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Relevant bibliographies by topics / Triple transgenic mice model

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Academic literature on the topic 'Triple transgenic mice model'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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Journal articles on the topic "Triple transgenic mice model"

1

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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Zhang, Yu, Zhenlong Xiao, Zhijun He, Junyu Chen, Xin Wang, and Liang Jiang. "Dendritic complexity change in the triple transgenic mouse model of Alzheimer’s disease." PeerJ 8 (January 9, 2020): e8178. http://dx.doi.org/10.7717/peerj.8178.

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Alzheimer’s disease (AD) is an irreversible, neurodegenerative disease that is characterized by memory impairment and executive dysfunction. However, the change of fine structure of neuronal morphology remains unclear in the AD model mouse. In this study, high-resolution mouse brain sectional images were scanned by Micro-Optical Sectioning Tomography (MOST) technology and reconstructed three-dimensionally to obtain the pyramidal neurons. The method of Sholl analysis was performed to analyze the neurons in the brains of 6- and 12-month-old AD mice. The results showed that dendritic complexity w

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He, Zhijun, Shuangxue Han, Chong Wu, et al. "Correction: Bis(ethylmaltolato)oxidovanadium(iv) inhibited the pathogenesis of Alzheimer's disease in triple transgenic model mice." Metallomics 12, no. 4 (2020): 631. http://dx.doi.org/10.1039/d0mt90008g.

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Correction for ‘Bis(ethylmaltolato)oxidovanadium(iv) inhibited the pathogenesis of Alzheimer's disease in triple transgenic model mice’ by Zhijun He et al., Metallomics, 2020, DOI: 10.1039/c9mt00271e.

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Paula, Pérez-Corredor, Sabogal-Guáqueta Angelica Maria, Carrillo-Hormaza Luis, and Cardona-Gómez Gloria Patricia. "Preventive Effect of Quercetin in a Triple Transgenic Alzheimer’s Disease Mice Model." Molecules 24, no. 12 (2019): 2287. http://dx.doi.org/10.3390/molecules24122287.

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Alzheimer’s disease (AD) is the most common type of dementia and is the leading cause of disability in elderly people worldwide. Current pharmacological therapies do not cure the disease, and for this reason, some pharmacotherapy studies have investigated preventive treatments focused on modifiable nutritional factors such as diet. Quercetin (Qc) is a flavonoid found in fruits and vegetables that has several biological properties. In this study, we evaluated the effect of chronic oral quercetin administration (100 mg/kg) on neurodegeneration markers and cognitive and emotional deficits in a tr

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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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Lieuw, Kenneth, Jayasree Krishnamurthy, and Mignon L. Loh. "CblY371H Transgene Combined with Hematopoietic Deletion of the Endogenous c-Cbl Gene Results in GM-CSF Hypersensitivity and Leukocytosis." Blood 126, no. 23 (2015): 3672. http://dx.doi.org/10.1182/blood.v126.23.3672.3672.

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Abstract Juvenile Myelomonocytic Leukemia (JMML) is a mixed myeloproliferative/myelodysplastic disease that is rapidly fatal with infiltration of myeloid cells into multiple organs. About 15% of JMML patient samples contain a mutation in c-Cbl, and germline mutation results in the predisposition for developing JMML. The c-Cbl gene encodes a multifunctional adaptor protein that contains an N-terminal tyrosine-kinase binding (TKB) domain, a RING finger motif that contains E3 ligase activity, and a C-terminal ubiquitin-associated domain. The TKB domain is involved in adaptor functions of the prot

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He, Zhijun, Shuangxue Han, Chong Wu, et al. "Bis(ethylmaltolato)oxidovanadium(iv) inhibited the pathogenesis of Alzheimer's disease in triple transgenic model mice." Metallomics 12, no. 4 (2020): 474–90. http://dx.doi.org/10.1039/c9mt00271e.

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BEOV activates PPARγ to affect JAK2/STAT3/SOCS1 signaling and eventually prevents Aβ generation. Meanwhile, BEOV inactivates PTP1B to affect PI3K/Akt/GSK3β signaling and finally reduces tau hyperphosphorylation.

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Polis, Baruh, Kolluru D. Srikanth, Vyacheslav Gurevich, Naamah Bloch, Hava Gil-Henn, and Abraham O. Samson. "Arginase Inhibition Supports Survival and Differentiation of Neuronal Precursors in Adult Alzheimer’s Disease Mice." International Journal of Molecular Sciences 21, no. 3 (2020): 1133. http://dx.doi.org/10.3390/ijms21031133.

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Adult neurogenesis is a complex physiological process, which plays a central role in maintaining cognitive functions, and consists of progenitor cell proliferation, newborn cell migration, and cell maturation. Adult neurogenesis is susceptible to alterations under various physiological and pathological conditions. A substantial decay of neurogenesis has been documented in Alzheimer’s disease (AD) patients and animal AD models; however, several treatment strategies can halt any further decline and even induce neurogenesis. Our previous results indicated a potential effect of arginase inhibition

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Salobrar-García, Elena, Ana C. Rodrigues-Neves, Ana I. Ramírez, et al. "Microglial Activation in the Retina of a Triple-Transgenic Alzheimer’s Disease Mouse Model (3xTg-AD)." International Journal of Molecular Sciences 21, no. 3 (2020): 816. http://dx.doi.org/10.3390/ijms21030816.

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Alzheimer’s disease (AD) is the most common type of dementia in the world. The main biomarkers associated with AD are protein amyloid-β (Aβ) plaques and protein tau neurofibrillary tangles, which are responsible for brain neuroinflammation mediated by microglial cells. Increasing evidence has shown that the retina can also be affected in AD, presenting some molecular and cellular changes in the brain, such as microglia activation. However, there are only a few studies assessing such changes in the retinal microglia in animal models of AD. These studies use retinal sections, which have some lim

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Bennardo, Sara, Stefano Iacovelli, Stefania Gobessi та ін. "The Nature of the Antigen Determines Leukemia Development and Behavior in the Eμ-TCL1 Transgenic Mouse Model of CLL". Blood 120, № 21 (2012): 181. http://dx.doi.org/10.1182/blood.v120.21.181.181.

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Abstract Abstract 181 Studies conducted over the past decade have revealed a strong association between the mutational status of the immunoglobulin heavy-chain variable region (IGHV) genes and clinical course in patients with chronic lymphocytic leukemia (CLL). In patients with aggressive CLL, the leukemic cells typically express B cell receptors (BCRs) encoded by unmutated IGHV genes, whereas these genes are most often mutated in leukemic cells from patients with indolent disease. The mutational status of the IGHV genes reflects features of the antigen, such as antigen structure, form, presen

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Dissertations / Theses on the topic "Triple transgenic mice model"

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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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蘇志良 and Chi-leung So. "Transgenic mouse model of human chondrodysplasia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31237678.

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衛永剛 and Wing-kong Wai. "Abnormal chondrocyte differentiation: a transgenic model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237800.

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Wai, Wing-kong. "Abnormal chondrocyte differentiation : a transgenic model /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19656439.

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Makinen, Kimmo. "Spontaneous model of experimental autoimmune uveoretinitis : IRBP-HEL transgenic mice." Thesis, University of Aberdeen, 2006. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU490269.

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To generate a spontaneous EAU model, transgenic mice expressing membrane-bound hen egg lysozyme (HEL) under control of the IRBP promoter were generated. The mice expressed HEL in the photoreceptors, and in the thymus as measured by immunofluorescent confocal microscopy and real-time RT-PCR, respectively. When crossed with the 3A9 TCR-transgenic mice whose CD4+ T cells are HEL-specific, double-transgenic mice developed spontaneous EAU with 100% incidence and an onset age of 22 days post-partum. The ocular inflammation was multifocal and affected the posterior segment of the eye, and led to comp

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Siu, Kwan-yin. "The development and characterization of a knockout model for secretin." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40887674.

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Chung, Chi-kin Samuel. "The development and characterization of a gene-knockout mouse model for secretin receptor /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31491121.

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Siu, Kwan-yin, and 蕭君言. "The development and characterization of a knockout model for secretin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40887674.

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Tsang, Kwok-yeung. "Molecular pathogenesis of abnormal chondrocyte differentiation in a transgenic mouse model /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B35132796.

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楊重文 and Chung-man Yeung. "Studies on the tissue specificity of the glucose-dependent insulinotropic polypeptide promoter by a transgenic mouse model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31220204.

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Books on the topic "Triple transgenic mice model"

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

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2

Tesseur, Ina. Expression of human apolipoprotein E₄ in the central nervous system of transgenic mice: Towards a model for alzheimer's disease. Leuven University Press, 2000.

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Brakebusch, Cord. Mouse as a Model Organism: From Animals to Cells. Springer Science+Business Media B.V., 2011.

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4

Razzaghi, Hamid. Establishment of transgenic mice carrying mutated human insulin gene: A model system for studying the immunological self-tolerance to a soluble antigen. National Library of Canada, 1993.

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5

Martin Hrabé de Angelis (Editor), Pierre Chambon (Editor), and Steve Brown (Editor), eds. Standards of Mouse Model Phenotyping. Wiley-VCH, 2006.

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

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Pihlajaniemi, Taina, and Cord Brakebusch. Mouse as a Model Organism: From Animals to Cells. Springer, 2014.

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Book chapters on the topic "Triple transgenic mice model"

1

Owens, Gabe E., Ruth A. Keri, and John H. Nilson. "LH Hypersecreting Mice: A Model for Ovarian Granulosa Cell Tumors." In Transgenic Models in Endocrinology. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1633-0_4.

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Lee, Seung-Sook, Ja-June Jang, Jeong Wook Seo, et al. "Thymic Tumor Progression in SV40T Transgenic Mice Model." In Epithelial Tumors of the Thymus. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0033-3_20.

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Higgins, Linda S., and Barbara Cordell. "Transgenic Mice as a Model of Alzheimer’s Disease." In Alzheimer Disease. Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-8149-9_64.

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Rubin, Edward, and Joshua Schultz. "Probing the Genetics of Atherosclerosis in Transgenic Mice." In Transgenic Animals as Model Systems for Human Diseases. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02925-1_2.

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Colas, D., J. London, R. Cespuglio, and N. Sarda. "Polysomnography in transgenic hSOD1 mice as Down syndrome model." In Advances in Down Syndrome Research. Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-6721-2_15.

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Coffey, Robert J., and Peter J. Dempsey. "Mammary Neoplasia in Mouse Mammary Tumor Virus-Transforming Growth Factor α Transgenic Mice." In Transgenic Animals as Model Systems for Human Diseases. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02925-1_6.

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Wagner, Erwin F., and Adriano Aguzzi. "Exploring the Pathogenic Potential of c-fos, Polyoma Middle T and Human Foamy Virus in Transgenic Mice." In Transgenic Animals as Model Systems for Human Diseases. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02925-1_7.

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Kollias, George A. "Transgenic Models of Chronic Arthritis and of Systemic Tumour Necrosis Factor-Mediated Disease in Mice Expressing Human Tumour Necrosis Factor." In Transgenic Animals as Model Systems for Human Diseases. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02925-1_5.

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Taniguchi, T., S. Matsuyama, K. Minoura, et al. "Learning Deficits in N279K Tau Transgenic Mice and an Assembly Model of Tau Protein." In Molecular Neurobiology of Alzheimer Disease and Related Disorders. KARGER, 2004. http://dx.doi.org/10.1159/000078538.

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Bulut, Gülay, and Aykut Üren. "Generation of K14-E7/∆N87βcat Double Transgenic Mice as a Model of Cervical Cancer." In Methods in Molecular Biology. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2013-6_29.

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Conference papers on the topic "Triple transgenic mice model"

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Sakai, Mizu, Tetsuya Kubota, Mayuka Isaka, et al. "Lung Injury Model Using Human MUC1 Transgenic Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5987.

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Zhang, Liangfen, Swati Dhar, Agnes M. Rimando, et al. "Abstract 3199: Pterostilbene supresses prostate cancer progression in transgenic mice model." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3199.

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Budiu, Raluca A., Esther Elishaev, Joan Brozick, et al. "Abstract 751: Vaccination with MUC1-pulsed dendritic cells prolongs survival in triple transgenic mice with orthotopic ovarian tumors." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-751.

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Budiu, Raluca A., Gina M. Mantia-Smaldone, Joan Brozick, Robert P. Edwards, and Anda M. Vlad. "Abstract 4793: MUC1 immunogenicity in a triple transgenic mouse model for epithelial ovarian 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.am10-4793.

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Rasheed, Ameer, Ji Hye Lee, Yoo-Hun Suh, and Cheil Moon. "Studies on the correlation with olfactory dysfunction in a transgenic mice model of Alzheimer's disease." In Nano-Bio Sensing, Imaging and Spectroscopy, edited by Shin Won Kang, Seung-Han Park, Luke P. Lee, Ki-Bong Song, and Yo Han Choi. SPIE, 2013. http://dx.doi.org/10.1117/12.2017726.

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Das, Krishna, Adriane Gardyan, Mathias Vormehr, et al. "Abstract 5012: Establishment of a transplantable, NY-BR-1 expressing breast cancer model in HLA-transgenic mice." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5012.

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Epperly, Michael W., J. Richard Chaillet, Shaonan Cao, Xichen Zhang, and Joel S. Greenberger. "Abstract 4355: Use of MnSOD tet on transgenic mice as a model for evaluating irradiation protection and mitigation." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4355.

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Emami, Kiarash, Amy Barulic, Yi Xin, et al. "Non-Invasive Assessment Of Pulmonary Developmental Deficiency In A Model Of Transgenic Mice Using Hyperpolarized Gas Diffusion MRI." 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.a3775.

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Bunin, Anna, Ann Marie Rossi, Christian Vidal, et al. "Abstract 1478: Human transgenic IL-15 NOG mice reconstituted with human NK cells as a model for NK cell depletion." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1478.

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Bunin, Anna, Ann Marie Rossi, Christian Vidal, et al. "Abstract 1478: Human transgenic IL-15 NOG mice reconstituted with human NK cells as a model for NK cell depletion." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1478.

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