Relevant bibliographies by topics / Mammalian cell cycle

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Mammalian cell cycle'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Mammalian cell cycle"

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OKAYAMA, HIROTO. "Mammalian Cell Cycle." RADIOISOTOPES 42, no. 8 (1993): 497–98. http://dx.doi.org/10.3769/radioisotopes.42.497.

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Martínez-Alonso, Diego, and Marcos Malumbres. "Mammalian cell cycle cyclins." Seminars in Cell & Developmental Biology 107 (November 2020): 28–35. http://dx.doi.org/10.1016/j.semcdb.2020.03.009.

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Noël, Vincent, Sergey Vakulenko, and Ovidiu Radulescu. "A hybrid mammalian cell cycle model." Electronic Proceedings in Theoretical Computer Science 125 (August 27, 2013): 68–83. http://dx.doi.org/10.4204/eptcs.125.5.

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Whitaker, M., and R. Patel. "Calcium and cell cycle control." Development 108, no. 4 (April 1, 1990): 525–42. http://dx.doi.org/10.1242/dev.108.4.525.

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The cell division cycle of the early sea urchin embryo is basic. Nonetheless, it has control points in common with the yeast and mammalian cell cycles, at START, mitosis ENTRY and mitosis EXIT. Progression through each control point in sea urchins is triggered by transient increases in intracellular free calcium. The Cai transients control cell cycle progression by translational and post-translational regulation of the cell cycle control proteins pp34 and cyclin. The START Cai transient leads to phosphorylation of pp34 and cyclin synthesis. The mitosis ENTRY Cai transient triggers cyclin phosphorylation. The motosis EXIT transient causes destruction of phosphorylated cyclin. We compare cell cycle regulation by calcium in sea urchin embryos to cell cycle regulation in other eggs and oocytes and in mammalian cells.
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Cooper, S. "Rethinking synchronization of mammalian cells for cell cycle analysis." Cellular and Molecular Life Sciences 60, no. 6 (June 2003): 1099–106. http://dx.doi.org/10.1007/s00018-003-2253-2.

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Davis, Penny K., Alan Ho, and Steven F. Dowdy. "Biological Methods for Cell-Cycle Synchronization of Mammalian Cells." BioTechniques 30, no. 6 (June 2001): 1322–31. http://dx.doi.org/10.2144/01306rv01.

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Müller, Rolf. "Transcriptional regulation during the mammalian cell cycle." Trends in Genetics 11, no. 5 (May 1995): 173–78. http://dx.doi.org/10.1016/s0168-9525(00)89039-3.

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Denhardt, David T., Dylan R. Edwards, and Craig L. J. Parfett. "Gene expression during the mammalian cell cycle." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 865, no. 2 (October 1986): 83–125. http://dx.doi.org/10.1016/0304-419x(86)90024-7.

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OSADA, HIROYUKI. "Bioprobes for Investigating Mammalian Cell Cycle Control." Journal of Antibiotics 51, no. 11 (1998): 973–82. http://dx.doi.org/10.7164/antibiotics.51.973.

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Rieder, Conly L., and Richard W. Cole. "Cold-Shock and the Mammalian Cell Cycle." Cell Cycle 1, no. 3 (May 2002): 168–74. http://dx.doi.org/10.4161/cc.1.3.119.

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Dissertations / Theses on the topic "Mammalian cell cycle"

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Kuleszewicz, Katarzyna. "Cell cycle regulation in mammalian oocytes." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/26148.

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An unusual feature of mammalian female germ cells is that they are arrested in meiotic prophase, equivalent to mitotic G2-phase, for an extended period of time. In this thesis I have investigated two aspects of this arrest. First, I examined whether cohesin replenishment is required for the maintenance of chromosome cohesion during protracted meiotic prophase arrest. Nipbl, an evolutionarily conserved protein, is a component of protein complex called kollerin, whose activity in loading cohesin onto chromosomes is necessary for accurate chromosome segregation during mitosis. However, until now its function in mammalian meiosis was unknown. I have showed that Nipbl is present on meiotic chromosomes throughout meiotic prophase in mouse spermatocytes and oocytes and it accumulates at chromosomal axes where it co-localises with cohesin. I employed conditional knockout strategy to inactivate Nipbl gene in mouse oocytes arrested in meiotic prophase. Although functional Nipbl transcripts were efficiently depleted, these oocytes underwent meiotic maturation with unaffected chiasmata and cohesion. Surprisingly, Nipbl-deleted eggs were fertile and the loading of mitotic cohesin containing Rad21 was unaffected in fertilized eggs. Aditionally, these eggs could develop into blastocysts upon parthenogenetic activation, however harbouring a high proportion of cells with misaligned chromosomes. These results suggest that Nipbl is very stable in the oocyte. In the second project we conceived that the maintenance of the cell cycle arrest in primordial oocytes is an important aspect of follicular survival. Previously proposed involvement of the anaphase promoting complex/cyclosome (APC/C), a cell cycle ubiquitin ligase complex in down-regulating the cyclin-dependent kinase activity in fully-grown oocyte led me to inactivate APC/C in dormant oocytes using conditional knockout system. I found that upon APC/C inactivation, primordial follicles were completely depleted before adulthood, within 5 weeks of birth, suggesting that the APC/C activity is required for the survival of primordial oocytes. These results propose the presence of previously unknown mechanism involving APC/C, essential for primordial follicle survival.
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Engstrom, Julia U. "Mammalian cell cycle regulates oligonucleotide-mediated repair." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 219 p, 2008. http://proquest.umi.com/pqdweb?did=1481658501&sid=9&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Weis, Michael Christian. "Computational Models of the Mammalian Cell Cycle." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1323278159.

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Sauvé, Gordon John. "Genetic complementation of a mammalian cell cycle mutant." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74037.

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Calegari, Federico, and Julieta Aprea. "Bioelectric State and Cell Cycle Control of Mammalian Neural Stem Cells." Sage-Hindawi, 2012. https://tud.qucosa.de/id/qucosa%3A27972.

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The concerted action of ion channels and pumps establishing a resting membrane potential has been most thoroughly studied in the context of excitable cells, most notably neurons, but emerging evidences indicate that they are also involved in controlling proliferation and differentiation of nonexcitable somatic stem cells. The importance of understanding stem cell contribution to tissue formation during embryonic development, adult homeostasis, and regeneration in disease has prompted many groups to study and manipulate the membrane potential of stem cells in a variety of systems. In this paper we aimed at summarizing the current knowledge on the role of ion channels and pumps in the context of mammalian corticogenesis with particular emphasis on their contribution to the switch of neural stem cells from proliferation to differentiation and generation of more committed progenitors and neurons, whose lineage during brain development has been recently elucidated.
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Calegari, Federico, and Julieta Aprea. "Bioelectric State and Cell Cycle Control of Mammalian Neural Stem Cells." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-185623.

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The concerted action of ion channels and pumps establishing a resting membrane potential has been most thoroughly studied in the context of excitable cells, most notably neurons, but emerging evidences indicate that they are also involved in controlling proliferation and differentiation of nonexcitable somatic stem cells. The importance of understanding stem cell contribution to tissue formation during embryonic development, adult homeostasis, and regeneration in disease has prompted many groups to study and manipulate the membrane potential of stem cells in a variety of systems. In this paper we aimed at summarizing the current knowledge on the role of ion channels and pumps in the context of mammalian corticogenesis with particular emphasis on their contribution to the switch of neural stem cells from proliferation to differentiation and generation of more committed progenitors and neurons, whose lineage during brain development has been recently elucidated.
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Greggains, Gareth David. "Cell cycle regulation and nuclear reprogramming in mammalian oocytes." Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538926.

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Swanton, Robert Charles. "Viral cyclin disruption of mammalian cell cycle control mechanisms." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286205.

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Lundgren, Andreas. "The ABC of the cell cycle: roles of the mammalian Cdc25 isoforms /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-639-5/.

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Avva, Jayant. "Complex Systems Biology of Mammalian Cell Cycle Signaling in Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1295625781.

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Books on the topic "Mammalian cell cycle"

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Wensing, Enrico J. Ribonucleotide reductase and ornithine decarboxylase mRNA expression in hydroxyurea resistant and cell cycle synchronized mammalian cells. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Burton, Derek, and Margaret Burton. Metabolism, homeostasis and growth. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198785552.003.0007.

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Metabolism consists of the sum of anabolism (construction) and catabolism (destruction) with the release of energy, and achieving a fairly constant internal environment (homeostasis). The aquatic external environment favours differences from mammalian pathways of excretion and requires osmoregulatory adjustments for fresh water and seawater though some taxa, notably marine elasmobranchs, avoid osmoregulatory problems by retaining osmotically active substances such as urea, and molecules protecting tissues from urea damage. Ion regulation may occur through chloride cells of the gills. Most fish are not temperature regulators but a few are regional heterotherms, conserving heat internally. The liver has many roles in metabolism, including in some fish the synthesis of antifreeze seasonally. Maturing females synthesize yolk proteins in the liver. Energy storage may include the liver and, surprisingly, white muscle. Fish growth can be indeterminate and highly variable, with very short (annual) life cycles or extremely long cycles with late and/or intermittent reproduction.
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Book chapters on the topic "Mammalian cell cycle"

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Ostheimer, Gerard J. "Cell Cycle of Mammalian Cells." In Encyclopedia of Systems Biology, 303–5. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_20.

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Balczon, Ron, Liming Bao, Warren E. Zimmer, Kevin Brown, Raymond P. Zinkowski, and B. R. Brinkley. "Analysis of Centrosome Replication Events in Mammalian Cells." In The Cell Cycle, 229–35. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_27.

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O’Connor, Patrick M., and Joany Jackman. "Synchronization of Mammalian Cells." In Cell Cycle — Materials and Methods, 63–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-57783-3_6.

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Sherr, Charles J., Hitoshi Matsushime, Jun-ya Kato, Dawn E. Quelle, and Martine F. Roussel. "Control of G1 Progression by Mammalian D-Type Cyclins." In The Cell Cycle, 17–23. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_2.

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Guo, Xiao-Wen, John P. H. Th’ng, Richard A. Swank, and E. Morton Bradbury. "Effects of Phosphatase Inhibitors on Mammalian p34cdc2 Kinase Activities." In The Cell Cycle, 41–49. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_5.

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Zwicker, Jörk, and Rolf Müller. "Cell cycle-regulated transcription in mammalian cells." In Progress in Cell Cycle Research, 91–99. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1809-9_7.

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Tapia-Alveal, Claudia, and Matthew J. O’Connell. "Methods for Studying the G2 DNA Damage Checkpoint in Mammalian Cells." In Cell Cycle Checkpoints, 23–31. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_3.

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Walsh, David, Li Zhe, Frank Zeng, Wu Yan, and Karen Li. "Heat Shock Genes and Cell Cycle Regulation During Early Mammalian Development." In The Cell Cycle, 271–81. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_32.

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Lee, Jongkuen, and David Dominguez-Sola. "Mammalian Cell Fusion Assays for the Study of Cell Cycle Progression by Functional Complementation." In Cell Cycle Checkpoints, 145–57. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1217-0_9.

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Misteli, Tom. "The mammalian Golgi apparatus during M-phase." In Progress in Cell Cycle Research, 267–77. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5873-6_24.

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Conference papers on the topic "Mammalian cell cycle"

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"A review of computational models of mammalian cell cycle." In 21st International Congress on Modelling and Simulation (MODSIM2015). Modelling and Simulation Society of Australia and New Zealand, 2015. http://dx.doi.org/10.36334/modsim.2015.c2.abroudi2.

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Faryabi, Babak, Golnaz Vahedi, Jean-Francois Chamberland, Aniruddha Datta, and Edward R. Dougherty. "Constrained intervention in a cancerous mammalian cell cycle network." In 2008 IEEE International Workshop on Genomic Signal Processing and Statistics (GENSIPS). IEEE, 2008. http://dx.doi.org/10.1109/gensips.2008.4555669.

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Ruz, Gonzalo A., and Eric Goles. "Reconstruction and update robustness of the mammalian cell cycle network." In 2012 IEEE Symposium on Computational Intelligence in Bioinformatics and Computational Biology (CIBCB). IEEE, 2012. http://dx.doi.org/10.1109/cibcb.2012.6217257.

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"System modelling of mammalian cell cycle regulation using multi-level hybrid petri nets." In 21st International Congress on Modelling and Simulation (MODSIM2015). Modelling and Simulation Society of Australia and New Zealand, 2015. http://dx.doi.org/10.36334/modsim.2015.c2.abroudi3.

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Gurumurthy, Channabasavaiah B., Jun H. Kim, Xiangshan Zhao, Mayumi Naramura, Hamid Band, and Vimla Band. "Abstract 1069: The role of mammalian Ecdysoneless in cell cycle regulation and 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.am10-1069.

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Diop, Ousmane, Laurent Tourniel, and Vincent Fromion. "Summarizing complex asynchronous Boolean attractors, application to the analysis of a mammalian cell cycle model." In 2019 18th European Control Conference (ECC). IEEE, 2019. http://dx.doi.org/10.23919/ecc.2019.8795712.

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Stumpf, Craig R., Melissa V. Moreno, Adam B. Olshen, Barry S. Taylor, and Davide Ruggero. "Abstract A57: Plasticity of the translational landscape during the mammalian cell cycle: Implications and new insights for cancer cell proliferation." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-a57.

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Tang, Binhua, Jiajun Liu, Li He, Qing Jing, and Bairong Shen. "In Silico Identification & Adaptive Control of the Motif in the Mammalian G1/S Cell Cycle Pathway." In 2008 2nd International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2008. http://dx.doi.org/10.1109/icbbe.2008.236.

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Meaud, Julien, Thomas Bowling, and Charlsie Lemons. "Computational Modeling of Spontaneous Otoacoustic Emissions by the Mammalian Cochlea." In ASME 2018 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dscc2018-9044.

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The mammalian cochlea is a sensory system with high sensitivity, sharp frequency selectivity and a broad dynamic range. These characteristics are due to the active nonlinear feedback by outer hair cells. Because it is an active nonlinear system, the cochlea sometimes emits spontaneous otoacoustic emissions (SOAEs) that are generated in the absence of any external stimulus due to the emergence of limit cycle oscillations. In this work, we use a computational physics-based model of the mammalian cochlea to investigate the generation of SOAEs. This model includes a three-dimensional model of the fluid mechanics in the cochlear ducts, a micromechanical model for the vibrations of the cochlear structures, and a realistic model of outer hair cell biophysics. Direct simulations of SOAEs in the time-domain demonstrate that the model is able to capture key experimental observations regarding SOAEs. Parametric studies and analysis of model simulations are used to demonstrate that SOAEs are a global phenomenon that arises due to the collective action of a distributed region of the cochlea rather than from spontaneous oscillations from individual outer hair cells.
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Li, G., S. S. Nair, S. J. Lees, and F. W. Booth. "Regulation of G2/M Transition in Mammalian Cells by Oxidative Stress." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-82349.

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The regulation of the G2/M transition for the mammalian cell cycle has been modeled using 19 states to investigate the G2 checkpoint dynamics in response to oxidative stress. A detailed network model of G2/M regulation is presented and then a “core” subsystem is extracted from the full network. An existing model of Mitosis control is extended by adding two important pathways regulating G2/M transition in response to DNA damage induced by oxidative stress. Model predictions indicate that the p53 dependent pathway is not required for initial G2 arrest as the Chk1/Cdc25C pathway can arrest the cell in G2 right after DNA damage. However, p53 and p21 expression is important for a more sustained G2 arrest by inhibiting the Thr161 phosphorylation by CAK. By eliminating the phosphorylation effect of Chk1 on p53, two completely independent pathways are obtained and it is shown that it does not affect the G2 arrest much. So the p53/p21 pathway makes an important, independent contribution to G2 arrest in response to oxidative stress, and any defect in this pathway may lead to genomic instability and predisposition to cancer. Such strict control mechanisms probably provide protection for survival in the face of various environmental changes. The controversial issue related to the mechanism of inactivation of Cdc2 by p21 is addressed and simulation predictions indicate that G2 arrest would not be affected much by considering the direct binding of p21 to Cdc2/Cyclin B given that the inhibition of CAK by p21 is already present if the binding efficiency is within a certain range. Lastly, we show that the G2 arrest time in response to oxidative stress is sensitive to the p53 synthesis rate.
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