Relevant bibliographies by topics / Cellular signals

Academic literature on the topic 'Cellular signals'

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

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Journal articles on the topic "Cellular signals"

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Nick, Peter. "Hijacking cellular signals." Protoplasma 254, no. 6 (October 11, 2017): 2053–54. http://dx.doi.org/10.1007/s00709-017-1174-0.

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Teplitz, Linda, and Deborah A. Siwik. "Cellular signals in atherosclerosis." Journal of Cardiovascular Nursing 8, no. 3 (April 1994): 28–52. http://dx.doi.org/10.1097/00005082-199404000-00004.

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Warren, G. "Sorting signals and cellular membranes." BMJ 295, no. 6608 (November 14, 1987): 1259–61. http://dx.doi.org/10.1136/bmj.295.6608.1259.

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Edgington, Thomas. "More Cellular Signals for Atherogenesis?" Circulation 98, no. 12 (September 22, 1998): 1151–52. http://dx.doi.org/10.1161/01.cir.98.12.1151.

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Tursz, T., and D. Hoessli. "Chemical Signals of Cellular Interactions." International Archives of Allergy and Immunology 83, no. 1 (1987): 21–35. http://dx.doi.org/10.1159/000234388.

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Tarn, Woan-Yuh. "Cellular signals modulate alternative splicing." Journal of Biomedical Science 14, no. 4 (March 24, 2007): 517–22. http://dx.doi.org/10.1007/s11373-007-9161-7.

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Macrez, N., and J. Mironneau. "Local Ca2+ Signals in Cellular Signalling." Current Molecular Medicine 4, no. 3 (May 1, 2004): 263–75. http://dx.doi.org/10.2174/1566524043360762.

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Ramanathan, Harish N., and Yihong Ye. "Cellular strategies for making monoubiquitin signals." Critical Reviews in Biochemistry and Molecular Biology 47, no. 1 (October 8, 2011): 17–28. http://dx.doi.org/10.3109/10409238.2011.620943.

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Chiarini, L. B. "Cellular prion protein transduces neuroprotective signals." EMBO Journal 21, no. 13 (July 1, 2002): 3317–26. http://dx.doi.org/10.1093/emboj/cdf324.

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DOWNES, C. Peter, and Colin H. MACPHEE. "myo-Inositol metabolites as cellular signals." European Journal of Biochemistry 193, no. 1 (October 1990): 1–18. http://dx.doi.org/10.1111/j.1432-1033.1990.tb19297.x.

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Dissertations / Theses on the topic "Cellular signals"

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Manktelow, Emily Frances. "Structural studies of viral and cellular recoding signals." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611943.

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Papaioannou, Alexandra. "Fine-tuning UPR signals and subsequent cellular outputs." Thesis, Rennes 1, 2019. http://www.theses.fr/2019REN1B013.

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La présente thèse explore le monde de la biologie du stress du RE (réticulum endoplasmique). Une vue globale du RE et du stress du RE est d'abord fournie en commençant par les mécanismes de base impliqués pour aller vers de possibles applications cliniques. L'accent est ensuite mis sur le rôle crucial de l'UPR dans la cancérogénèse, qui est activée en réponse au stress du RE dans la micro-environnement de la tumeur. Après avoir passé en revue ces aspects, nous mettons en évidence des éléments manquants dans notre compréhension de la façon dont les signaux UPR sont affinés et conduisent soit à la restauration de l'homéostasie du RE et des cellules soit à la mort cellulaire. Parmi les branches de l'UPR, les signaux ATF6 et IRE1 deviennent notre sujet d'investigation en raison de leur convergence dans la régulation du facteur XBP1 favorisant la survie. D'une part, nous découvrons les mécanismes provenant du lumen du RE qui régulent l'activation de l'ATF6 en réponse au stress du RE et affectant la signalisation adaptative cellulaire de l'ATF6 en aval. D'autre part, nous observons l'existence d'un réseau autorégulateur de l'activité RNase de l’IRE1 consistant en un système tyrosine kinase-phosphatase ciblant la RtcB et impactant l'épissage de l'ARNm de XBP1. Ainsi, grâce à nos études, nous avons découvert un circuit de signalisation intégré capable d’ajuster avec précision les sorties cellulaires de l’activation conjointe ATF6 et IRE1 en réponse au stress du RE
The present thesis explores the world of ER (endoplasmic reticulum) stress biology. A global view of ER and ER stress is first provided with a transition from the basic mechanisms involved to possible clinical applications. The focus is then placed to the crucial role of the UPR in carcinogenesis that is activated in response to ER stress in the micro-environment of the tumor. After reviewing these aspects, we point to missing parts in our comprehension of how UPR signals are fine-tuned and lead to either restoration of ER and cell homeostasis or cell death. Among the UPR branches, ATF6 and IRE1 signaling become our focus of investigation because of their convergence in the regulation of the pro-survival factor XBP1s. On the one hand, we unravel mechanisms originating from the ER lumen that regulate the ATF6 activation in response to ER stress and affect its downstream cell adaptive signaling. On the other hand, we witness the existence of an auto-regulatory network of IRE1 RNase activity consisted of a tyrosine kinase-phosphatase system that targets RtcB and impacts on XBP1 mRNA splicing. Hence, through our studies we uncover an integrated signaling circuit that can fine-tune the cellular outputs of the joint ATF6 and IRE1 activation in response to ER stress
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Thomson, Ty M., and Drew Endy. "Rapid Characterization of Cellular Pathways Using Time-Varying Signals." International Conference on Systems Biology, 2005. http://hdl.handle.net/1721.1/29803.

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The use of traditional tools for the discovery and characterization of biological systems has resulted in a wealth of biological knowledge. Unfortunately, only a small portion of the biological world is well-understood to date, and the study of the rest remains a daunting task. This work involves using time-varying stimuli in order to more rapidly interrogate and characterize signaling pathways. The time-dependent stimulation of a signaling pathway can be used in conjunction with a model of the pathway to efficiently evaluate and test hypotheses. We are developing this technology using the yeast pheromone signal transduction pathway as a model system. The time-varying stimuli will be applied to the yeast cells via a novel microfluidic device, and the pathway output will be measured via various fluorescent reporters. The output of the pathway can then be compared to the output from a computational model of the pathway in order to test hypotheses and constrain our knowledge of the pathway. Initial work shows that a computational model can be used to identify stimuli time-courses that increase the parameter sensitivity, meaning that corresponding experiments could potentially be much more informative.
Poster presented at the 2005 ICSB meeting, held at Harvard Medical School in Boston, MA.
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Madhavan, Shashi D. "Biomechanical signals mediate cellular mechano-transduction and gene regulation." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1195234773.

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Brandman, Onn. "Feedback loops shape cellular signals in space and time /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Osuna, José A. "The recognition of acoustical alarm signals with cellular neural networks /." [S.l.] : [s.n.], 1995. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=11058.

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Wong, Stephanie A. "Physical and Molecular Pathways Involved in Cellular Sensing of Mechanical Signals." Research Showcase @ CMU, 2016. http://repository.cmu.edu/dissertations/878.

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Mechanical properties of the extracellular environment provide important cues that regulate cell behavior. Particularly, the cellular response to substrate rigidity has become an important parameter to consider in disease treatment as well as tissue engineering. The goal of this thesis is to understand how adherent cells sense and respond to external rigidity cues. It has been challenging to study the mechanism that drives the preferential migration of cells towards stiffer substrates at a rigidity border due to difficulties in capturing cells as they transiently encounter a rigidity interface. Using a model system developed for testing cellular responses at a simulated rigidity border, I find that NIH 3T3 cells preferentially localize to the rigid portion of the model system. Cells use filopodia extensions to probe substrate rigidity in front of the leading edge and use substrate strain to determine whether the filopodia protrusions retract or expand to occupy the area. Myosin II mediated contractility is necessary to generate forces for both probing the substrate and retraction in response to substrate strain. Focal adhesion kinase null (FAK -/-) cells, known to be defective in durotaxis, are able to readily cross the rigidity border, while reexpression of focal adhesion kinase (FAK) rescues rigidity sensing. The model experimental system allows efficient analyses of conditions affecting rigidity sensing of cells. The results suggest that enhanced Rho activity, likely through Rho downstream effector mDia1, may underlie many rigidity sensing defects including those caused by FAK deficiency and microtubule disassembly. Additionally, I show that probing mechanisms at the front of a cell are used not only for probing rigidity but for sensing the state of migration. Design of a new checkerboard micropattern with alternating adhesive and non-adhesive areas revealed that the appearance of new traction forces and focal adhesions at the leading edge promotes the downregulation of pre-existing traction forces and focal adhesions that lag behind. These results suggest that in migrating cells continuous protrusion and mechanical probing directly in front of existing adhesions modulates traction force build up and serves as a key mechanism for regulating mechanical output in response to physical cues.
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Lau, See-yan. "A study of intracellular signals of K-opioids in non-neuronal cells /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19667139.

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Park, Edward S. "Microfluidic chamber arrays for testing cellular responses to soluble-matrix and gradient signals." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/39471.

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This work develops microfluidic technologies to advance the state-of-the-art in living cell-based assays. Current cell-based assay platforms are limited in their capabilities, particularly with respect to spatial and temporal control of external signaling factors, sample usage, and throughput. The emergence of highly quantitative, data-driven systems approaches to studying biology have added further challenges to develop assay technologies with greater throughput, content, and physiological relevance. The primary objectives of this research are to (i) develop a method to reliably fabricate 3-D flow networks and (ii) apply 3-D flow networks to the development and testing of microfluidic chamber arrays to query cellular response to soluble-matrix signal combinations and gradient signaling fields. An equally important objective is for the chamber arrays to be scaled efficiently for higher-throughput applications, which is another reason for 3-D flow networks. Two prototype chamber arrays are designed, modeled, fabricated, and characterized. Furthermore, tests are performed wherein cells are introduced into the chambers and microenvironments are presented to elicit complex responses. Specifically, soluble-matrix signaling combinations and soluble signal gradients are presented. The study of complex biological processes necessitates improved assay techniques to control the microenvironment and increase throughput. Quantitative morphological, migrational, and fluorescence readouts, along with qualitative observations, suggest that the chamber arrays elicit responses; however further experiments are required to confirm specific phenotypes. The experiments provide initial proof-of-concept that the developed arrays can one day serve as effective and versatile screening platforms. Understanding the integration of extracellular signals on complex cellular behaviors has significance in the study of embryonic development, tissue repair and regeneration, and pathological conditions such as cancer. The microfluidic chamber arrays developed in this work could form the basis for enhanced assay platforms to perform massively parallel interrogation of complex signaling events upon living cells. This could lead to the rapid identification of synergistic and antagonistic signaling mechanisms that regulate complex behaviors. In addition, the same technology could be used to rapidly screen potential therapeutic compounds and identify suitable candidates to regulate pathological processes, such as cancer and fibrosis.
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Heessen, Stijn. "Regulation of the ubiquitin-proteasome system : characterization of viral and cellular stabilization signals /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-600-6/.

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Books on the topic "Cellular signals"

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University), International Washington Spring Symposium (9th 1989 George Washington. Biology of cellular transducing signals. New York: Plenum Press, 1990.

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A, Lavia Lynn, ed. Cellular signals controlling uterine function. New York: Plenum Press, 1991.

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Vanderhoek, Jack Y., ed. Biology of Cellular Transducing Signals. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0559-0.

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Lavia, Lynn A., ed. Cellular Signals Controlling Uterine Function. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3724-3.

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Fukada, Toshiyuki, and Taiho Kambe, eds. Zinc Signals in Cellular Functions and Disorders. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-55114-0.

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Osuna, José A. The recognition of acoustical alarm signals with cellular neural networks. Konstanz: Hartung-Gorre Verlag, 1995.

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Luan, Sheng. Coding and decoding of calcium signals in plants. Heidelberg: Springer, 2011.

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Verma, D. P. S. 1944-, ed. Molecular signals in plant-microbe communications. Boca Raton: CRC Press, 1991.

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J, Bowles Dianna, ed. Molecular botany: Signals and the environment. London: Portland Press, 1994.

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Molecular mechanisms for sensory signals: Recognition and transformation. Princeton, N.J: Princeton University Press, 1991.

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Book chapters on the topic "Cellular signals"

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Reading, Anthony. "Cellular Signals." In SpringerBriefs in Biology, 97–103. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0158-2_12.

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Marks, Friedrich, Ursula Klingmüller, and Karin Müller-Decker. "Signals Controlling mRNA Translation." In Cellular Signal Processing, 329–58. Second edition. | New York, NY: Garland Science, 2017.: Garland Science, 2017. http://dx.doi.org/10.4324/9781315165479-9.

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Delorme, Marianne, and Jacques Mazoyer. "Signals on Cellular Automata." In Collision-Based Computing, 231–75. London: Springer London, 2002. http://dx.doi.org/10.1007/978-1-4471-0129-1_9.

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Gomez-Barquero, David, Peter Unger, Karim Nasr, Jussi Poikonen, and Kristian Nybom. "Hybrid Cellular and Broadcasting Networks." In Signals and Communication Technology, 547–76. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2315-6_13.

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Rink, Lothar, and Martina Maywald. "Zinc Signals in Immunology." In Zinc Signals in Cellular Functions and Disorders, 197–226. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-55114-0_10.

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Lavia, Lynn A. "Prologue." In Cellular Signals Controlling Uterine Function, 1–4. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3724-3_1.

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Bazer, F. W. "Uterine-conceptus Interactions During the Peri-implantation Period." In Cellular Signals Controlling Uterine Function, 119–36. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3724-3_10.

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Talamantes, F., J. N. Southard, L. Ogren, and G. Thordarson. "The Endocrine Function of the Rodent Placenta: Placental Lactogens." In Cellular Signals Controlling Uterine Function, 137–43. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3724-3_11.

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Clark, David A. "The Origin and Role of Cytokines Determining Success and Failure in the Post-Implantation Period." In Cellular Signals Controlling Uterine Function, 145–55. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3724-3_12.

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Lavia, Lynn A. "Epilogue." In Cellular Signals Controlling Uterine Function, 157–59. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3724-3_13.

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Conference papers on the topic "Cellular signals"

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McCune, Earl. "Modern cellular wireless signals." In 2010 75th ARFTG Microwave Measurement Conference. IEEE, 2010. http://dx.doi.org/10.1109/arftg.2010.5496316.

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Steward, Robert L., Chao-Min Cheng, and Philip R. LeDuc. "Probing Nonlinear Cellular Responses to Integrated Mechanical Signals Through Examining Cell Alignment." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19205.

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Cells are complex systems that continuously receive signals in a variety of forms including both physical and chemical. The ability of cells to integrate these signals and already be hard wired to have coupled responses indicates the complexity at which cells function in terms of signal integration. One of the important areas in signal response is in mechanical stimulation, which has been shown to influence many cellular functions through the cytoskeleton and most often induces various cellular alignment. Most studies generally probe the affects of mechanical stimulation on cell behaviour by one mode of mechanical stimulation, though cells in fact experience multiple modes of mechanical stimulation simultaneously. From this comes the question of how does the cell process these multiple mechanical inputs? In this study we probed the effects of uniaxial stretch and/or shear fluid flow on NIH 3T3 fibroblast behaviour, specifically cell alignment. We used fluorescence microscopy to examine the orientation of the actin cytoskeleton and observed alignment along the direction of force for both uniaxial stretching and shear fluid flow in comparison to cells exposed to both mechanical modes. The cellular response surprisingly revealed an alignment that was neither parallel nor perpendicular to the direction of force. Furthermore, the integration of these 2 modes revealed a nonlinear response to combinations of shear stress and uniaxial stretching. These intriguing results have potential implications in a variety of fields including bioengineering, mechanotransduction, and cell structure.
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Khalife, Joe J., Souradeep Bhattacharya, and Zak M. Kassas. "Centimeter-Accurate UAV Navigation With Cellular Signals." In 31st International Technical Meeting of The Satellite Division of the Institute of Navigation (ION GNSS+ 2018). Institute of Navigation, 2018. http://dx.doi.org/10.33012/2018.16105.

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"BIO-INSPIRED DATA AND SIGNALS CELLULAR SYSTEMS." In International Conference on Bio-inspired Systems and Signal Processing. SciTePress - Science and and Technology Publications, 2008. http://dx.doi.org/10.5220/0001057402030207.

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He, Tai-Ran, Guo-Long Li, Jia Lee, and Ferdinand Peper. "Reliable Crossing of Signals in Asynchronous Cellular Automata." In 2014 Second International Symposium on Computing and Networking (CANDAR). IEEE, 2014. http://dx.doi.org/10.1109/candar.2014.106.

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Carolan, Emmett, Seamus C. McLoone, and Ronan Farrell. "Predictive modelling of cellular load." In 2015 26th Irish Signals and Systems Conference (ISSC). IEEE, 2015. http://dx.doi.org/10.1109/issc.2015.7163784.

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Sawchuk, A. A. "Cellular optical digital computers." In Twenty-Third Asilomar Conference on Signals, Systems and Computers, 1989. IEEE, 1989. http://dx.doi.org/10.1109/acssc.1989.1200757.

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"Session MP3: 5G Cellular networks." In 2015 49th Asilomar Conference on Signals, Systems and Computers. IEEE, 2015. http://dx.doi.org/10.1109/acssc.2015.7421135.

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"Session TP1b: 5G cellular theory." In 2016 50th Asilomar Conference on Signals, Systems and Computers. IEEE, 2016. http://dx.doi.org/10.1109/acssc.2016.7869607.

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Xue, Lixia, Yan Cheng, Yongxing Zhou, and Bingyu Qu. "Next generation TDD cellular communication." In 2015 49th Asilomar Conference on Signals, Systems and Computers. IEEE, 2015. http://dx.doi.org/10.1109/acssc.2015.7421296.

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Reports on the topic "Cellular signals"

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Jones, Robert M., Alison K. Thurston, Robyn A. Barbato, and Eftihia V. Barnes. Evaluating the Conductive Properties of Melanin-Producing Fungus, Curvularia lunata, after Copper Doping. Engineer Research and Development Center (U.S.), November 2020. http://dx.doi.org/10.21079/11681/38641.

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Melanins are pigmented biomacromolecules found throughout all domains of life. Of melanins’ many unique properties, their malleable electrically conductive properties and their ability to chelate could allow them to serve as material for bioelectronics. Studies have shown that sheets or pellets of melanin conduct low levels of electricity; however, electrical conductance of melanin within a cellular context has not been thoroughly investigated. In addition, given the chelating properties of melanin, it is possible that introducing traditionally con-ductive metal ions could improve the conductivity. Therefore, this study investigated the conductive properties of melanized cells and how metal ions change these. We measured the con-ductivity of pulverized Curvularia lunata, a melanized filamentous fungi, with and without the addition of copper ions. We then com-pared the conductivity measurements of the fungus to chemically synthesized, commercially bought melanin. Our data showed that the conductivity of the melanized fungal biomass was an order of magnitude higher when grown in the presence of copper. However, it was two orders of magnitude less than that of synthetic melanin. Interestingly, conductance was measurable despite additional constituents in the pellet that may inhibit conductivity. Therefore, these data show promising results for using melanized cells to carry electrical signals.
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Merrill, Alfred H., and Jr. Subcellular Signal Transduction Systems in the Cellular Trauma of Ischemia. Fort Belvoir, VA: Defense Technical Information Center, November 1990. http://dx.doi.org/10.21236/ada229876.

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Naim, Michael, Andrew Spielman, Shlomo Nir, and Ann Noble. Bitter Taste Transduction: Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7695839.bard.

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Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.
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Tschoellitsch, Thomas, Martin Dünser, Matthias Noitz, and Michael Türk. Clinical indicators of systemic tissue hypoperfusion (‘shock’): A protocol for a systematic review and qualitative analysis of the literature. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0047.

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Review question / Objective: The objective of this review is to identify the current scientific evidence on the value of clinical signs to indicate systemic tissue hypoperfusion or shock. Condition being studied: In the literature and clinical studies, shock has traditionally been defined by a drop in arterial blood pressure under a critical threshold, e.g., a systolic blood pressure of 90 mmHg, a mean arterial blood pressure <65 mmHg or a relative drop in systolic blood pressure of ≥40 mmHg. From a pathophysiologic point of view, shock relates to an imbalance between tissue oxygen delivery as well as cellular oxygen consumption and utilization. In most cases, shock results from systemic tissue hypoperfusion with consequent decreased tissue oxygen delivery (commonly referred to as circulatory shock). Impaired cellular oxygen consumption and utilization appear to play contributory roles in specific disease states (e.g., sepsis) or conditions (e.g., intoxications).
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Barg, Rivka, Erich Grotewold, and Yechiam Salts. Regulation of Tomato Fruit Development by Interacting MYB Proteins. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7592647.bard.

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Background to the topic: Early tomato fruit development is executed via extensive cell divisions followed by cell expansion concomitantly with endoreduplication. The signals involved in activating the different modes of growth during fruit development are still inadequately understood. Addressing this developmental process, we identified SlFSM1 as a gene expressed specifically during the cell-division dependent stages of fruit development. SlFSM1 is the founder of a class of small plant specific proteins containing a divergent SANT/MYB domain (Barg et al 2005). Before initiating this project, we found that low ectopic over-expression (OEX) of SlFSM1 leads to a significant decrease in the final size of the cells in mature leaves and fruits, and the outer pericarp is substantially narrower, suggesting a role in determining cell size and shape. We also found the interacting partners of the Arabidopsis homologs of FSM1 (two, belonging to the same family), and cloned their tomato single homolog, which we named SlFSB1 (Fruit SANT/MYB–Binding1). SlFSB1 is a novel plant specific single MYB-like protein, which function was unknown. The present project aimed at elucidating the function and mode of action of these two single MYB proteins in regulating tomato fruit development. The specific objectives were: 1. Functional analysis of SlFSM1 and its interacting protein SlFSB1 in relation to fruit development. 2. Identification of the SlFSM1 and/or SlFSB1 cellular targets. The plan of work included: 1) Detailed phenotypic, histological and cellular analyses of plants ectopically expressing FSM1, and plants either ectopically over-expressing or silenced for FSB1. 2) Extensive SELEX analysis, which did not reveal any specific DNA target of SlFSM1 binding, hence the originally offered ChIP analysis was omitted. 3) Genome-wide transcriptional impact of gain- and loss- of SlFSM1 and SlFSB1 function by Affymetrix microarray analyses. This part is still in progress and therefore results are not reported, 4) Search for additional candidate partners of SlFSB1 revealed SlMYBI to be an alternative partner of FSB1, and 5) Study of the physical basis of the interaction between SlFSM1 and SlFSB1 and between FSB1 and MYBI. Major conclusions, solutions, achievements: We established that FSM1 negatively affects cell expansion, particularly of those cells with the highest potential to expand, such as the ones residing inner to the vascular bundles in the fruit pericarp. On the other hand, FSB1 which is expressed throughout fruit development acts as a positive regulator of cell expansion. It was also established that besides interacting with FSM1, FSB1 interacts also with the transcription factor MYBI, and that the formation of the FSB1-MYBI complex is competed by FSM1, which recognizes in FSB1 the same region as MYBI does. Based on these findings a model was developed explaining the role of this novel network of the three different MYB containing proteins FSM1/FSB1/MYBI in the control of tomato cell expansion, particularly during fruit development. In short, during early stages of fruit development (Phase II), the formation of the FSM1-FSB1 complex serves to restrict the expansion of the cells with the greatest expansion potential, those non-dividing cells residing in the inner mesocarp layers of the pericarp. Alternatively, during growth phase III, after transcription of FSM1 sharply declines, FSB1, possibly through complexing with the transcription factor MYBI serves as a positive regulator of the differential cell expansion which drives fruit enlargement during this phase. Additionally, a novel mechanism was revealed by which competing MYB-MYB interactions could participate in the control of gene expression. Implications, both scientific and agricultural: The demonstrated role of the FSM1/FSB1/MYBI complex in controlling differential cell growth in the developing tomato fruit highlights potential exploitations of these genes for improving fruit quality characteristics. Modulation of expression of these genes or their paralogs in other organs could serve to modify leaf and canopy architecture in various crops.
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Avni, Adi, and Kirankumar S. Mysore. Functional Genomics Approach to Identify Signaling Components Involved in Defense Responses Induced by the Ethylene Inducing Xyalanase Elicitor. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7697100.bard.

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Plant-microbe interactions involve a large number of global regulatory systems, which are essential for plants to protect themselves against pathogen attack. An ethylene-inducing xylanase (EIX) of Trichoderma viride is a potent elicitor of plant defense responses, like hypersensitive response (HR), in specific cultivars of tobacco (Nicotiana tabacum) and tomato (Lycopersicon esculentum). The central goal of this proposal was to investigate the molecular mechanisms that allow plants to specifically activate defense responses after EIX treatment. We proposed to identify cellular signaling components involved in the induction of HR by the EIX elicitor. The molecular genetic analysis of the signal transduction pathway that modulates hypersensitive responses is an important step in understanding the induction of plant defense responses. The genes that mediate LeEIX2-EIX dependent activation of resistance mechanisms remain to be identified. We used two approaches to identify the cellular signaling components that induce HR mediated by the EIX elicitor. In the first approach, we performed a yeast two-hybrid screening using LeEix2 as bait to identify plant proteins that interact with it. In the second approach, we used virus-induced gene silencing (VIGS) for a high-throughput screen to identify genes that are required for the induction of LeEIX2-EIX mediated HR. VIGS will also be used for functional characterization of genes that will be identified during the yeast two-hybrid screen. This investigation will shed light on cellular processes and signaling components involved in induction of general plant defense against pathogens and will provide the basis for future biotechnological approaches to improve plant resistance to pathogens. Several genes were indentified by the two approaches. We used the VIGS and yeast two hybrid approaches to confirm that activity of the genes initially identified by different procedure. Two genes inhibit the induction of HR by the fungal elicitor in the different systems; Tobacco-Harpin binding protein 1 and cyclopropyl isomerase.
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Lers, Amnon, and Pamela J. Green. Analysis of Small RNAs Associated with Plant Senescence. United States Department of Agriculture, March 2013. http://dx.doi.org/10.32747/2013.7593393.bard.

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Senescence is an agriculturally significant process due to its negative impact to crop yield and postharvest quality. The genetic regulatory systems controlling senescence induction and progress respond to both developmental and environmental stress signals and involve numerous gene expression changes. Knowledge about the key molecular factors which control senescence is very limited. MicroRNAs (miRNAs) are a class of small RNAs which typically function by guiding cleavage of target messenger RNAs. They have been shown to play major roles in a variety of plant processes including development, responses to environmental stresses, and senescence. The long-term goal of this work is to elucidate roles of small RNAs associated with plant senescence. The hypothesis underlying this research is that miRNA-mediated regulation makes important contributions to the senescence process in plants. Specific, original research objectives included: 1) Profiling of small RNAs from senescing plants; 2) Data Analysis and public access via a user-friendly web interface; 3) Validation of senescence-associated miRNAs and target RNAs; 4) Development of transgenic plants for functional analysis of miRNAs in Arabidopsis. Major revisions made in the research compared to the original work plan included 1) Exclusion of the planned work with tomato as recommended by the BARD review panel; 2) Performing miRNA study also in senescing Arabidopsis siliques, in addition to senescing leaves. To identify senescenceregulation of miRNAs in Arabidopsis thaliana, eight small RNA libraries were constructed and sequenced at four different stages of development and senescence from both leaves and siliques, resulting in more than 200 million genome-matched sequences. Parallel Analysis of RNA Ends (PARE) libraries, which enable the large-scale examination of miRNA-guided cleavage products, were also constructed and sequenced, resulting in over 750 million genome-matched sequences. These massive datasets lead to the identification of new miRNAs, as well as new regulation of known miRNAs and their target genes during senescence, many of which have established roles in nutrient responsiveness and cell structural integrity. In keeping with remobilization of nutrients thought to occur during senescence, many miRNAs and targets had opposite expression pattern changes between leaf and silique tissues during the progression of senescence. Taken together, these findings highlight the integral role that miRNAs may play in the remobilization of resources and alteration of cellular structure that is known to occur in senescence. Experiments were initiated for functional analysis of specific senescence-associated miRNAs and respective target genes. Transgenic Arabidopsis plants were generated in which miR408, found in this study to be significantly induced in leaf senescence, was over-expressed either constitutively or under a senescence-specific promoter. These plants are currently being characterized for any altered phenotypes. In addition T-DNA knock out mutants for various target genes identified in this research are being analyzed. This work provides insights about specific miRNAs that contribute to leaf and silique senescence. The knowledge generated may suggest new strategies to monitor and alter the progression of senescence in crops for agricultural improvement.
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Philosoph-Hadas, Sonia, Peter B. Kaufman, Shimon Meir, and Abraham H. Halevy. Inhibition of the Gravitropic Shoot Bending in Stored Cut Flowers Through Control of Their Graviperception: Involvement of the Cytoskeleton and Cytosolic Calcium. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7586533.bard.

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Original objectives: The basic goal of the present project was to study the mechanism involved in shoot graviperception and early transduction, in order to determine the sequence of events operating in this process. This will enable to control the entire process of gravity-induced differential growth without affecting vertical growth processes essential for development. Thus, several new postulated interactions, operating at the perception and early transduction stages of the signaling cascade leading to auxin-mediated bending, were proposed to be examined in snapdragon spikes and oat shoot pulvini, according to the following research goals: 1) Establish the role of amyloplasts as gravireceptors in shoots; 2) Investigate gravity-induced changes in the integrity of shoot actin cytoskeleton (CK); 3) Study the cellular interactions among actin CK, statoliths and cell membranes (endoplasmic reticulum - ER, plasma membrane - PM) during shoot graviperception; 4) Examine mediation of graviperception by modulations of cytosolic calcium - [Ca2+]cyt, and other second messengers (protein phosphorylation, inositol 1,4,5-trisphosphate - IP3). Revisions: 1) Model system: in addition to snapdragon (Antirrhinum majus L.) spikes and oat (Avena sativa) shoot pulvini, the model system of maize (Zea mays) primary roots was targeted to confirm a more general mechanism for graviperception. 2) Research topic: brassinolide, which were not included in the original plan, were examined for their regulatory role in gravity perception and signal transduction in roots, in relation to auxin and ethylene. Background to the topic: The negative gravitropic response of shoots is a complex multi-step process that requires the participation of various cellular components acting in succession or in parallel. Most of the long-lasting studies regarding the link between graviperception and cellular components were focused mainly on roots, and there are relatively few reports on shoot graviperception. Our previous project has successfully characterized several key events occurring during shoot bending of cut flowers and oat pulvini, including amyloplast displacement, hormonal interactions and differential growth analysis. Based on this evidence, the present project has focused on studying the initial graviperception process in flowering stems and cereal shoots. Major conclusions and achievements: 1) The actin and not the microtubule (MT) CK is involved in the graviperception of snapdragon shoots. 2) Gravisensing, exhibited by amyloplast displacement, and early transduction events (auxin redistribution) in the gravitropic response of snapdragon spikes are mediated by the acto-myosin complex. 3) MTs are involved in stem directional growth, which occurs during gravitropism of cut snapdragon spikes, but they are not necessary for the gravity-induced differential growth. 4) The role of amyloplasts as gravisensors in the shoot endodermis was demonstrated for both plant systems. 5) A gravity-induced increase in IP.
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Sadot, Einat, Christopher Staiger, and Mohamad Abu-Abied. Studies of Novel Cytoskeletal Regulatory Proteins that are Involved in Abiotic Stress Signaling. United States Department of Agriculture, September 2011. http://dx.doi.org/10.32747/2011.7592652.bard.

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In the original proposal we planned to focus on two proteins related to the actin cytoskeleton: TCH2, a touch-induced calmodulin-like protein which was found by us to interact with the IQ domain of myosin VIII, ATM1; and ERD10, a dehydrin which was found to associate with actin filaments. As reported previously, no other dehydrins were found to interact with actin filaments. In addition so far we were unsuccessful in confirming the interaction of TCH2 with myosin VIII using other methods. In addition, no other myosin light chain candidates were found in a yeast two hybrid survey. Nevertheless we have made a significant progress in our studies of the role of myosins in plant cells. Plant myosins have been implicated in various cellular activities, such as cytoplasmic streaming (1, 2), plasmodesmata function (3-5), organelle movement (6-10), cytokinesis (4, 11, 12), endocytosis (4, 5, 13-15) and targeted RNA transport (16). Plant myosins belong to two main groups of unconventional myosins: myosin XI and myosin VIII, both closely related to myosin V (17-19). The Arabidopsis myosin family contains 17 members: 13 myosin XI and four myosin VIII (19, 20). The data obtained from our research of myosins was published in two papers acknowledging BARD funding. To address whether specific myosins are involved with the motility of specific organelles, we cloned the cDNAs from neck to tail of all 17 Arabidopsis myosins. These were fused to GFP and used as dominant negative mutants that interact with their cargo but are unable to walk along actin filaments. Therefore arrested organelle movement in the presence of such a construct shows that a particular myosin is involved with the movement of that particular organelle. While no mutually exclusive connections between specific myosins and organelles were found, based on overexpression of dominant negative tail constructs, a group of six myosins (XIC, XIE, XIK, XI-I, MYA1 and MYA2) were found to be more important for the motility of Golgi bodies and mitochondria in Nicotiana benthamiana and Nicotiana tabacum (8). Further deep and thorough analysis of myosin XIK revealed a potential regulation by head and tail interaction (Avisar et al., 2011). A similar regulatory mechanism has been reported for animal myosin V and VIIa (21, 22). In was shown that myosin V in the inhibited state is in a folded conformation such that the tail domain interacts with the head domain, inhibiting its ATPase and actinbinding activities. Cargo binding, high Ca2+, and/or phosphorylation may reduce the interaction between the head and tail domains, thus restoring its activity (23). Our collaborative work focuses on the characterization of the head tail interaction of myosin XIK. For this purpose the Israeli group built yeast expression vectors encoding the myosin XIK head. In addition, GST fusions of the wild-type tail as well as a tail mutated in the amino acids that mediate head to tail interaction. These were sent to the US group who is working on the isolation of recombinant proteins and performing the in vitro assays. While stress signals involve changes in Ca2+ levels in plants cells, the cytoplasmic streaming is sensitive to Ca2+. Therefore plant myosin activity is possibly regulated by stress. This finding is directly related to the goal of the original proposal.
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10

O'Neill, Sharman, Abraham Halevy, and Amihud Borochov. Molecular Genetic Analysis of Pollination-Induced Senescence in Phalaenopsis Orchids. United States Department of Agriculture, 1991. http://dx.doi.org/10.32747/1991.7612837.bard.

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The project investigated the molecular genetic and biochemical basis of pollination-induced senescence of Phalaenopsis flowers. This experimental system offered unique advantages in that senescence is strictly regulated by pollination, providing the basis to experimentally initiate and synchronize senescence in populations of flowers. The postpollination syndrome in the Phalaenopsis orchid system was dissected by investigating the temporal and spatial regulation of ACC synthase gene expression. In the stigma, pollen-borne auxin induces the expression of the auxin-regulated ACC synthase (PS-ACS2) gene, resulting in ACC synthesis within 1 h following pollination. Newly formed ACC is oxidized by basal constitutive ACC oxidase to ethylene, which then induces the expression of the ethylene-regulated ACC synthase(PS-ACS1) and oxidase (ACO1) genes for further autocatalytic production of ethylene. It is speculated that during the 6-h period following pollination, emasculation leads to the production or release of a sensitivity factor that sensitizes the cells of the stigma to ethylene. ACC and ethylene molecules are translocated from the stigma to the labellum and perianth where ethylene induces the expression of PS-ACS1 and ACO1 resulting in an increased production of ACC and ethylene. Organ-localized ethylene is responsible for inrolling and senescence of the labellum and perianth. The regulation of ethylene sensitivity and signal transduction events in pollinated flowers was also investigated. The increase in ethylene sensitivity appeared in both the flower column and the perianth, and was detected as early as 4 h after pollination. The increase in ethylene sensitivity following pollination was not dependent on endogenous ethylene production. Application of linoleic and linoleic acids to Phalaenopsis and Dendrobium flowers enhanced their senescence and promoted ethylene production. Several major lipoxygenase pathway products including JA-ME, traumatic acid, trans-2-hexenal and cis-3-hexenol, also enhanced flower senescence. However, lipoxygenase appears to not be directly involved in the endogenous regulation of pollination-induced Phalaenopsis and Dendrobium flower senescence. The data suggest that short-chain saturated fatty acids may be the ethylene "sensitivity factors" produced following pollination, and that their mode of action involves a decrease in the order of specific regions i the membrane lipid bilayer, consequently altering ethylene action. Examination of potential signal transduction intermediates indicate a direct involvement of GTP-binding proteins, calcium ions and protein phosphorylation in the cellular signal transduction response to ethylene following pollination. Modulations of cytosolic calcium levels allowed us to modify the flowers responsiveness to ethylene.
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