Relevant bibliographies by topics / Intracellular signal transduction

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Intracellular signal transduction'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Intracellular signal transduction"

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Beeram, Muralidhar, and Amita Patnaik. "Targeting intracellular signal transduction." Hematology/Oncology Clinics of North America 16, no. 5 (October 2002): 1089–100. http://dx.doi.org/10.1016/s0889-8588(02)00054-0.

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Burrow, G. N., and M. Eggo. "Signal transduction and intracellular chatter." Endocrinology 135, no. 2 (August 1994): 491–92. http://dx.doi.org/10.1210/endo.135.2.8033798.

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Hurtley, S. M. "CELL BIOLOGY: Intracellular Signal Transduction." Science 296, no. 5567 (April 19, 2002): 433a—433. http://dx.doi.org/10.1126/science.296.5567.433a.

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Kobayashi, T., M. Murakami, T. Kawasaki, A. Yoshimura, and A. Kusumi. "S2L1 Single molecule analysis of intracellular signal transduction in living cells." Seibutsu Butsuri 42, supplement2 (2002): S11. http://dx.doi.org/10.2142/biophys.42.s11_1.

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Hidaka, Hiroyoshi. "Intracellular Signal Transduction and Cell Function." membrane 21, no. 1 (1996): 9–17. http://dx.doi.org/10.5360/membrane.21.9.

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SODEOKA, Mikiko. "Development of Intracellular Signal Transduction Modulators." Journal of the agricultural chemical society of Japan 78, no. 12 (2004): 1156a—1157. http://dx.doi.org/10.1271/nogeikagaku1924.78.1156a.

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Saito, Hideaki, Woodae Kang, and Shigeo Ikeda. "Nutrition and phagocyte intracellular signal transduction." International Congress Series 1255 (August 2003): 61–64. http://dx.doi.org/10.1016/s0531-5131(03)00653-8.

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Louie, Dexter S. "Cholecystokinin-Stimulated Intracellular Signal Transduction Pathways." Journal of Nutrition 124, suppl_8 (August 1, 1994): 1315S—1320S. http://dx.doi.org/10.1093/jn/124.suppl_8.1315s.

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Müller, Werner E. G., Durdica Ugarković, Vera Gamulin, Barbara E. Weiler, and Heinz C. Schröder. "Intracellular signal transduction pathways in sponges." Electron Microscopy Reviews 3, no. 1 (January 1990): 97–114. http://dx.doi.org/10.1016/0892-0354(90)90016-l.

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Klesse, Laura J., and Luis F. Parada. "Trks: Signal transduction and intracellular pathways." Microscopy Research and Technique 45, no. 4-5 (May 15, 1999): 210–16. http://dx.doi.org/10.1002/(sici)1097-0029(19990515/01)45:4/5<210::aid-jemt4>3.0.co;2-f.

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Dissertations / Theses on the topic "Intracellular signal transduction"

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McKay, Jodi Ho-Jung. "HRas intracellular trafficking and signal transduction." [Ames, Iowa : Iowa State University], 2007.

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Legewie, Stefan. "Systems biological analyses of intracellular signal transduction." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/16018.

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An der Interpretation extrazellulärer Signale beteiligte Regulationsnetzwerke sind von zentraler Bedeutung für alle Organismen. Extrazelluläre Signale werden gewöhnlich durch enzymatische Kaskaden innerhalb weniger Minuten in den Zellkern weitergeleitet, wo sie langsame Änderungen der Genexpression bewirken und so das Schicksal der Zelle beeinflussen. Im ersten Teil der Arbeit wird durch mathematische Modellierung untersucht, wie die MAPK Kaskade Signale von der Zellmembran in den Kern weiterleitet. Es wurden Netzwerkeigenschaften herausgearbeitet, die verhindern, dass die MAPK Kaskade fälschlicherweise durch genetische Mutationen aktiviert wird. Desweiteren wurde eine versteckte positive Rückkopplungsschleife identifiziert, welche die Aktivierung der MAPK Kaskade oberhalb eines gewissen Schwellwert-Stimulus verstärkt. Der zweite Teil der Arbeit konzentriert sich darauf, wie Änderungen der Genexpression auf langsamer Zeitskala in das Signalnetzwerk rückkoppeln. Eine systematische Genexpressionsdaten-Analyse ergab, dass transkriptionelle Rückkopplung in Eukaryoten generell über Induktion kurzlebiger Signalinhibitoren geschieht. Dynamische Modellierung und experimentelle Validierung von Modellvorhersagen ergab, dass das Inhibitorprotein SnoN als zentraler negativer Feedback Regulator im TGFbeta Signalweg fungiert. Der dritte Teil der Arbeit untersucht, wie die Genexpressionsmaschinerie intrazelluläre Signale interpretiert (“dekodiert“). Eine experimentelle und theoretische Analyse der cyanobakteriellen Eisenstress-Antwort ergab, dass IsrR, eine kleine regulatorische RNA, die Genexpression auf ausreichend starke und lange Stimulation beschränkt. Des Weiteren wurde ein “Reverse Engineering“-Algorithmus auf Hochdurchsatz-RNAi-Daten angewendet, um die Topologie eines krebsrelevanten Transkriptionsfaktornetzwerks abzuleiten. Zusammenfassend wurde in dieser Dissertation gezeigt, wie mathematische Modellierung die experimentelle Analyse biologischer Systeme unterstützen kann.
Intracellular regulatory networks involved in sensing extracellular cues are crucial to all living organisms. Extracellular signals are rapidly transmitted from the cell membrane to the nucleus by activation of enzymatic cascades which ultimately elicit slow changes in gene expression, and thereby affect the cell fate. In the first part of this thesis, the Ras-MAPK cascade transducing signals from the cell membrane to the nucleus is analyzed using mathematical modeling. Model analysis reveals network properties which prevent the MAPK cascade from being inappropriately activated by mutations. Moreover, the simulations unveil a hidden positive feedback loop which ensures strong amplification of MAPK signalling once extracellular stimulation exceeds a certain threshold. The second part of the thesis focuses on how slow gene expression responses feed back into the upstream signalling network. A systematic analysis of gene expression data gathered in mammalian cells demonstrates that such transcriptional feedback generally involves induction of highly unstable signalling inhibitors, thereby establishing negative feedback regulation. Dynamic data-based modelling identifies the SnoN oncoprotein as the central negative feedback regulator in the TGFbeta signalling pathway, and corresponding model predictions are verified experimentally in SnoN-depleted cells. The third part of the thesis focuses on how intracellular signals are decoded by the downstream gene expression machinery. A combined experimental and theoretical analysis of the cyanobacterial iron stress response reveals that small non-coding RNAs allow cells to selectively respond to sufficiently strong and sustained stimuli. Finally, a reverse engineering approach is applied to derive the topology of a complex mammalian transcription factor network from high-throughput knock-down data. In conclusion, this thesis demonstrates how mathematical modelling can support experimental analysis of biological systems.
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Bottomley, Matthew James. "Biophysical studies of intracellular signal transduction proteins : investigating the structure-function relationship." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286570.

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Hao, Baixia, and 郝佰侠. "Regulatory and functional studies of store-operated calcium entry." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196486.

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Ca2+ signaling is essential for a wide variety of cellular activities, ranging from short term activities, such as synaptic and muscle contraction, to long term processes, such as proliferation and differentiation. Store-operated Ca2+ entry (SOCE), an important Ca2+ influx pathway in non-excitable cells, well coordinates Ca2+ release from ER and Ca2+ influx through plasma membrane. STIM1 and Orai1, serving as ER Ca2+ sensor and pore forming subunit, respectively, are the two essential components of SOCE machinery. In addition to activate Orai1 channel, studies have shown that STIM1 regulates other plasma membrane Ca2+ channels and senses a variety of cellular stresses to regulate SOCE. Therefore, it is of great interests to investigate the mechanisms and physiological functions of STIM1 and Orai1 mediated SOCE. Here, we performed tandem affinity purification to identify STIM1 associated proteins in Hela cells stably expressing STIM1-His6-3×Flag. Four candidate proteins, including GRP78, HSP70, IQGAP1, and Actin, were identified by mass spectrometry analyses. Surprisingly, IQGAP1 failed to affect the activity of SOCE. Interestingly, GRP78 knockdown only affected the inactivation phase while exerted no effect on the activation phase of SOCE. In addition, GRP78 knockdown markedly induced cell apoptosis and dramatically increased the ER Ca2+ concentration. Moreover, GRP78 was involved in the regulation of SOCE by the ER stress. These data indicate that GRP78 is an important regulator of SOCE to prevent Ca2+ overload in cells. HSP70, however, significantly reduced the activity of SOCE by inhibiting STIM1 translocation to ER-PM junctions. Future studies will explore the mechanism of GRP78 and HSP70 in regulating SOCE by confocal and TIRF imaging. Embryonic stem (ES) cells proliferate unlimitedly and can differentiate into all fetal and adult cell types. This property endows ES cells to be the promising candidates in the therapy of neurodegenerative diseases. Thus, it is important to identify novel signaling molecules or events that could play a role in the neural commitment of ES cells. Accumulated evidences have documented the role of STIM1 and Orai1 mediated SOCE in neuronal activities. Yet, the role of SOCE in early neural development remains to be determined. Here we examined the role of STIM1 and Orai1 during neural differentiation of mouse ES cells. Both of STIM1 and Orai1 were expressed and functionally active in ES cells, and expressions of STIM1 and Orai1 were dynamically regulated during neural differentiation of mouse ES cells. STIM1 knockdown inhibited the differentiation of mouse ES cells into neural progenitors, neurons, and astrocytes. In addition, STIM1 knockdown caused severe cell death and markedly suppressed the proliferation of neural progenitors. Surprisingly, Orai1 knockdown had little effect on neural differentiation of mouse ES cells, but the neurons derived from Orai1 knockdown ES cells, like those from STIM1 knockdown cells, had defective SOCE. Taken together, our data indicate that STIM1 is required for neural differentiation of mouse ES cells independent of Orai1-mediated SOCE.
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Kemp, Daniel M. "Reporter gene analysis of regulatory mechanisms in cAMP signalling." Thesis, University of Kent, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310202.

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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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Kawano, Yuichi. "Effect of hyperglycemia on glucose transport and intracellular signal transduction in skeletal muscle /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3593-9/.

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劉思恩 and See-yan Lau. "A study of intracellular signals of K-opioids in non-neuronal cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31214290.

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Sadreev, Ildar. "Mathematical modelling of inter- and intracellular signal transduction : the regulatory role of multisite interactions." Thesis, University of Exeter, 2015. http://hdl.handle.net/10871/21212.

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Signalling processes regulate various aspects of living cells via modulation of protein activity. The interactions between the signalling proteins can occur at single or multiple sites. Although single site protein interactions are relatively easy to understand, these rarely occur in living systems. It is therefore important to investigate multisite interactions. Despite the recent progress in experimental studies, the underlying molecular mechanisms and molecular functions of the multisite interactions are still not clear and therefore require systems approaches for deeper understanding, for example to understand how the system will react to perturbation of one of its components. The examples of the molecular functions that are studied in this thesis are: kinetics of multisite calcium binding to proteins such as calmodulin (CaM), multisite phosphorylation of interferon regulatory factor 5 (IRF-5) and signal transducers and activators of transcription (STATs). We also study the role of STATs in the overall immune response and in T cell phenotype switching as well as multisite phosphorylation of high osmolarity glycerol factor 1 (Hog1) in mitogen activated protein kinase (MAPK) cascade during the adaptation of Candida glabrata to osmotic stress. In this thesis, these examples are studied using the systems approach in the context of human diseases: cancer, candidiasis, immunity-related pathologies such as rheumatoid arthritis, inflammatory bowel disease and systemic lupus erythematosus. We discuss potential therapeutic implications of the proposed models in these diseases. The predictions of the models developed in this thesis are supported by the experimental data and propose possible mechanisms of the multisite interactions involved in the cellular regulation.
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Li, Sen, and 李森. "Intracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46940546.

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Books on the topic "Intracellular signal transduction"

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W, Taylor Colin, ed. Intracellular messengers. Oxford: Pergamon Press, 1993.

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1961-, Yang Zhenbiao, ed. Intracellular signaling in plants. Oxford: Wiley-Blackwell Pub., 2008.

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Wilks, Andrew F., and Ailsa G. Harpur. Intracellular Signal Transduction: The JAK-STAT Pathway. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.

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Wilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. New York: Springer, 1996.

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1961-, Yang Zhenbiao, ed. Intracellular signaling in plants. Oxford, UK: Blackwell Pub., 2008.

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B, Hoek Jan, and National Institute on Alcohol Abuse and Alcoholism (U.S.), eds. Ethanol and intracellular signaling: From molecules to behavior. Bethesda, MD (6000 Executive Blvd., Bethesda 20892): U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism, 2000.

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Intracellular parasitism of microorganisms. New York: Springer, 1996.

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Hoek, Jan B. Ethanol and intracellular signaling: From molecules to behavior. Bethesda, MD (6000 Executive Boulevard, Bethesda, 20892): U.S. Department of Health and Human Services, Public Health Service, National Institute of Health, National Institute on Alcohol Abuse and Alcoholism, 2000.

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R, Nahorski S., ed. Transmembrane signalling, intracellular messengers, and implications for drug development. Chichester: Wiley, 1990.

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Karin, Müller-Decker, and Klingmüller Ursula, eds. Cellular signal processing. New York, NY: Garland Science, 2009.

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Book chapters on the topic "Intracellular signal transduction"

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Wilks, Andrew F., and Ailsa G. Harpur. "Intracellular Signal Transduction." In Intracellular Signal Transduction: The JAK-STAT Pathway, 1–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4_1.

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Fasolato, C., M. Zottini, P. Chiozzi, S. Treves, A. Villa, E. Clementi, J. Meldolesi, and T. Pozzan. "Intracellular Ca2+ Homeostasis: Receptor-Activated Ca2+ Channels and Intracellular Ca2+ Pools." In Biological Signal Transduction, 403–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75136-3_29.

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Mithöfer, Axel, Christian Mazars, and Massimo E. Maffei. "Probing Spatio-temporal Intracellular Calcium Variations in Plants." In Plant Signal Transduction, 79–92. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-289-2_5.

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Reith, Maarten E. A. "Intracellular Messengers in Drug Addiction." In Introduction to Cellular Signal Transduction, 287–304. Boston, MA: Birkhäuser Boston, 1999. http://dx.doi.org/10.1007/978-1-4612-1990-3_12.

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Garvin, Jeffrey L. "Nitric Oxide: Synthesis and Intracellular Actions." In Introduction to Cellular Signal Transduction, 177–212. Boston, MA: Birkhäuser Boston, 1999. http://dx.doi.org/10.1007/978-1-4612-1990-3_8.

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Ravesloot, Jan H. "Strategies for Studying Intracellular pH Regulation." In Signal Transduction — Single Cell Techniques, 318–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80368-0_24.

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Silveira, Neidiquele Maria, Eduardo Caruso Machado, and Rafael Vasconcelos Ribeiro. "Extracellular and Intracellular NO Detection in Plants by Diaminofluoresceins." In Redox-Mediated Signal Transduction, 103–8. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9463-2_9.

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Hoek, Jan B., and Emanuel Rubin. "Intracellular signal transduction in liver regeneration." In Liver Growth and Repair, 366–401. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4932-7_14.

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Schäfer, Eberhard, Stefan Kircher, Patricia Gil, Klaus Harter, Lana Kim, Frank Wellmer, Lazlo Kozma-Bognar, Eva Adam, and Ferenc Nagy. "Signal Transduction in Photomorphogenesis: Intracellular Partitioning of Factors and Photoreceptors." In Signal Transduction in Plants, 19–24. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1365-0_3.

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Belyi, Yuri F. "General Comments on Signal Transduction in Eukaryotic Cells." In Intracellular Parasitism of Microorganisms, 101–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22047-4_10.

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Conference papers on the topic "Intracellular signal transduction"

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Ishiyama, Hiroki, Takashi Nakakuki, Chiharu Ishii, and Mitsuo Kobayashi. "Frequency analysis of intracellular signal transduction systems." In 2010 International Conference on Control, Automation and Systems (ICCAS 2010). IEEE, 2010. http://dx.doi.org/10.1109/iccas.2010.5669745.

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Jinghua Gu, Chen Wang, Le-Ming Shih, Tian-Li Wang, Yue Wang, R. Clarke, and Jianhua Xuan. "GIST: A Gibbs sampler to identify intracellular signal transduction pathways." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090677.

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Bartholome, Kilian, Jens Timmer, and Markus Kollmann. "Design principles of signal transduction pathways to compensate intracellular perturbations." In 2006 IEEE Conference on Computer Aided Control System Design, 2006 IEEE International Conference on Control Applications, 2006 IEEE International Symposium on Intelligent Control. IEEE, 2006. http://dx.doi.org/10.1109/cacsd-cca-isic.2006.4776902.

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Bartholome, Kilian, Jens Timmer, and Markus Kollmann. "Design Principles of Signal Transduction Pathways to compensate Intracellular Perturbations." In 2006 IEEE International Conference on Control Applications. IEEE, 2006. http://dx.doi.org/10.1109/cca.2006.286134.

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Agarwal, Rakhee, Junaid Khan, Bozena Laska, Rahul Mehta, Parimal Chowdhury, Nawab Ali, and Olga Tarasenko. "ALTERATIONS IN SIGNAL TRANSDUCTION AND INTRACELLULAR SIGNALING PROCESSES DURING SIMULATED MICROGRAVITY." In BIOLOGY, NANOTECHNOLOGY, TOXICOLOGY AND APPLICATIONS: 4th BioNanoTox (Biology, Nanotechnology, Toxicology) and Applications. AIP, 2010. http://dx.doi.org/10.1063/1.3419702.

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Wu, Chia-Chou, and Bor-Sen Chen. "Signal transduction ability measurement of signaling pathways in intracellular communication via fuzzy method." In 2011 IEEE International Conference on Fuzzy Systems (FUZZ-IEEE). IEEE, 2011. http://dx.doi.org/10.1109/fuzzy.2011.6007659.

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Mir, T. A., and H. Shinohara. "2D-SPR biosensor detects the intracellular signal transduction in PC 12 cells at single cell level." In 2012 Sixth International Conference on Sensing Technology (ICST 2012). IEEE, 2012. http://dx.doi.org/10.1109/icsenst.2012.6461763.

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de Chaffov de Courcelles, D., F. De Clerck, and P. Roevens. "EVALUATION OF THE PROPOSED FUNCTIONS OF PROTEIN KINASE C IN PLATELET SIGNAL TRANSDUCTION BY THE USE OF A DIACYLGLYCEROL KINASE INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644632.

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Protein kinase C is suggested to play a major role in propagation as well as in termination of excitatory signal transduction in the platelet. Most of its properties were discovered by the use of synthetic diacylglycerol analogs or phorbol esters that directly stimulate protein kinase C. It is, however, unknown to what extent activation of the protein kinase C by these exogenously added compounds can be compared to that after receptor activation. To evaluate the role of protein kinase C in excitatory signal transduction, we transiently elevated the endogenous diacylglycerol level after receptor activation by the use of a diacylglycerol kinase inhibitor (R 59 949). On addition of the agonist vasopressin to platelets prelabeled with [32P] orthophosphate, 32P-phosphatidic acid (PA) formation was inhibited by R 59 949 in a dose-dependent manner (IC50 α 10−6 M). Vasopressin induced formation of 32P-phosphatidylinositol-4’-phosphate (PIP) and the phosphorylation of the 40 k Da protein (major substrate of the protein kinase C) were increased in the presence of the compound. In platelets prelabeled with [3H]-inositol, the agonist-induced formation of all the water-soluble inositol phosphates was inhibited in the presence of the diacylglycerol kinase inhibitor and Li+. Vasopressin induced increase in intracellular Ca2+ was lower in the presence of R 59 949. The platelet shape change induced by a threshold concentration of vasopressin was reduced by the compound. By contrast, the rate and the maximum of the first-wave aggregation was enhanced in the presence of R 59 949.These data evidence that protein kinase C, stimulated by endogenously generated diacylglycerol after receptor activation, plays a major inhibitory role on the primary steps of signal transduction since its activation reduces i) phospholipase C activity and ii) the increase in intracellular Ca2+ and the concomitant shape change reaction. The inhibitory role of protein kinase C on signal transduction is largely independent of its stimulatory role on platelet aggregation. Our data further confirm that stimulation of protein kinase C induces the formation of PIP but questions the role of the kinase in the breakdown process of inositoltrisphosphate.
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Zibaii, M. I., H. Latifi, A. Asadollahi, Z. Noraeipoor, and L. Dargahi. "Real-time monitoring of intracellular signal transduction in PC12 cells by non-adiabatic tapered optical fiber biosensor." In OFS2014 23rd International Conference on Optical Fiber Sensors, edited by José M. López-Higuera, Julian D. C. Jones, Manuel López-Amo, and José L. Santos. SPIE, 2014. http://dx.doi.org/10.1117/12.2058939.

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Fakhroo, Aisha, Fatma Ali, Gheyath K. Nasrallah, Nico Marr, and Hadi Mohamad Yassine. "Detection of antinuclear antibodies targeting intracellular signal transduction, metabolism, apoptotic processes and cell death in critical COVID-19 patients." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0095.

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Background: The heterogeneity of COVID-19 lies within its diverse symptoms and severity, ranging from mild to lethal. Acute respiratory distress syndrome (ARDS) has been shown to be the leading cause of mortality in COVID-19 patients, characterized by a hyper cytokine storm. Autoimmunity is proposed to occur as a result of COVID-19, given the high similarity of the immune responses observed in COVID-19 and autoimmune diseases. Results: Here, we investigate the level of autoimmune antibodies in COVID-19 patients with different severities. Initial screening for antinuclear antibodies (ANA) IgG revealed that 1.6% (2/126) and 4% (5/126) of ICU COVID-19 cases developed strong and moderate ANA levels, respectively. However, all the non-ICU cases (n = 273) were ANA negative. The high ANA level was confirmed by immunofluorescence (IFA) and large-scale autoantibody screening by phage immunoprecipitation-sequencing (PhIP-Seq). Indeed, the majority of the samples showed "speckled" ANA pattern by microscopy, and we demonstrate that samples of ICU patients with strong and moderate ANA levels contain autoantibody specificities that predominantly targeted proteins involved in intracellular signal transduction, metabolism, apoptotic processes, and cell death; further denoting reactivity to nuclear and cytoplasmic antigens. Conclusion:Our results further support the notion of routine screening for autoimmune responses in COVID-19 patients, which might help improve disease prognosis and patient management. Further, results provide compelling evidence that ANA-positive individuals should be excluded from being donors for convalescent plasma therapy in the context of Covid-19.
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Reports on the topic "Intracellular signal transduction"

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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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2

Bazer, Fuller W., Arieh Gertler, and Elisha Gootwine. Role of Placental Lactogen in Sheep. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7574339.bard.

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Central problems in sheep and dairy cattle production are reproductive failure due to embryonic/fetal mortality and low birth weights, especially in prolific breeds, and reduced milk yields which adversely affect neonatal survival and economy of production. The sheep placenta expresses lactogenic (ovine placental lactogen, oPL) and somatogenic (ovine placental growth hormone, oGH) hormones. Our research has focused on the biological roles of oPL and oGH in function of the uterine endometrium during gestation and the mammary gland during pregnancy and lactation. Major conclusions were that: ( 1 ) immunization of prepubertal ewes against oPL resulted in increased birth weights of their lambs and their milk production during lactation; (2) neither oPL nor oGH had an antiluteolytic effect on uterine endometrium to affect lifespan of the corpus luteum; (3) only sequential exposure of the progesterone stimulated uterus to oIFNt and oPL or oGH increased endometrial gland proliferation and secretory protein gene expression; (4) oPL signals through a homodimer of ovine prolactin receptor (PRL-R) and heterodimer of oPRL-R and growth hormone receptor (GH-R); (5) exogenous recombinant oPL and oGH stimulated mammogenesis and milk yield during lactation; and (6) mutation of oPL and oGH was used to define specific biological effects and a rational basis for design of a specific receptor agonists or antagonists. This project was very productive in elucidating basic biological effects of oPL and oGH on intracellular signal transduction pathways, uterine development and secretory function, as well as mammogenesis and lactogenesis. We determined that immunization of prepubertal ewes against roPL increased birth weights of their lambs, especially those born as twins and triplets, as well as enhanced lactational performance. These studies significantly extended our knowledge of uterine and fetal-placental physiology and provided a foundation for new strategies to enhance reproductive and lactation efficiency. Based on these results, the major achievements were: 1) creation of a practical and cost effective management tool for producers to increase reproductive performance, neonatal survival, and milk yield of ewes in commercial flocks; and 2) define, for the first time, biological effects of oPL on endometrial functions and gene expression by uterine gland epithelium.
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