Relevant bibliographies by topics / N mouse

Academic literature on the topic 'N mouse'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "N mouse"

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Salinger, A. P., and M. J. Justice. "Mouse Mutagenesis Using N-Ethyl-N-Nitrosourea (ENU)." Cold Spring Harbor Protocols 2008, no. 5 (April 1, 2008): pdb.prot4985. http://dx.doi.org/10.1101/pdb.prot4985.

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Yan, Lan, Diane M. Otterness, Timothy L. Craddock, and Richard M. Weinshilboum. "Mouse Liver Nicotinamide N-Methyltransferase:." Biochemical Pharmacology 54, no. 10 (November 1997): 1139–49. http://dx.doi.org/10.1016/s0006-2952(97)00325-0.

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Cordes, Sabine P. "N-Ethyl-N-Nitrosourea Mutagenesis: Boarding the Mouse Mutant Express." Microbiology and Molecular Biology Reviews 69, no. 3 (September 2005): 426–39. http://dx.doi.org/10.1128/mmbr.69.3.426-439.2005.

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SUMMARY In the mouse, random mutagenesis with N-ethyl-N-nitrosourea (ENU) has been used since the 1970s in forward mutagenesis screens. However, only in the last decade has ENU mutagenesis been harnessed to generate a myriad of new mouse mutations in large-scale genetic screens and focused, smaller efforts. The development of additional genetic tools, such as balancer chromosomes, refinements in genetic mapping strategies, and evolution of specialized assays, has allowed these screens to achieve new levels of sophistication. The impressive productivity of these screens has led to a deluge of mouse mutants that wait to be harnessed. Here the basic large- and small-scale strategies are described, as are the basics of screen design. Finally, and importantly, this review describes the mechanisms by which such mutants may be accessed now and in the future. Thus, this review should serve both as an overview of the power of forward mutagenesis in the mouse and as a resource for those interested in developing their own screens, adding onto existing efforts, or obtaining specific mouse mutants that have already been generated.
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Tanaka, M., A. Fukuhara, and I. Shimomura. "N-Linked Glycosylation of Mouse Adiponectin." Hormone and Metabolic Research 43, no. 08 (July 2011): 545–50. http://dx.doi.org/10.1055/s-0031-1280782.

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Tinwell, H., J. Yendle, and J. Ashby. "Mutagenicity to the mouse bone marrow by the mouse germ cell mutagen N-propyl-N-nitrosourea." Mutation Research/Genetic Toxicology 370, no. 3-4 (October 1996): 141–43. http://dx.doi.org/10.1016/s0165-1218(96)00047-x.

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Shibuya, T., T. Murota, T. Tokiwa, H. Matsumoto, N. Horiya, and T. Hara. "N-Propyl-N-nitrosourea-induced recessive mutations in mouse spermatogonia." Mutation Research/Environmental Mutagenesis and Related Subjects 203, no. 5 (October 1988): 387–88. http://dx.doi.org/10.1016/0165-1161(88)90080-5.

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Lu, Shajia, Diane E. Borst, and Robert Horowits. "N-RAP expression during mouse heart development." Developmental Dynamics 233, no. 1 (2005): 201–12. http://dx.doi.org/10.1002/dvdy.20314.

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Château, Marie-Thérèse, Herisoa Rabesandratana, and René Caravano. "Suspended mouse peritoneal macrophages." Journal of Immunological Methods 143, no. 1 (September 1991): 103–9. http://dx.doi.org/10.1016/0022-1759(91)90278-n.

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Noveroske, J. K., J. S. Weber, and M. J. Justice. "The mutagenic action of N-ethyl-N-nitrosourea in the mouse." Mammalian Genome 11, no. 7 (July 2000): 478–83. http://dx.doi.org/10.1007/s003350010093.

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Grosse, Johannes, Patrick Tarnow, Holger Römpler, Boris Schneider, Reinhard Sedlmeier, Ulrike Huffstadt, Dirk Korthaus, et al. "N-ethyl-N-nitrosourea-based generation of mouse models for mutant G protein-coupled receptors." Physiological Genomics 26, no. 3 (August 2006): 209–17. http://dx.doi.org/10.1152/physiolgenomics.00289.2005.

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Chemical random mutagenesis techniques with the germ line supermutagen N-ethyl- N-nitrosourea (ENU) have been established to provide comprehensive collections of mouse models, which were then mined and analyzed in phenotype-driven studies. Here, we applied ENU mutagenesis in a high-throughput fashion for a gene-driven identification of new mutations. Selected members of the large superfamily of G protein-coupled receptors (GPCR), melanocortin type 3 (Mc3r) and type 4 (Mc4r) receptors, and the orphan chemoattractant receptor GPR33, were used as model targets to prove the feasibility of this approach. Parallel archives of DNA and sperm from mice mutagenized with ENU were screened for mutations in these GPCR, and in vitro assays served as a preselection step before in vitro fertilization was performed to generate the appropriate mouse model. For example, mouse models for inherited obesity were established by selecting fully or partially inactivating mutations in Mc4r. Our technology described herein has the potential to provide mouse models for a GPCR dysfunction of choice within <4 mo and can be extended to other gene classes of interest.
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Dissertations / Theses on the topic "N mouse"

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Lommel, Silvia. "Conditional inactivation of N-WASP in the mouse analyses of N-WASP function /." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964801922.

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Dagälv, Anders. "Role of Heparan Sulfate N-sulfation in Mouse Embryonic Development." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-123474.

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Heparan sulfate (HS) is a sulfated glycosaminoglycan expressed by all cells in the body. It is found at the cell surface and in the extracellular matrix where it binds a large amount of various ligands including growth factors and morphogens. HS is important for building up morphogen gradients during embryonic development and to act as coreceptors for signaling molecules. Many different Golgi enzymes are involved in the biosynthesis of HS. It is known that some of these enzymes interact with each other but not how the whole biosynthesis machinery works or how the cell regulates the structure of the HS that it produces. In this thesis, cells and mice deficient in two of these biosynthetic enzymes, glucosaminyl N-deacetylase/N-sulfotransferase-1 (NDST1) and the isoform NDST2 have been studied. NDSTs perform the first modifications during biosynthesis where they replace N-acetyl groups on N-acetyl-glucosamine units with sulfate groups. It is known that deficiency of NDST1 is lethal, while lack of NDST2 only results in abnormal connective tissue type mast cells. Here it is shown that deficiency of both NDST1 and NDST2 is embryonically lethal. The embryonic stem (ES) cells extracted from the inner cell mass of double knockout blastocysts show in addition an impaired differentiation capacity compared to wild-type ES cells and fail completely to differentiate into cardiac muscle cells which NDST1-/-, NDST2-/- and wild-type ES cells all do. Cultured mast cells that lack NDST2 produce heparin that is low-sulfated compared to wild-type HS. To our surprise, we could show that mast cells deficient in NDST1 instead produce a more highly sulfated heparin than wild-type cells. We use a model that predicts that the biosynthesis enzymes work together in a multienzyme complex, the GAGosome, to explain our results. We hypothesize that NDST1 has a higher affinity for the GAGosome than NDST2 which only in the absence of NDST1 gets incorporated into the enzyme complex. When all GAGosomes contain NDST2, a more highly sulfated glycosaminoglycan chain will be synthesized. A splice variant of NDST1, NDST1S, has also been studied. We could show that NDST1S lacks enzyme activity but that it probably has the capacity to incorporate into GAGosomes. Overexpression of NDST1S results in altered structure of the HS produced by the cells. We speculate that expression of the splice variant during development may be one way to regulate HS structure.
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Mazza, Graziella. "Antibody responses to Schistosoma mansoni in the CBA/N mouse." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303138.

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Barron, Catherine Mary. "Effects of Trimethylamine N-Oxide on Mouse Embryonic Stem Cell Properties." Thesis, Virginia Tech, 2020. http://hdl.handle.net/10919/99602.

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Trimethylamine N-oxide (TMAO) is a metabolite derived from dietary choline, betaine, and carnitine via intestinal microbiota metabolism. In several recent studies, TMAO has been shown to directly induce inflammation and reactive oxygen species (ROS) generation in numerous cell types, resulting in cell dysfunction. However, whether TMAO will impact stem cell properties remains unknown. This project aims to explore the potential impact of TMAO on mouse embryonic stem cells (mESCs), which serve as an in vitro model of the early embryo and of other potent stem cell types. Briefly, mESCs were cultured in the absence (0mM) or presence of TMAO under two different sets of treatment conditions: long-term (21 days), low-dose (20µM, 200µM, and 1000µM) treatment or short-term (5 days), high-dose (5mM, 10mM, 15mM) treatment. Under these treatment conditions, mESC viability, proliferation, and stemness were analyzed. mESC properties were not negatively impacted under long-term, low-dose TMAO treatment; however, short-term, high-dose treatment resulted in significant reduction of mESC viability and proliferation. Additionally, mESC stemness was significantly reduced when high-dose treatment was extended to 21 days. To investigate an underlying cause for TMAO-induced loss in mESC stemness, metabolic activity of the mESCs under short-term, high-dose TMAO treatment was measured with a Seahorse XFe96 Analyzer. TMAO treatment significantly decreased the rate of glycolysis, and it increased the rate of compensatory glycolysis upon inhibition of oxidative phosphorylation (OxPHOS). It also significantly increased the rate of OxPHOS, maximal respiratory capacity, and respiratory reserve. These findings indicate that TMAO induced a metabolic switch of mESCs from high glycolytic activity to greater OxPHOS activity to promote mESC differentiation. Additionally, TMAO resulted in increased proton leak, indicating increased oxidative stress, and elucidating a potential underlying mechanism for TMAO-induced loss in mESC stemness. Altogether, these findings indicate that TMAO decreases stem cell potency potentially via modulation of metabolic activity.
Master of Science
Trimethylamine N-oxide (TMAO) is a metabolite that is produced by the bacteria in the gut after the consumption of specific dietary ingredients (e.g., choline, carnitine, betaine). These ingredients are commonly found in meat and dairy products, and thus make up a large part of the average American diet. Recently, it was discovered that high TMAO levels in the bloodstream put people at an increased risk for heart disease, neurodegenerative diseases (e.g., Alzheimer's Disease), diabetes, stroke, and chronic kidney disease. At the cellular level, there is evidence that TMAO increases inflammation and the production of oxygen radicals, which causes cells to lose their function and promotes the onset of disease. TMAO has been well studied in adult cell types; however, no one has investigated whether TMAO will impact cells of the early embryo. This project aims to explore the impact of TMAO on mouse embryonic stem cells (mESCs), which are cells that represent the early stage of embryonic development and are critical for proper development of the final offspring. In addition, mESCs may also help to provide insight into how TMAO impacts other stem cell types, some of which are present throughout the entire human lifespan and play an important role in the body's ability to repair itself and maintain overall health. My project demonstrated that TMAO does not impact the overall health of mESCs under normal conditions, which signifies that TMAO generated by a pregnant mother may not directly impact the early embryonic stage of development. Further studies should be conducted to determine the potential impact of TMAO on late stages of embryonic and fetal development. Next, to simulate diseased conditions, the mESCs were treated with extremely high concentrations of TMAO in order to determine what concentration of TMAO will negatively impact these cells. It was found that at 5mM TMAO, mESCs begin to lose their basic properties and become dysfunctional. They are impaired in their viability, growth, ability to become other cell types, and in their metabolic activity. These mESC properties are shared with several types of adult stem cells, and therefore, these findings help to provide insight into how TMAO may impact stem cells found in the adult body which are exposed to a lifetime of high TMAO levels. In the future, we would like to further explore the impact of TMAO on mESCs at the molecular level as well as examine the direct impact of TMAO on other stem cell types.
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Ly, Lan H. "Immunosuppressive dietary n-3 polyunsaturated fatty acids differentially modulate costimulatory regulation of murine CD4+ T-cell function." Texas A&M University, 2004. http://hdl.handle.net/1969.1/1535.

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Consumption of fish oils (FO) enriched with the n-3 polyunsaturated fatty acids (PUFA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), is beneficial to a variety of inflammatory disorders due, in part, to the alteration of membrane composition of T-lymphocytes and other immune cells. We previously observed that down-regulation of proliferation and cytokine synthesis by CD4+ T-cells in mice fed diets rich in n-3 PUFA was dependent on the involvement of CD28, a co-stimulatory molecule necessary for T-cell activation. Since the co-receptor homologues, CD28 and CTLA-4, have opposing effects on T-cell activation, we hypothesized that the balance of costimulatory and downregulatory properties of CD28 and CTLA-4, respectively, would be altered by diet. A significant increase (p<0.05) in CD28 and CTLA-4 surface expression was observed in CD4+ T-cells post-stimulation with phorbol ester and calcium ionophore (PMA/Iono) or anti-CD3 and anti-CD28 (αCD3/CD28) antibodies in all diet groups. A significant increase (p<0.01; 20%) in the number of CD28 molecules was observed in n-3 PUFA vs. CO-fed mice after 48 h of in vitro CD4+ T-cell activation, and both CTLA-4 mRNA transcript and protein levels were upregulated by 50% at 72 h post-activation (p<0.01). Treatment with anti-CTLA-4 mAb in vivo in Mycobacterium bovis (BCG)-vaccinated mice did not alter the suppressive effects of dietary n-3 PUFA on antigen (PPD)-induced lymphocyte proliferation or delayed hypersensitivity reactions. T-cells from both the C57BL/6 and IL-10mice fed dietary n-3 PUFA after 72 h of in vitro stimulation with αCD3/CD28. CD4T-cells from C57BL/6 mice fed DHA produced significantly less IFNγ and IL-10, while CD4T-cells from IL-10Ligation of CD28 upregulates IL-10 receptor (IL-10R) expression on CD4+ T-cells. Therefore, we hypothesized that dietary n-3 PUFA would suppress T-cell function through the effects of IL-10. Surprisingly, the proliferation of purified splenic CD4+ T-cells activated in vitro with αCD3/CD28 was suppressed by dietary n-3 PUFA in both conventional mice (C57BL/6) and IL-10 gene knockout (IL-10(-/-)) mice. Furthermore, IL-10R cell surface expression was significantly down-regulated on CD4+ T-cells from both the C67BL/6 and IL-10(-/-) mice fed dietary n-3 PUFA produced significantly more IFNγ compared to the CO-fed group.
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Munro, Sandra Bronwen. "Characterization of a composite cDNA clone encoding mouse testicular N-Cadherin and the mouse homologue of a human breast tumor autoantigen." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=69645.

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A mouse testis cDNA library was screened with an oligonucleotide probe corresponding to a sequence in the 5$ sp prime$ region of mouse N-cadherin cDNA. A composite clone containing three individual cDNAs was isolated. These included a 711 bp cDNA encoding part of mouse testicular N-cadherin, an unidentified 392 bp cDNA, and a 1500 bp cDNA encoding the mouse homologue of a human breast tumor autoantigen.
The cadherins, the influenza strain A hemagglutinins, and the fibroblast growth factor receptors are three different families of integral membrane glycoproteins that harbour the amino acid motif histidine-alanine-valine (HAV) in regions involved in protein-protein interactions. In order to identify other proteins that possess the HAV motif in functionally important regions, the SwissProt database was searched using a consensus sequence derived from the cadherins, influenza strain A hemagglutinins, and fibroblast growth factor receptors. This search identified the $ alpha$ chains of the HLA class I histocompatibility antigens as a fourth family of integral membrane glycoproteins with an HAV-containing region that is involved in a protein-protein interaction. (Abstract shortened by UMI.)
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Yu-Plant, Violeta Lynn. "The development of gene targeted mouse strains for studying arylamine N-acetyltransferase function." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34082.pdf.

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Neale, Sondra-Ann. "Characterization of the neural cell adhesion molecule N-CAM in splotch mutant mouse embryos." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=69646.

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Cell adhesion molecules are known to play crucial roles in a variety of developmental processes. The neural cell adhesion molecule N-CAM is strongly implicated in neurulation and neural crest cell (NCC) migration and was thus studied in splotch (Sp) neural tube defect mutant embryos. At the 20 somite-stage of gestation day 9, Sp N-CAM was found to contain polysialic acid (PSA) side chains which are normally only present beginning at gestational day 11. Younger embryos at 12 and 14 somites also showed the presence of PSA on N-CAM, which was absent in controls. Enzymatic removal of PSA from N-CAM resulted in isoforms which migrated identically to PSA-free N-CAM isoforms in SDS-polyacrylamide gels. The post-translational modification of N-CAM appears to be the primary target of the Sp gene. In view of N-CAM's importance during development, an alteration at a critical stage is likely to result in the cascade of abnormalities seen in Sp mutants.
A new genotyping assay was also implemented for examination of N-CAM in Sp and other related wildtype strains.
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Rago, Luciano F. [Verfasser], and Rolf [Akademischer Betreuer] Kemler. "N-cadherin expression regulation by microRNAs in the mouse developing neocortex = N-Cadherin-Expressionsregulation von microRNAs in der Maus entwickelt Neokortex." Freiburg : Universität, 2014. http://d-nb.info/1122646674/34.

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Muraveika, Liudmila [Verfasser], and Daniela N. [Akademischer Betreuer] Männel. "Binding specificity of mouse ficolin to different bacterial strains / Liudmila Muraveika. Betreuer: Daniela N. Männel." Regensburg : Universitätsbibliothek Regensburg, 2012. http://d-nb.info/1028392583/34.

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Books on the topic "N mouse"

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Brennan, Laurie Anne. Low expression of the LSP1 gene in early mouse T-lymphomas induced by N-methyl-N-nitrosourea. Ottawa: National Library of Canada, 1996.

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Yu-Plant, Violeta Lynn. The development of gene targeted mouse strains for studying arylamine N-aceyltransferase function. Ottawa: National Library of Canada, 1998.

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Larrivey, Wayne. Nutcracker--: The musical : a 2-act play : based on E.T.A. Hoffman[n]'s "The Nutcracker and Mouse King" : music adapted from Peter Illytch Tchaikovsky's "Nutcracker suite". Schulenburg, TX: I.E. Clark, 1996.

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Moses as a character in the Fourth Gospel: A study of ancient reading techniques. London: Sheffield Academic Press, 2002.

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The descent of Christ: Ephesians 4:7-11 and traditional Hebrew imagery. Grand Rapids, Mich: Baker Books, 1998.

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The descent of Christ: Ephesians 4:7-11 and traditional Hebrew imagery. Leiden: E.J. Brill, 1996.

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The wicked tenants and Gethsemane: Isaiah in the wicked tenants' vineyard, and Moses and the high priest in Gethsemane : Judaic traditions in Mark 12:1-9 and 14:32-42. Atlanta, Ga: Scholars Press, 1996.

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Paul, Moses, and the history of Israel: The letter/spirit contrast and the argument from Scripture in 2 Corinthians 3. Peabody, Mass: Hendrickson Publishers, 1996.

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Paul, Moses, and the history of Israel: The letter/spirit contrast and the argument from Scripture in 2 Corinthians 3. Tübingen: J.C.B. Mohr (Paul Siebeck), 1995.

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Awesome Super Nintendo Secrets 2. Lahaina, USA: Sandwich Islands Publishing, 1993.

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Book chapters on the topic "N mouse"

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Oliveira, Paula A., Cármen Vasconcelos-Nóbrega, Rui M. Gil da Costa, and Regina Arantes-Rodrigues. "The N-butyl-N-4-hydroxybutyl Nitrosamine Mouse Urinary Bladder Cancer Model." In Urothelial Carcinoma, 155–67. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7234-0_13.

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Williams, Suzannah A., and Pamela Stanley. "Roles for N- and O-Glycans in Early Mouse Development." In Advances in Experimental Medicine and Biology, 397–410. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7877-6_20.

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Kennelly, James C., and R. Colin Garner. "The Mutagenicity of Benzidine, 4,4″-Diaminoterphenyl, N,N-Dimethyl-4-aminoazobenzene and 4-Cyano-N,N-dimethylaniline in the L51787 Mouse Lymphoma Assay." In Comparative Genetic Toxicology, 311–18. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07901-8_37.

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Pan, Xiaoping. "Determination of the N-Nitroso Compounds in Mouse Following RDX Exposure." In Environmental Toxicology and Toxicogenomics, 315–25. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1514-0_23.

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Russo, James E. "Inhibition of Mouse and Human Class 1 Aldehyde Dehydrogenase by 4-(N,N-Dialkylamino)Benzaldehyde Compounds." In Advances in Experimental Medicine and Biology, 217–24. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5871-2_25.

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Guzman, Raphael C., Rebecca C. Osborn, Shigeki Miyamoto, Ramasamy Sakthivel, Soo-In Hwang, and Satyabrata Nandi. "Hormone-Dependent Activation of c-Ki-ras in N-Methyl-N-Nitrosourea (MNU)-Induced Mouse Mammary Tumors." In Hormonal Carcinogenesis, 285–87. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4613-9208-8_41.

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Taherzadeh, Ghazaleh, Matthew Campbell, and Yaoqi Zhou. "Computational Prediction of N- and O-Linked Glycosylation Sites for Human and Mouse Proteins." In Methods in Molecular Biology, 177–86. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2317-6_9.

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Hesk, D., and C. J. Logan. "In vitro Metabolism of 4-Cyano-N,N-dimethyl-[14C] aniline (CDA) by Rat, Mouse, Chicken and Induced Rat S9 Fractions." In Comparative Genetic Toxicology, 543–46. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07901-8_64.

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Brouwer, Judith R., Laurent Foiry, and Geneviève Gourdon. "Cell Recovery from DM1 Transgenic Mouse Tissue to Study (CTG) n Instability and DM1 Pathogenesis." In Methods in Molecular Biology, 253–64. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-411-1_16.

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Silva, S., Y. Wang, M. Babonits, H. Axelson, F. Wiener, and G. Klein. "An Exceptional Mouse Plasmacytoma with a New Kappa/N-myc [T(6; 12) (C1; B)] Translocation Expresses N-myc But Not c-myc." In Current Topics in Microbiology and Immunology, 251–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77633-5_31.

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Conference papers on the topic "N mouse"

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Pendleton, N. "E-111 Analysis of intracerebral hemorrhage in n established mouse model." In SNIS 19th Annual Meeting Abstracts. BMA House, Tavistock Square, London, WC1H 9JR: BMJ Publishing Group Ltd., 2022. http://dx.doi.org/10.1136/neurintsurg-2022-snis.222.

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Feng, Gong, Patricia Hicks, Charles W. Prince, Candece Gladson, and Pi-Ling Chang. "OSTEOPONTIN ENHANCES PROTO-ONCOGENE (Junb) EXPRESSION IN PRENEOPLASTIC MOUSE CELLS." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.253.

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Kowalski, Aaron J., Susan R. Rittling, and David T. Denhardt. "MOUSE ANTIMOUSE AND ANTIHUMAN OSTEOPONTIN ANTIBODIES: CREATION, CHARACTERIZATION, AND APPLICATION." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.275.

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Zhu, Hongyan, Dawei Deng, Haiyan Chen, Zhiyu Qian, and Yueqing Gu. "The targeted behavior of folate-decorated N-succinyl-N'-octyl chitosan evaluated by NIR system in mouse model." In Photonics Asia 2010, edited by Qingming Luo, Ying Gu, and Xingde Li. SPIE, 2010. http://dx.doi.org/10.1117/12.870163.

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Ginwala, Rashida, Jodie Franklin, James R. White, Uttam Satyal, Abhishek Srivastava, and Philip H. Abbosh. "Abstract 2912: Changes in mouse bladder cancer microbiome associated with exposure to bladder carcinogen N-butyl-N-(4-hydroxybutyl) nitrosamine." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2912.

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Price, Ann. "Mouse FSP27 Mediates Lipid Droplet Accumulation in Vegetative Tissues of Arabidopsis and N. benthamiana." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1063453.

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Atay, Stefan M., and Philip V. Bayly. "Magnetic Resonance Elastography of the Mouse Brain In Vivo." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175375.

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In the current study we apply the magnetic resonance elastography (MRE) technique to estimate the dynamic shear modulus of mouse brain tissue in vivo. The frequency used (1200 Hz) is well above those reported previously [1]. Estimates of dynamic shear modulus range from 12,600–14,800 N/m2 at 1200 Hz. These data are strictly relevant only to small oscillations at this specific frequency, but these values are obtained at high frequencies (and thus high deformation rates) and non-invasively throughout the brain. These data complement measurements of nonlinear viscoelastic properties obtained by others at slower rates, either ex vivo or invasively.
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Fan, Yang-Yi, Shinya Toyokuni, Evelyn S. Callaway, Qitao Ran, Joanne R. Lupton, and Robert S. Chapkin. "Abstract 955: n-3 polyunsaturated fatty acids promote apoptosis in oxidatively stressed transgenic mouse models." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-955.

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Wang, Tzu-Chien, Pei-Chi Chang, and Chi-Yuan Chen. "Abstract A146: Study of anti-leukemia activity of N-(1-pyrenlyl) maleimideinvivousing a bioluminescent mouse model." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-a146.

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Su, Yanrong, Jifen Li, Leeanne Griffith, and Glenn Radice. "Abstract 4178: N-cadherin haploinsufficiency prolongs survival in a genetically engineered mouse model of pancreatic cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4178.

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Reports on the topic "N mouse"

1

Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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