After sacrificed, large amounts of lipid were found deposited in adipose (p < 0.01) and ectopically deposited in the non-adipose tissues (p < 0.05 or 0.01) of the animals in the Tg HFHSD group. The weights of kidneys and hearts of Tg animals were significantly increased (p < 0.01). Serum C peptide (C-P) was decreased due to Tg effects, and insulin levels were increased due to the effects of the HFHSD in the Tg HFHSD group, indicating that damaged insulin secretion and insulin resistance hyperinsulinemia existed simultaneously in these animals. The serum corticosterone of Tg was slightly higher than those of Nc due to the effects of the 11βHSD-1 transgene and obesity. In Tg HFHSD, hepatic adipose deposition was more severe and the pancreatic islet area was enlarged under compensation, accompanying apoptosis. In the transgenic control diet (Tg ControlD) group, hepatic adipose deposition was also severe, pancreatic islets were damaged, and their areas were decreased (p < 0.05), and apoptosis of pancreatic cells occurred. Taken together, these data show the transgenes led to early-stage pathological changes characteristic of type 2 diabetes in the triple-transgene HFHSD group. The disease of triple-transgenic mice was more severe than that of dual or single-transgenic mice. Conclusion The use of multi-transgenes involved in insulin resistance and pancreatic apoptosis is a better way to generate polygene-related early-stage diabetes models.

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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 (June 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 broad range of tissues in the animal. Although the presence of the hybrid intron increased the frequency of transgenics with significant CAT activity, it did not affect the integration site-dependent variation commonly seen in transgene expression. To determine whether the enhancement is a general outcome of splicing or is dependent on the particular intron, we also produced equivalent transgenics carrying the widely used simian virus 40 small-t intron. We found that the hybrid intron is significantly more effective in elevating transgene expression. Our results suggest that inclusion of the generic intron in cDNA constructs may be valuable in achieving high levels of expression in transgenic mice.

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Heinzelmann, Andy, Subbiah Kumar, Scott Noggle, Ine Goedegebuur, K. Morgan Sauer, Satyajit Rath, and Jeannine M. Durdik. "Deletion of a Recombined Ig Heavy Chain Transgene in B-Lineage Cells of Transgenic Mice." Journal of Immunology 161, no. 2 (July 15, 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 transgene we have been studying show a significant net loss of transgene copies. This loss is more marked in the B cells expressing endogenous heavy chains than in those expressing transgenic heavy chains. We have also examined cells of the B lineage in the bone marrow, and a small degree of deletion is also evident in CD19+CD23−IgM− immature B-lineage cells. As greater deletion is observed in mature B cells, it is possible that the deletion process either continues into B cell maturity and/or provides a selective advantage. We have investigated the relationship between transgene expression and deletion, and we find that while thymocytes in these mice express the transgene well, T cell hybridomas derived from transgenic thymus do not show any loss of the transgene. Thus, a recombined Ig heavy chain transgene prominently undergoes somatic deletion in B-lineage cells independent of its insertion site or expression. This transgenic instability is significant to the analysis of genomic stability as well as to the design of gene therapy strategies.

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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 (November 16, 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 mice are viable and fertile, and they displayed normal blood cell counts. This proves that the V617F mutation but not gene overexpression per se caused MPD phenotypes in JAK2V617F transgenic mice. We then crossed the JAK2 and JAK2V617F transgenic mice to generate JAK2/JAK2V617F double transgenic hybrids. Interestingly, these hybrid mice developed no or mild MPD phenotypes with only a slight increase in blood counts in contrast to the striking elevation observed in JAK2V617F transgenic mice. Expression of wild type JAK2 also blocked the constitutive activation of signal transduction components caused by JAK2V617F. Our data indicates that over-expression of wild type JAK2 suppresses the pathogenic function of mutant JAK2V617F. Therefore, JAK2V617F is not a typical dominant oncogene. Homozygous mutation or in the case of heterozygous mutation, its amplification with concurrent deletion or suppression of wild type JAK2, is required to produce MPD phenotypes. Our transgenic mouse models will serve as an invaluable tool to study the interplay of JAK2 and JAK2V617F and the mechanism by which specific MPD phenotypes develop.

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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 (May 1, 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+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. Moreover, in contrast to the predominant peri-insulitis observed in TNF-beta transgenic mice, the majority of the infiltrate in the TNF-alpha transgenic mice was within the islet itself. These unique patterns of infiltration were observed in the F1 progeny of crosses with C57BL/6 as well as NOD. Both TNF-alpha and TNF-beta transgenic mice show elevated expression of leukocyte adhesion molecules VCAM-1 and ICAM-1 in islet endothelia and increased expression of MHC class I on islet cells. This inflammation did not result in reduced insulin content of the islets, nor did it lead to diabetes. These data suggest that additional stimuli are necessary to initiate the process of islet destruction.

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Дисертації з теми "Transgenic Mice"

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.
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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Cosentino, Lidia. "A comparison of transgenic and endogenous loci in vivo." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/NQ56223.pdf.

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

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

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

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

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

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The present dissertation describes the use of a novel system to achieve specific cell ablation in fat tissue. The method is based on the use of E.coli nitroreductase (NTR) enzyme that activates certain nitro compounds into cytotoxic DNA interstrand cross-linking agents. This system was assessed first in vitro, 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 in vivo, 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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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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Книги з теми "Transgenic Mice"

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

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

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

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

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

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

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

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

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

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

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Частини книг з теми "Transgenic Mice"

Lo, Lilian H., and Vincent W. Keng. "Transgenic Mice." In Encyclopedia of Gerontology and Population Aging, 1–8. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_967-1.

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Lo, Lilian H., and Vincent W. Keng. "Transgenic Mice." In Encyclopedia of Gerontology and Population Aging, 5197–204. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_967.

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Diack, Abigail B., Rona Wilson, Enrico Cancellotti, Barry Bradford, Matthew Bishop, and Jean C. Manson. "Transgenic Mice Modelling." In Prions and Diseases, 155–69. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5338-3_10.

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Chen, X., Y. Matsuura, and J. F. Kearney. "CD5 Transgenic Mice." In Current Topics in Microbiology and Immunology, 209–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_25.

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Rüther, Ulrich. "Insertional Mutagenesis in Transgenic Mice." In Transgenic Animals, 361–63. London: CRC Press, 2022. http://dx.doi.org/10.1201/9781003211099-68.

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Lowell, Bradford B. "Genetically Engineered Mice in Obesity Research." In Transgenic Animals, 449–54. London: CRC Press, 2022. http://dx.doi.org/10.1201/9781003211099-80.

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Strange, Robert, and Robert D. Cardiff. "Transgenic Mice and Transgenic Mammary Glands." In Breast Cancer: Progress in Biology, Clinical Management and Prevention, 1–14. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1617-6_1.

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Jaenisch, Rudolf, Douglas Gray, Tetsuo Noda, and Hans Weiher. "Mutations in Transgenic Mice." In Vectors as Tools for the Study of Normal and Abnormal Growth and Differentiation, 63–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74197-5_6.

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Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts, et al. "Ataxin-3 Transgenic Mice." In Encyclopedia of Psychopharmacology, 158. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_659.

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Wagner, E. F. "Oncogenes and Transgenic Mice." In Growth Factors, Differentiation Factors, and Cytokines, 366–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74856-1_27.

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Тези доповідей конференцій з теми "Transgenic Mice"

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

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

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

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The study of the molecular mechanisms of interaction between the innate immune system and the bacterial pathogen Pseudomonas aeruginosa may contribute to the development of new approaches to combat bacterial infections. In this work, we showed that overexpression of human TRIM14 led to a decrease in the survival rate of transgenic mice upon P. aeruginosa infection. At the same time, the amount of phosho-STAT3 (p-STAT3) protein in the nuclear fraction in the lungs of transgenic mice increased after infection.

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Luo, Xue-Gang, Ting-Ting Qin, Zhong-Shuai Xin, Dao-Zhu Huangfu, and Tao Xi. "Construction of SMYD3 liver-specific expression transgene for the eestablishment of transgenic mice." In 2010 International Conference on Bioinformatics and Biomedical Technology. IEEE, 2010. http://dx.doi.org/10.1109/icbbt.2010.5478970.

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

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Sakai, Mizu, Tetsuya Kubota, Mayuka Isaka, Takashi Yamane, Naoki Shiota, Hiroshi Ohnishi, Hiroshi Iwamoto, and Akihito Yokoyama. "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 Mustn1^PRO-GFPtpz transgenic mice." In 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413256.

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Irungbam, K., M. Roderfeld, Y. Churin, H. Glimm, I. Yüce, G. Morlock, and E. Roeb. "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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Звіти організацій з теми "Transgenic Mice"

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

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

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

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Shankar, Deepa. Analysis of Multistep Mammary Tumorigenesis in WNT-1 Transgenic Mice. Fort Belvoir, VA: Defense Technical Information Center, September 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. Fort Belvoir, VA: Defense Technical Information Center, October 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. Fort Belvoir, VA: Defense Technical Information Center, October 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. Fort Belvoir, VA: Defense Technical Information Center, July 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. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada506317.

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

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