Relevant bibliographies by topics / Mice Notch genes Mice

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Mice Notch genes Mice'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Mice Notch genes Mice"

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Broner, Esther Channah, Genia Alpert, Udi Gluschnaider, et al. "AL101 mediated tumor inhibition in notch-altered TNBC PDX models." Journal of Clinical Oncology 37, no. 15_suppl (2019): 1064. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.1064.

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1064 Background: The Notch pathway is activated during mammary gland development and has been implicated as a key driver in breast cancer. There is an urgent need to identify new therapeutic strategies for triple-negative breast cancer (TNBC), a sub-type associated with poor prognosis and no available targeted therapies. Notch gain of function (GOF) genetic alterations are potential tumor drivers found in ~10% of TNBC. This motivated the development of Notch inhibitors, including AL101 a pan-Notch, gamma secretase inhibitor (J Clin Oncol 36, 2018 abstract 2515). AL101 is currently being evalua
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Kramer, Jan, Ralf Schwanbeck, Horst Pagel, Figen Cakiroglu, Jürgen Rohwedel та Ursula Just. "Inhibition of Notch Signaling Ameliorates Acute Kidney Failure and Downregulates Platelet-Derived Growth Factor Receptor β in the Mouse Model". Cells Tissues Organs 201, № 2 (2016): 109–17. http://dx.doi.org/10.1159/000442463.

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Ischemic acute kidney injury (AKI) is associated with high morbidity and frequent complications. Repeated episodes of AKI may lead to end-stage renal failure. The pathobiology of regeneration in AKI is not well understood and there is no effective clinical therapy that improves regeneration. The Notch signaling pathway plays an essential role in kidney development and has been implicated in tissue repair in the adult kidney. Here, we found that kidneys after experimental AKI in mice showed increased expression of Notch receptors, specifically Notch1-3, of the Notch ligands Jagged-1 (Jag1), Jag
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Wu, Lizi, Ivan Maillard, Makoto Nakamura, Warren S. Pear, and James D. Griffin. "The MAML1 Transcriptional Co-Activator Is Required for the Development of Marginal Zone B Cells." Blood 108, no. 11 (2006): 777. http://dx.doi.org/10.1182/blood.v108.11.777.777.

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Abstract Notch1 and Notch2 receptor-mediated signaling appear to have important and unique roles in lymphoid lineage commitment. Notch1 is required for T cell development, while Notch2 is essential for marginal zone B cell development. This specificity is not completely explained by differential expression patterns of Notch1 and 2 or Notch ligands, suggesting that there are other genes that contribute to specifying Notch receptor functions. We have previously shown that the MAML family of transcriptional co-activators is essential for Notch-induced transcriptional events, and functions by form
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Hamada, Y., Y. Kadokawa, M. Okabe, M. Ikawa, J. R. Coleman, and Y. Tsujimoto. "Mutation in ankyrin repeats of the mouse Notch2 gene induces early embryonic lethality." Development 126, no. 15 (1999): 3415–24. http://dx.doi.org/10.1242/dev.126.15.3415.

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Notch family genes encode transmembrane proteins involved in cell-fate determination. Using gene targeting procedures, we disrupted the mouse Notch2 gene by replacing all but one of the ankyrin repeat sequences in the cytoplasmic domain with the E. coli (beta)-galactosidase gene. The mutant Notch2 gene encodes a 380 kDa Notch2-(beta)-gal fusion protein with (beta)-galactosidase activity. Notch2 homozygous mutant mice die prior to embryonic day 11.5, whereas heterozygotes show no apparent abnormalities and are fully viable. Analysis of Notch2 expression patterns, revealed by X-gal staining, dem
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Canalis, Ernesto, Tamar R. Grossman, Michele Carrer, Lauren Schilling, and Jungeun Yu. "Antisense oligonucleotides targeting Notch2 ameliorate the osteopenic phenotype in a mouse model of Hajdu-Cheney syndrome." Journal of Biological Chemistry 295, no. 12 (2020): 3952–64. http://dx.doi.org/10.1074/jbc.ra119.011440.

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Notch receptors play critical roles in cell-fate decisions and in the regulation of skeletal development and bone remodeling. Gain–of–function NOTCH2 mutations can cause Hajdu-Cheney syndrome, an untreatable disease characterized by osteoporosis and fractures, craniofacial developmental abnormalities, and acro-osteolysis. We have previously created a mouse model harboring a point 6955C→T mutation in the Notch2 locus upstream of the PEST domain, and we termed this model Notch2tm1.1Ecan. Heterozygous Notch2tm1.1Ecan mutant mice exhibit severe cancellous and cortical bone osteopenia due to increa
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Wang, Qing, Ran Yan, Nancy Pinnell, et al. "The Direct Notch1 Cofactor Zmiz1 Differentially Regulates Notch1 Signals in a Stage-Specific Manner to Preserve Early T-Cell Precursors and Expand Committed T Cells." Blood 128, no. 22 (2016): 426. http://dx.doi.org/10.1182/blood.v128.22.426.426.

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Abstract When stem cells first enter the thymus and become early T-cell precursor (ETP) cells, they are exposed to high levels of Notch1 ligand. Notch1 signal strength must be tightly regulated because on one hand, excessive Notch1 signals drive premature T-cell commitment, resulting in loss of ETP cells and alternative cell fates. On the other hand, complete loss of Notch1 signals impairs ETP proliferation, also resulting in loss of ETP cells. Thus, keeping Notch signals finely balanced in ETP cells preserves "stemness". However, after ETP cells commit to the T-cell lineage by the DN3 cell st
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Vanorny, Dallas A., Rexxi D. Prasasya, Abha J. Chalpe, Signe M. Kilen, and Kelly E. Mayo. "Notch Signaling Regulates Ovarian Follicle Formation and Coordinates Follicular Growth." Molecular Endocrinology 28, no. 4 (2014): 499–511. http://dx.doi.org/10.1210/me.2013-1288.

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Abstract Ovarian follicles form through a process in which somatic pregranulosa cells encapsulate individual germ cells from germ cell syncytia. Complementary expression of the Notch ligand, Jagged1, in germ cells and the Notch receptor, Notch2, in pregranulosa cells suggests a role for Notch signaling in mediating cellular interactions during follicle assembly. Using a Notch reporter mouse, we demonstrate that Notch signaling is active within somatic cells of the embryonic ovary, and these cells undergo dramatic reorganization during follicle histogenesis. This coincides with a significant in
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Ziouti, Fani, Regina Ebert, Maximilian Rummler, et al. "NOTCH Signaling Is Activated through Mechanical Strain in Human Bone Marrow-Derived Mesenchymal Stromal Cells." Stem Cells International 2019 (February 26, 2019): 1–13. http://dx.doi.org/10.1155/2019/5150634.

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Skeletal development and remodeling of adult bone are critically controlled by activated NOTCH signaling in genetically modified mice. It is yet unclear whether NOTCH signaling is activated by mechanical strain sensed by bone cells. We found that expression of specific NOTCH target genes is induced after in vivo tibial mechanical loading in wild-type mice. We further applied mechanical strain through cyclic stretching in human bone marrow-derived mesenchymal stromal cells (BMSCs) in vitro by using a bioreactor system and detected upregulation of NOTCH target gene expression. Inhibition of the
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Wu, Lizi, Ivan Maillard, Makoto Nakamura, Warren S. Pear, and James D. Griffin. "The transcriptional coactivator Maml1 is required for Notch2-mediated marginal zone B-cell development." Blood 110, no. 10 (2007): 3618–23. http://dx.doi.org/10.1182/blood-2007-06-097030.

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Abstract Signaling mediated by various Notch receptors and their ligands regulates diverse biological processes, including lymphoid cell fate decisions. Notch1 is required during T-cell development, while Notch2 and the Notch ligand Delta-like1 control marginal zone B (MZB) cell development. We previously determined that Mastermind-like (MAML) transcriptional coactivators are required for Notchinduced transcription by forming ternary nuclear complexes with Notch and the transcription factor CSL. The 3 MAML family members (MAML1-MAML3) are collectively essential for Notch activity in vivo, but
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Luo, B., J. C. Aster, R. P. Hasserjian, F. Kuo, and J. Sklar. "Isolation and functional analysis of a cDNA for human Jagged2, a gene encoding a ligand for the Notch1 receptor." Molecular and Cellular Biology 17, no. 10 (1997): 6057–67. http://dx.doi.org/10.1128/mcb.17.10.6057.

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Signaling through Notch receptors has been implicated in the control of cellular differentiation in animals ranging from nematodes to humans. Starting from a human expressed sequence tag-containing sequence resembling that of Serrate, the gene for a ligand of Drosophila melanogaster Notch, we assembled a full-length cDNA, now called human Jagged2, from overlapping cDNA clones. The full-length cDNA encodes a polypeptide having extensive sequence homology to Serrate (40.6% identity and 58.7% similarity) and even greater homology to several putative mammalian Notch ligands that have subsequently
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Dissertations / Theses on the topic "Mice Notch genes Mice"

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Ruivenkamp, Claudia Antoinette Laetitia. "Colon cancer susceptibility genes in mice and humans." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/67685.

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Jakt, Lars Martin. "Isolation of mouse Hoxb-3 protein binding sequences : a whole genome approach /." Thesis, Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21185505.

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Rigby, Robert James. "The identification of lupus susceptibility genes in New Zealand mice." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429877.

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Randhawa, J. S. "Molecular characterisation of the pneumonia virus of mice glycoprotein genes." Thesis, University of Warwick, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387336.

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Boukouvala, Sotiria. "Expression of the genes for arylamine N-acetyltransferases in mice." Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:ed864a10-2cb9-4ebe-8a2c-934d707c5a0d.

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Freland, Sofia. "Lymphoid development and function in MHC class I deficient mice /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3714-1/.

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Keshavarz, Maryam [Verfasser]. "Analysis of candidate genes for behavioral differences in mice / Maryam Keshavarz." Kiel : Universitätsbibliothek Kiel, 2019. http://d-nb.info/1187242616/34.

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Faulkes, David Julian. "The analysis of human serum amyloid A genes using transgenic mice." Thesis, Open University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287010.

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Scherer, Christina Ann. "An in vitro screen to isolate developmentally regulated genes in mice." Thesis, Massachusetts Institute of Technology, 1995. http://hdl.handle.net/1721.1/32638.

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Dershem, Victoria Lynne. "The Expression of Dopamine-Related Genes and Behavioral Performance in Mice." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1484217370390211.

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Books on the topic "Mice Notch genes Mice"

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Ormestad, Mattias. FoxF genes in embryonic development. Department of Cell and Molecular Biology, Göteborg University, 2006.

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Haddad, George E. Expression of HLA class II genes in transgenic mice. National Library of Canada, 1994.

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Randhawa, J. S. Molecular characterisation of the pneumonia virus of mice glycoprotein genes. typescript, 1993.

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Tsang, Michael Wai Kok. Characterisation of structure and function of mouse dishevelled genes. University College Dublin, 1996.

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Howard, Lorraine Tamar. The construction and characterization of hypoxia responsive reporter genes for use in transgenic mice. National Library of Canada, 2001.

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Barr, John Nicholas. Expression of the nucleoprotein and phosphoprotein genes of pneumonia virus of mice and specific interactions ofthe gene products. typescript, 1993.

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Thomas, David Peter. Studies on tumourigenesis in transgenic mice expressing the early region genes of human papillomavirus type 16 (HPV-16). University of Birmingham, 1996.

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E, Davies K., and Tilghman Shirley M, eds. Genes and phenotypes. Cold Spring Harbor Laboratory Press, 1991.

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(Foreword), Thomas R. Cech, and Maya Pines (Introduction), eds. Genes We Share With Yeast, Flies, Worms and Mice: New Clues to Human Health and Disease. Diane Pub Co, 2003.

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Maya, Pines, and Howard Hughes Medical Institute, eds. The genes we share with yeast, flies, worms, and mice: New clues to human health and disease. Howard Hughes Medical Institute, 2001.

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Book chapters on the topic "Mice Notch genes Mice"

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Aiba, Atsu, and Motoya Katsuki. "Mutant Mice Lacking Dopamine Receptor Genes." In Catecholamine Research. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3538-3_37.

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Kono, D. H., and A. N. Theofilopoulos. "Genetic Susceptibility to Spontaneous Lupus in Mice." In Genes and Genetics of Autoimmunity. KARGER, 1999. http://dx.doi.org/10.1159/000060497.

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Kohda, Takashi, Fumitoshi Ishino, and Atsuo Ogura. "Expression of Imprinted Genes in Cloned Mice." In Methods in Molecular Biology. Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-154-3_16.

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Lovell-Badge, Robin, Clare Canning, and Ryohei Sekido. "Sex-Determining Genes in Mice: Building Pathways." In The Genetics and Biology of Sex Determination. John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470868732.ch2.

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Jami, J., and R. Pictet. "Expression of Foreign Genes in Transgenic Mice." In Future Aspects in Human In Vitro Fertilization. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71412-2_26.

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Kawade, Yoshimi, Masahide Asano, Hitoshi Nagashima, and Yoichiro Iwakura. "Transgenic Mice Carrying Exogenous Mouse Interferon Genes." In The Biology of the Interferon System 1986. Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3543-3_43.

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Wilder, R. L., E. F. Remmers, Y. Kawahito, P. S. Gulko, G. W. Cannon, and M. M. Griffiths. "Genetic Factors Regulating Experimental Arthritis in Mice and Rats." In Genes and Genetics of Autoimmunity. KARGER, 1999. http://dx.doi.org/10.1159/000060492.

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Storb, U., P. Engler, E. Klotz, et al. "Rearrangement and Expression of Immunoglobulin Genes in Transgenic Mice." In Current Topics in Microbiology and Immunology. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77633-5_16.

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Kozak, C. A., and R. R. O’Neill. "Xenotropic and MCF Related Retroviral Genes in Wild Mice." In The Wild Mouse in Immunology. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71304-0_42.

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Levine, Arnold J. "Expression of SV40 Early Region Genes in Transgenic Mice." In Concepts in Viral Pathogenesis III. Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-8890-6_18.

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Conference papers on the topic "Mice Notch genes Mice"

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Estrella, A. M., E. Dobrinskikh, C. E. Hennessy, I. V. Yang, and D. A. Schwartz. "Muc5b and Other Genes Predispose Mice to Lung Fibrosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2159.

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Trivedi, S., J. Ciencewicki, HY Cho, K. Horvath, I. Jaspers, and SR Kleeberger. "Expression of Notch and Its Ligands in Mice Exposed to Ozone." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2572.

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Yongbin, Chen, Zhang Liyan, and Guo Guozhen. "Effect of EMP on mice polydactylia and related genes expression (Gli3, Shh and Fgf4) during the development of mice limbs." In 2006 4th Asia-Pacific Conference on Environmental Electromagnetics. IEEE, 2006. http://dx.doi.org/10.1109/ceem.2006.257966.

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Turner, Charles H., and Alexander G. Robling. "Genetic Effects on Skeletal Mechanosensitivity in Mice." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32596.

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The accumulation of bone mass during growth can be enhanced by environmental factors such as mechanical loading (exercise) or calcium intake, but 60–70% of the variance in adult bone mineral density (BMD) is explained by heredity. Consequently, understanding the signaling pathways targeted by the genes governing bone accumulation holds perhaps the greatest potential in reducing fracture incidence later in life. Rodent models are particularly useful for studying the genetics of skeletal traits. Of the available inbred mouse strains, three in particular have been studied extensively in skeletal
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Evert, K., Y. Qiao, J. Wang та ін. "Loss of Axin1 induced hepatocarcinogenesis requires intact β-Catenin but not Notch cascade in mice". У 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677207.

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Hall, R., M. Krawczyk, S. Weber, M. Milkiewicz, P. Milkiewicz, and F. Lammert. "Genes involved in hepatic cholesterol homeostasis identified as modifiers of cholestasis in Abcb4 deficient mice." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402110.

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Leikauf, George D., Hannah Pope-Varsalona, Vincent J. Concel, et al. "Candidate Susceptibility Genes Identified By Genomewide Analysis Of Chloride-induced Acute Lung Injury In Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5370.

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Chen, Richard, Daniel Nemeth, Jason Mora, Mohan Muvvala, Derek Wu, and Yuri Griko. "Changes in Differential Expression of Genes in Normal and Metabolically Suppressed Mice in Response to Radiation." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8513624.

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El-fadl, Rihab, Nasser Rizk, Amena Fadel, and Abdelrahman El Gamal. "The Profile of Hepatic Gene Expression of Glucose Metabolism in Mice on High Fat Diet." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0213.

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Obesity is a growing problem worldwide, and recent data indicated that 20% of the populations would be obese. Obesity arises as a multifactorial disease caused by inherited traits that interact with lifestyle factors such as diet and physical activity. The liver plays an essential role in the gluco-regulation via regulating glucose, lipid and protein metabolism. The process of glucose metabolism is controlled by a range of molecular mechanisms and genes which affect the metabolism of the liver during intake of high fat diet (HFD). The objective of this research is to investigate the profile of
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Duarte, Antonio, Marina Badenes, Alexandre Trindade, Ren Liu, and Parkash S. Gill. "Abstract LB-285: Blocking Dll4/Notch signaling inhibits development of chronic colitis-associated colorectal cancer in mice." 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-lb-285.

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Reports on the topic "Mice Notch genes Mice"

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Connolly, Denise C. Modeling Human Epithelial Ovarian Cancer in Mice by Alteration of Expression of the BRCA1 and/or p53 Genes. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada485053.

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Connolly, Denise C. Modeling Human Epithelial Ovarian Cancer in Mice by Alteration of Expression of the BRCA1 and/or P53 Genes. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada436423.

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Blackburn, Anneke C., and Joseph Jerry. Development of Spontaneous Mammary Tumors in BALB/c-p53+-Mice: Detection of Early Genetic Alterations and the Mapping of BALB/c Susceptibility Genes. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada410279.

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Smith, Sallie, and Joseph Jerry. Development of Spontaneous Mammary Tumors in BALB/c-p53+/-Mice: Detection of Early Genetic Alterations and the Mapping of BALB/c Susceptibility Genes. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada424523.

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