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Academic literature on the topic 'Intracellular signals'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Intracellular signals"

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Imboden, J. B., and G. A. Koretsky. "Intracellular Signalling: Switching off signals." Current Biology 5, no. 7 (July 1995): 727–29. http://dx.doi.org/10.1016/s0960-9822(95)00145-x.

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Kalaidzidis, Yannis, Hernán Morales-Navarrete, Inna Kalaidzidis, and Marino Zerial. "Intracellular Background Estimation for Quantitative Fluorescence Microscopy." Proceedings 33, no. 1 (December 6, 2019): 22. http://dx.doi.org/10.3390/proceedings2019033022.

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Fluorescently targeted proteins are widely used for studies of intracellular organelles dynamic. Peripheral proteins are transiently associated with organelles and a significant fraction of them are located at the cytosol. Image analysis of peripheral proteins poses a problem on properly discriminating membrane-associated signal from the cytosolic one. In most cases, signals from organelles are compact in comparison with diffuse signal from cytosol. Commonly used methods for background estimation depend on the assumption that background and foreground signals are separable by spatial frequency filters. However, large non-stained organelles (e.g., nuclei) result in abrupt changes in the cytosol intensity and lead to errors in the background estimation. Such mistakes result in artifacts in the reconstructed foreground signal. We developed a new algorithm that estimates background intensity in fluorescence microscopy images and does not produce artifacts on the borders of nuclei.
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IKATAYAMA, Yoshiki. "Polymer Drugs Responding to Intracellular Signals." Kobunshi 55, no. 5 (2006): 326–29. http://dx.doi.org/10.1295/kobunshi.55.326.

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Song, Jianxun, Fengyang Tylan Lei, Xiaofang Xiong, and Rizwanul Haque. "Intracellular Signals of T Cell Costimulation." Cellular & Molecular Immunology 5, no. 4 (August 2008): 239–47. http://dx.doi.org/10.1038/cmi.2008.30.

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Cao, Y., A. T. Pearman, G. A. Zimmerman, T. M. McIntyre, and S. M. Prescott. "Intracellular unesterified arachidonic acid signals apoptosis." Proceedings of the National Academy of Sciences 97, no. 21 (September 26, 2000): 11280–85. http://dx.doi.org/10.1073/pnas.200367597.

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Konieczny, Vera, Michael V. Keebler, and Colin W. Taylor. "Spatial organization of intracellular Ca2+ signals." Seminars in Cell & Developmental Biology 23, no. 2 (April 2012): 172–80. http://dx.doi.org/10.1016/j.semcdb.2011.09.006.

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Rüdiger, Sten. "Stochastic models of intracellular calcium signals." Physics Reports 534, no. 2 (January 2014): 39–87. http://dx.doi.org/10.1016/j.physrep.2013.09.002.

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Seuwen, Klaus, and Jaques Pouysségur. "Intracellular signals in the mitogenic response." Fresenius' Zeitschrift für analytische Chemie 330, no. 4-5 (January 1988): 308–9. http://dx.doi.org/10.1007/bf00469223.

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Ramseyer, Lorenz T. H., Janet Barker-Harrel, David J. Smith, Kari A. McBride, Robert N. Jarman, and Robert H. Broyles. "Intracellular signals for developmental hemoglobin switching." Developmental Biology 133, no. 1 (May 1989): 262–71. http://dx.doi.org/10.1016/0012-1606(89)90317-5.

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Gruol, D. L., J. G. Netzeband, and K. L. Parsons. "Ca2+ signaling pathways linked to glutamate receptor activation in the somatic and dendritic regions of cultured cerebellar purkinje neurons." Journal of Neurophysiology 76, no. 5 (November 1, 1996): 3325–40. http://dx.doi.org/10.1152/jn.1996.76.5.3325.

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1. Ca2+ signaling elicited by ionotropic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate (iGluR) and metabotropic (mGluR) glutamate receptor agonists was studied in the somatic and dendritic regions of cultured cerebellar Purkinje neurons using microscopic video imaging and the Ca2+ sensitive dye fura-2. 2. iGluR and mGluR agonists and K+ depolarization applied by brief micropressure pulses evoked Ca2+ signals in both the somatic and dendritic regions of all Purkinje neurons studied. The Ca2+ signals were generated simultaneously in both cellular regions. The Ca+ signals to these stimulants were similar in general form, consisting of an initial peak and slow recovery phase, but differed in details of amplitude, time course, and complexity. 3. Removal of extracellular Ca2+ abolished the Ca2+ signal to the iGluR agonist AMPA, indicating that Ca2+ influx was essential to the generation of Ca2+ signals by iGluR agonists. The Ca2+ channel blocker lanthanum almost completely eliminated the Ca2+ signals to AMPA, indicating that Ca2+ influx through voltage-sensitive Ca2+ channels was the main pathway for Ca2+ influx. Omega-agatoxin IVA, a P-type Ca2+ channel blocker, significantly reduced the Ca2+ signals to AMPA suggesting that Ca2+ influx was predominately through P-type Ca2+ channels. 4. Pharmacological manipulation of intracellular Ca2+ stores significantly reduced the Ca2+ signals to AMPA, indicating that release of Ca2+ from intracellular Ca2+ stores also plays a prominent role in the generation of the Ca2+ signals to iGluR agonists. These manipulations included blocking Ca2+ release from intracellular stores with dantrolene, an antagonist at the ryanodine receptor that controls Ca2+ release from one pool of intracellular Ca2+ stores, and depletion of intracellular Ca2+ stores with caffeine or ryanodine. 5. Ca2+ influx through voltage-sensitive Ca2+ channels did not appear to be involved in the Ca2+ signals to mGluR activation, because neither lanthanum nor omega-agatoxin IVA altered Ca2+ signals to mGluR agonists. Manipulation of intracellular stores with Ca(2+)-ATPase inhibitors and dantrolene significantly reduced the Ca2+ signal to mGluR agonists, indicating that Ca2+ signals were derived from both the inositol trisphosphate (IP3) and the ryanodine receptor-controlled intracellular Ca2+ stores. 6. Ca2+ signals to the iGluR agonist AMPA correlated temporally with the prolonged, multiphasic membrane responses elicited by similar agonist application in parallel electrophysiological studies. Pharmacological manipulation of Ca2+ influx and release of Ca2+ from intracellular stores significantly influenced components of the membrane response to AMPA, indicating a potential modulator or mediator role for Ca2+ in the membrane response to iGluR activation.
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Dissertations / Theses on the topic "Intracellular signals"

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Nair, Prashant. "Signals involved in protein intracellular sorting /." Basel : [s.n.], 2005. http://edoc.unibas.ch/diss/DissB_6999.

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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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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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Liu, Ke, University of Western Sydney, of Science Technology and Environment College, and of Science Food and Horticulture School. "Role of second messengers in controlling growth patterns of corneal epithelial cells." THESIS_CSTE_SFH_Liu_K.xml, 2002. http://handle.uws.edu.au:8081/1959.7/387.

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The purpose of this thesis was to investigate mechanisms contolling the growth of corneal epithelial cells, particularly the intracellular signals involved with stratification compared with cellular migration and maturation. Buttons of epithelium were cultured in different culture media. The explants were monitored microscopically for their growth patterns and finally fixed and examined for cytokeratin, vimentin and actin. Different growth patterns were observed in the different media, indicating that different signalling patterns must be operating in these cells depending upon the media in which they were grown. To investigate the intracellular pathways controlling the different growth patterns, the protein phosphorylation of different cultures was investigated. The two proteins, p57 and p30, are strongly suggested to be associated with stratification of the epithelial cells. The possible involvement of the common serine kinase, PKC, in controlling the growth pattern of corneal epithelial cells were also investigated. The results suggested that an intracellular pathway involving PKC promotes the maturation and spread of the cells but is not involved in their stratification. These experiments taken together indicate that the different aspects of corneal epithelia cell growth are tightly controlled and may occur quite independently. Specific protein expression appears to be important for stratification, and phosphorylation of proteins by PKC appears to be involved with the maturation of epithelial cells from basal cells. It also indicates that the mature cells are capable of producing the extracellular matrix protein fibronectin which appears to have an important role in causing the spread as distinct from the stratification of the corneal epithelial cells.
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Levings, Megan K. "Biological and biochemical analyses of the distinctive intracellular signals activated by interleukin-4." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0025/NQ38928.pdf.

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Raraty, Michael Gordon Thomas. "Cytosolic calcium signals and intracellular enzyme activation in the pathogenesis of acute pancreatitis." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250238.

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Bradley, J. "Analysis of the mechanisms responsible for the generation and decoding of intracellular calcium signals." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596849.

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In many cells, including hepatocytes, receptors coupled to phosphoinositide hydrolysis stimulate oscillatory changes in cytosolic [Ca2+] ([Ca2+]i). I have used two methods to examine the means whereby such [Ca2+]i transients are linked to the stimulation of glycogenolysis. By perifusing rat hepatocytes prelabelled with [3H]-glucose, I showed that phenylephrine increases the rate of [3H]-glucose release by 2-3 fold, and confirmed this effect using a colorimetric assay for glucose. When cultured hepatocytes were loaded with Fura-2 and incubated with thapsigargin in a Ca2+-free medium, restoration of external Ca2+ caused Ca2+ entry. Brief pulses (10s or 30s) of extracellular medium containing Ca2+ (5mM), produced [Ca2+]i transients comparable to those observed in single hepatocytes treated with Areg8-vasopressin (duration = 1.0 -1.5min). Using a similar protocol to manipulate [Ca2+]i in hepatocytes prelabelled with [3H]-glucose, I demonstrated that single [Ca2+]i transients stimulate a 2-fold increase in [3H]-glucose release (n=4). Moreover, stimulated glucose release outlasted the transient elevation of [Ca2+]i having a duration of 7.4 ± 0.6min (n=4). In conclusion, stimulation of glucose release by imposed transients of [Ca2+]i in a population of hepatocytes indicates that the discontinuous signal of [Ca2+]i transients can be decoded to produce a continuous response. Further characterisation of this decoding process requires single cell measurements of glucose and [Ca2+]i. Such measurements are not yet possible with the presently available techniques for enzyme immobilisation on glucose microbiosensors. Overexpression of type I and type III InsP3 receptors results in cell death, the mechanism of which requires further study. It is possible, however, to induce the expression of the type I InsP3 receptor and the effects of increasing InsP3 receptor level on elementary Ca2+ release events should provide insight into the mechanism by which [Ca2+]i waves are generated.
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Righetti, Karima Maria. "Study of Rsm/Gac post-transcriptional regulation by quorum sensing, extracellular and intracellular signals in Pseugomonas aeruginosa." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/13853/.

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Bacteria have evolved ways to sense and respond to changes in their population density through quorum sensing (QS) systems, and to adapt to changes in the extracellular environment through two component systems (TCS). In Pseudomonas aeruginosa, QS and the GacS/GacA TCS are global regulatory systems that modulate the expression of virulence genes at the transcriptional and post-transcriptional level, respectively. Although in P. aeruginosa the QS network has been extensively characterized, the way the Gac/Rsm global regulatory system is regulated is still unclear. The study of QS and Gac/Rsm networks is crucial for the development of new drugs able to interfere with these regulatory systems. This thesis is dedicated to the study of the Gac/Rsm global regulatory system and its interaction with the QS network. An introduction to these systems is presented in Chapter 1. The materials and methods used in this study are described in Chapter 2. In Chapter 3 the methods to detect and identify the extracellular signals modulating Gac/Rsm system are investigated. This analysis led to the identification of the Pseudomonas Quinolone Signal (PQS) molecule, which is responsible for the activation of the gene coding for the small RNA RsmZ. RsmZ (in synergy with RsmY) antagonises by titration the effects of the global post-transcriptional regulator RsmA, a small RNA-binding protein which targets specific mRNAs. Since the discovery of QS, there have been many studies showing the importance of this type of regulatory mechanism in the global transcriptional control of gene expression. However, there has been no clear evidence to attribute to QS a key role in post-transcriptional regulation of terminal gene targets. In Chapter 4, the importance of PQS in the control of lecA is demonstrated. lecA encodes for the PA-I galactophilic lectin protein whose translation rates is modulated by the activity of the regulatory small RNA rsmZ in concert with RsmA. These results demonstrate that QS not only controls terminal target gene expression at the transcriptional level, but also at the translational level. Using a genetic bank, a transposon mutagenesis and a promoter pull-down approach, new regulators were identified together with regulatory networks involved in the modulation of the global Gac/Rsm system. These results are described in Chapter 5. Chapter 6 is focused on the effect of a library of compounds available in our laboratory, for their QS-inhibiting potential. The conclusions and future directions are presented in Chapter 7.
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Huang, Yun. "Integration of Extracellular and Intracellular Calcium Signals: Roles of Calcium-Sensing Receptor (CASR), Calmodulin and Stromal Interaction Molecule 1 (STIM1)." Atlanta, Ga. : Georgia State University, 2008. http://digitalarchive.gsu.edu/chemistry_diss/28/.

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Thesis (Ph. D.)--Georgia State University, 2008.
Title from title page (Digital Archive@GSU, viewed July 1, 2010) Jenny J. Yang, committee chair; Edward Brown, Giovanni Gadda, Zhi-ren Liu, committee members. Includes bibliographical references (p. 230-258).
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Lemaire, Mathieu. "Intracellular signals underlying the inductive effects of agrin during neuromuscular junction formation : study on the roles of ras and Shc." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0030/MQ64388.pdf.

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Books on the topic "Intracellular signals"

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

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

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

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C, Mobley William, Christen Yves, and SpringerLink (Online service), eds. Intracellular Traffic and Neurodegenerative Disorders. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009.

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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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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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Jeroen, Pasterkamp R., ed. Semaphorins: Receptor and intracellular signaling mechanisms. New York, N.Y: Springer Science+Business Media, 2007.

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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 signals"

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Atherton, Philip J., and Nathaniel J. Szewczyk. "Chapter 5. Regulation of Muscle Proteostasis via Extramuscular Signals." In Extracellular and Intracellular Signaling, 77–104. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733434-00077.

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Salehi, Ahmad, Chengbiao Wu, Ke Zhan, and William C. Mobley. "Axonal Transport of Neurotrophic Signals: An Achilles' Heel for Neurodegeneration?" In Intracellular Traffic and Neurodegenerative Disorders, 87–101. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-87941-1_7.

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Denizot, Audrey, Hugues Berry, and Sharmila Venugopal. "Intracellular Calcium Signals in Astrocytes, Computational Modeling of." In Encyclopedia of Computational Neuroscience, 1–12. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-7320-6_100693-1.

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Hessels, Anne M., and Maarten Merkx. "Genetically Encoded Fluorescent Probes for Intracellular Zn2+ Imaging." In Zinc Signals in Cellular Functions and Disorders, 135–59. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-55114-0_7.

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Iino, Masamitsu. "Dynamic regulation of intracellular calcium signals through calcium release channels." In Muscle Physiology and Biochemistry, 185–90. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5543-8_23.

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Schulz, I., H. Streb, and F. Thevenod. "Intracellular Signals in Stimulation of Enzyme Secretion from Exocrine Glands." In Calcium Electrogenesis and Neuronal Functioning, 166–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70744-5_15.

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Negro-Vilar, A., M. M. Valenca, and M. D. Culler. "Transmembrane Signals and Intracellular Messengers Mediating LHRH and LH Secretion." In Advances in Experimental Medicine and Biology, 85–108. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5395-9_5.

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Graff van Creveld, Shiri, Avia Mizrachi, and Assaf Vardi. "An Ocean of Signals: Intracellular and Extracellular Signaling in Diatoms." In The Molecular Life of Diatoms, 641–78. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92499-7_22.

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Neagu, Monica, and Carolina Constantin. "Signal Transduction in Immune Cells and Protein Kinases." In Advances in Experimental Medicine and Biology, 133–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49844-3_5.

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AbstractImmune response relies upon several intracellular signaling events. Among the protein kinases involved in these pathways, members of the protein kinase C (PKC) family are prominent molecules because they have the capacity to acutely and reversibly modulate effector protein functions, controlling both spatial distribution and dynamic properties of the signals. Different PKC isoforms are involved in distinct signaling pathways, with selective functions in a cell-specific manner.In innate system, Toll-like receptor signaling is the main molecular event triggering effector functions. Various isoforms of PKC can be common to different TLRs, while some of them are specific for a certain type of TLR. Protein kinases involvement in innate immune cells are presented within the chapter emphasizing their coordination in many aspects of immune cell function and, as important players in immune regulation.In adaptive immunity T-cell receptor and B-cell receptor signaling are the main intracellular pathways involved in seminal immune specific cellular events. Activation through TCR and BCR can have common intracellular pathways while others can be specific for the type of receptor involved or for the specific function triggered. Various PKC isoforms involvement in TCR and BCR Intracellular signaling will be presented as positive and negative regulators of the immune response events triggered in adaptive immunity.
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Li, Ming, and Songwei Wu. "Regulation of T-Type Ca2+ Channels by Intercellular and Intracellular Signals." In T-type Calcium Channels in Basic and Clinical Science, 19–35. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-1413-1_2.

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Conference papers on the topic "Intracellular signals"

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Harootunian, A. T., J. P. Kao, and Roger Y. Tsien. "Fluorescence Ratio Imaging Of Dynamic Intracellular Signals." In 33rd Annual Techincal Symposium, edited by John E. Wampler. SPIE, 1989. http://dx.doi.org/10.1117/12.962706.

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Erickson, Geoffrey R., and Farshid Guilak. "Osmotic Stress Initiates Intracellular Calcium Waves in Chondrocytes Through Extracellular Influx and the Inositol Phosphate Pathway." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0580.

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Abstract The biophysical environment of the chondrocytes plays an important role in the health, turnover, and homeostasis of articular cartilage. Under normal physiologic loading, chondrocytes are exposed to a complex and diverse array of biophysical signals, including mechanical and osmotic stresses, fluid flow, and fluid pressures [4]. Due to the charged and hydrated nature of the extracellular matrix, mechanical compression causes exudation of interstitial fluid in cartilage, which alters the osmotic environment of the chondrocytes. Confocal microscopy studies have shown that chondrocytes lose or gain volume in response to tissue compression [4] or changes in extracellular osmolarity [3]. The active process of volume recovery subsequent to osmotic shock has been shown to initiate intracellular signaling cascades [2], which may in turn alter cellular metabolism [6]. Although the mechanisms of intracellular signaling in response to osmotic stress are not fully understood, it has been hypothesized that intracellular transients and oscillations of calcium ion (Ca2+) are involved. The objective of this study was to examine the hypothesis that osmotic stress initiates a transient increase in the concentration of intracellular calcium ion ([Ca2+]i), and to determine the mechanisms of Ca2+ mobilization in isolated chondrocytes exposed to hypo- and hyper-osmotic stress.
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Nolte, David, Shadia Jalal, and Ran An. "Twin-Neural-Network Differential Autoencoder and Dynamic-Contrast Optical Coherence Tomography for Cancer Diagnostics." In CLEO: Applications and Technology. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleo_at.2022.am5i.6.

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Dynamic-contrast optical coherence tomography (OCT) using en face digital holography senses intracellular dynamics in living tumor tissue. Intracellular motions produce ultra-low-frequency Doppler shifts for speeds down to nanometers per second (10 mHz) and up to microns per second (10 Hz). Cancer drugs applied to human tumor biopsies induce changes in these dynamics and produce specific Doppler signatures of therapeutic efficacy. We have developed a new type of deep neural network that performs as a differential autoencoder with high common-mode rejection that isolates Doppler signatures associated with drug response and patient outcomes. The differential autoencoder is applied to Doppler signals from a clinical trial of esophageal cancer patients.
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Mayalu, Michaëlle N., and H. Harry Asada. "Integrated Mechanistic-Empirical Modeling of Cellular Response Based on Intracellular Signaling Dynamics." In ASME 2013 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/dscc2013-3806.

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A hybrid modeling framework integrating a highly specific mechanistic model with highly abstract empirical model is presented. With the growing interest in the scientific and medical community for identification of therapeutic targets in treatment of disease, it is necessary to develop predictive models that can describe cellular behavior in response to environmental cues. Intracellular signaling pathways form complex networks that regulate cellular response in both health and disease. Mechanistic (or white-box) models of biochemical networks are often unable to explain comprehensive cellular response due to lack of knowledge and/or intractable complexity (especially in events distal from the cell membrane). Empirical (or black-box) models may provide a less than accurate representation of cellular response due to data deficiency and/or loss of mechanistic detail. In the proposed framework, we use a mechanistic model to capture early signaling events and apply the resulting generated internal signals (along with external inputs) to a downstream empirical sub-model. The key construct in the approach is the treatment of a cell’s biochemical network as an encoder that creates a functional internal representation of external environmental cues. The signals derived from this representation are then used to inform downstream behaviors. Using this idea, we are able to create a comprehensive framework that describes important mechanisms with sufficient detail, while representing complex or unknown mechanisms in a more abstract form. The model is verified using published biological data describing T-Cells in immune response.
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Shiraishi, Toshihiko, Kazuhiro Sakata, Shin Morishita, and Ryohei Takeuchi. "Investigation of a Cell Mechanosensing System by Measuring Cytoskeletal Deformation and Intracellular Calcium Ion Concentration." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-64843.

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This paper describes a method to investigate the relationship between cytoskeletal deformation by mechanical stimulation and its corresponding intracellular signals for identifying mechanosensors of cells. Gene transfection of green fluorescent protein to osteoblasts enabled visualization of actin in cells. When local deformation was applied to a cell by a micropipette, the distribution of cytoskeletal actin deformation in the whole cell was automatically obtained from the two images of the cell before and after deformation by using KLT method. Calcium ion signaling response to the same mechanical stimulation was measured as the spatial and temporal changes of fluorescent intensity of fluo-4 loaded to osteoblasts. As a result, we obtained the relationship between the deformation and the biochemical signals in cells.
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Sun, Xuanhao, Vipuil Kishore, Kateri Fites, and Ozan Akkus. "Mechanically Induced Calcium Release From Bone Matrix Triggers Intracellular Ca2+ Signalling in Osteoblasts: A Novel Mechanotransduction Mechanism." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53446.

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Bone cells are responsible for sensing and converting the mechanical signals into cellular signals to drive bone adaptation and damage repair [1]. Cell-mediated repair of bone is reported to be in preferential association with regions filled with microdamage [2]. Although different theories have been proposed for mechanisms involved in those processes (such as substrate deformation, fluid flow shear, and hydrostatic pressure in mechanotransduction [3], or microcrack and osteocyte apoptosis in damage detection [4]), knowledge on the exact form of physical stimuli which trigger bone cells, especially in critically loaded regions of bone, is still elusive.
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Lages, B., and H. J. Weiss. "TIME DEPENDENCE OF AEQUORIN-INDICATED CALCIUM SIGNALS IN STIMULATED AND UNSTIMULATED PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644530.

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The photoprotein aequorin (aeq) has been used as an indicator of intracellular calcium levels ([Ca]i) in platelets (pits). Aeq is believed to monitor aspects of [Ca]i somewhat different from those reported by quin-2, since it reports a higher basal [Ca]i than quin-2 and the presence, rather than the absence, of increased [Ca]i following epinephrine (epi) stimulation. To characterize further aeq-indicated pit Ca signals we measured their time dependence in both stimulated and untimulated pits. Aeq was loaded into pits by membrane permeabilization and resealing at 0°C. The maximum aeq signal (Lmax), obtained by Triton X-100 lysis of pits in the presence of 1 mM Ca, decreased over 40-60 min in a non-linear manner to about 60% of its initial value. Basal [Ca]i also decreased in a similar manner, even after correction for the changes in Lmax. The decreases in both responses were greater in pits isolated in the presence of 1 mM Ca than in the absence of Ca, indicating a sensitivity to external Ca. Epi (1-50 uM) induced an aeq signal in pits of most, but not all, subjects initially, but this response disappeared completely over 40-60 min in most subjects, without a concomitant loss of aggregation response. In contrast, the endoperoxide analog U44069 (10 uM) induced aeq signals in pits from all subjects, which decreased only slightly with time. These results suggest 1) that a portion of pit aeq may be localized in a region of high [Ca]i which may be partially accessible to external Ca, and this may account, in part, for the higher basal [Ca]i reported by aeq than by quin-2; and 2) that the epi-induced aeq signal, which is not prerequisite for aggregation, may be derived primarily from this labile aeq pool since the time courses for the decay of Lmax and basal [Ca]i and the loss of the epi-induced aeq signal are similar.
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Rich, T., N. S. Annamdevula, A. Britain, and S. Leavesley. "PGE1 Triggers Camp Signals Generated at the Plasma Membrane and at Intracellular Locations in Pulmonary Microvascular Endothelial Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7844.

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9

Gu, W. Y., W. M. Lai, C. T. Hung, Z. P. Liu, and V. C. Mow. "Analysis of Transient Swelling and Electrical Responses of an Isolated Cell to Sudden Osmotic Loading." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0292.

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Abstract The cell volume changes in response to changes in the osmolality of an extracellular medium. When the medium osmolality decreases, extracellular water will move into the cell so that the cell volume increases (swelling). The rate of change in cell volume depends on the material properties of the cell, such as the tensile stiffness and hydraulic permeability. During cell swelling, the cell membrane is stretched, possibly affecting membrane permeability to various ions (i.e., stretch-activated ion-channels). The transport of ions and water will result in a change in membrane potential [e.g., 1] as well as a change in intracellular ion concentrations. Therefore, mechanical, chemical and electrical events are coupled within a cell. It is important to understand these coupled events in order to separate mechanical and chemical signals and to begin to elucidate the biophysical signal transduction pathways. As a first step to model a cell, we have begun to study mechanical, chemical and electrical phenomena across a cell membrane using recently developed theories [1–3]. In this study, we report our analysis of transient swelling and electrical responses of an isolated cell to an osmotic load, which has been studied experimentally [e.g., 4]. The objective of this study was to relate the changes in cell volume, intracellular ion concentration and electrical potential (which can be readily measured) to the cell material properties (e.g., stiffness, hydraulic permeability and ion-channels).
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Oswald, Elizabeth S., Pen-hsiu Grace Chao, J. Chloe Bulinski, Gerard A. Ateshian, and Clark T. Hung. "The Role of Microtubule Organization in Chondrocyte Response to Osmotic Loading." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176634.

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The cytoskeleton, including actin filaments and microtubules, provides chondrocytes with structure, cytoplasmic organization, and intracellular transport. The cytoskeleton is known to be involved in cellular responses to physiologic mechanical and osmotic loading signals, including morphological changes and mechanostransduction [1, 2]. Here, we examine microtubule (MT) involvement in volume response of chondrocytes to osmotic loading, as well as organization of stable MT with hypoosmotic loading. We also explore the hypothesis that chondrocytes from different zones of cartilage possess cytoskeletons with different properties, which help explain variations in their volume response to osmotic loading in situ and in vitro [3].
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Reports on the topic "Intracellular signals"

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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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Horwitz, Benjamin, and Nicole M. Donofrio. Identifying unique and overlapping roles of reactive oxygen species in rice blast and Southern corn leaf blight. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604290.bard.

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Plants and their fungal pathogens both produce reactive oxygen species (ROS). CytotoxicROS act both as stressors and signals in the plant-fungal interaction. In biotrophs, a compatible interaction generates little ROS, but is followed by disease. An incompatible interaction results in a strong oxidative burst by the host, limiting infection. Necrotrophs, in contrast, thrive on dead and dying cells in an oxidant-rich local environment. Rice blast, Magnaportheoryzae, a hemibiotroph, occurs worldwide on rice and related hosts and can decimate enough rice each year to feed sixty million people. Cochliobolusheterostrophus, a necrotroph, causes Southern corn leaf blight (SLB), responsible for a major epidemic in the 1970s. The objectives of our study of ROS signaling and response in these two cereal pathogens were: Confocal imaging of ROS production using genetically encoded redox sensor in two pathosystems over time. Forward genetic screening of HyPer sensor lines in two pathosystems for fungal genes involved in altered ROSphenotypes. RNA-seq for discovery of genes involved in ROS-related stress and signaling in two pathosystems. Revisions to the research plan: Library construction in SLB was limited by low transformation efficiency, compounded by a protoplasting enzyme being unavailable during most of year 3. Thus Objective 2 for SLB re-focused to construction of sensor lines carrying deletion mutations in known or candidate genes involved in ROS response. Imaging on rice proved extremely challenging, so mutant screening and imaging were done with a barley-infecting line, already from the first year. In this project, ROS imaging at unprecedented time and spatial resolution was achieved, using genetically-encoded ratio sensors in both pathogens. This technology is currently in use for a large library of rice blast mutants in the ROS sensor background, and Southern corn leaf blight mutants in final stages of construction. The imaging methods developed here to follow the redox state of plant pathogens in the host tissue should be applicable to fungal pathogens in general. Upon completion of mutant construction for SCLB we hope to achieve our goal of comparison between intracellular ROS status and response in hemibiotroph and necrotroph cereal pathogens.
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Avni, Adi, and Gitta L. Coaker. Proteomic investigation of a tomato receptor like protein recognizing fungal pathogens. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600030.bard.

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Maximizing food production with minimal negative effects on the environment remains a long-term challenge for sustainable food production. Microbial pathogens cause devastating diseases, minimizing crop losses by controlling plant diseases can contribute significantly to this goal. All plants possess an innate immune system that is activated after recognition of microbial-derived molecules. The fungal protein Eix induces defense responses in tomato and tobacco. Plants recognize Eix through a leucine-rich-repeat receptor- like-protein (LRR-RLP) termed LeEix. Despite the knowledge obtained from studies on tomato, relatively little is known about signaling initiated by RLP-type immune receptors. The focus of this grant proposal is to generate a foundational understanding of how the tomato xylanase receptor LeEix2 signals to confer defense responses. LeEix2 recognition results in pattern triggered immunity (PTI). The grant has two main aims: (1) Isolate the LeEix2 protein complex in an active and resting state; (2) Examine the biological function of the identified proteins in relation to LeEix2 signaling upon perception of the xylanase elicitor Eix. We used two separate approaches to isolate receptor interacting proteins. Transgenic tomato plants expressing LeEix2 fused to the GFP tag were used to identify complex components at a resting and activated state. LeEix2 complexes were purified by mass spectrometry and associated proteins identified by mass spectrometry. We identified novel proteins that interact with LeEix receptor by proteomics analysis. We identified two dynamin related proteins (DRPs), a coiled coil – nucleotide binding site leucine rich repeat (SlNRC4a) protein. In the second approach we used the split ubiquitin yeast two hybrid (Y2H) screen system to identified receptor-like protein kinase At5g24010-like (SlRLK-like) (Solyc01g094920.2.1) as an interactor of LeEIX2. We examined the role of SlNRC4a in plant immunity. Co-immunoprecipitation demonstrates that SlNRC4a is able to associate with different PRRs. Physiological assays with specific elicitors revealed that SlNRC4a generally alters PRR-mediated responses. SlNRC4a overexpression enhances defense responses while silencing SlNRC4 reduces plant immunity. We propose that SlNRC4a acts as a non-canonical positive regulator of immunity mediated by diverse PRRs. Thus, SlNRC4a could link both intracellular and extracellular immune perception. SlDRP2A localizes at the plasma membrane. Overexpression of SlDRP2A increases the sub-population of LeEIX2 inVHAa1 endosomes, and enhances LeEIX2- and FLS2-mediated defense. The effect of SlDRP2A on induction of plant immunity highlights the importance of endomembrane components and endocytosis in signal propagation during plant immune . The interaction of LeEIX2 with SlRLK-like was verified using co- immunoprecipitation and a bimolecular fluorescence complementation assay. The defence responses induced by EIX were markedly reduced when SlRLK-like was over-expressed, and mutation of slrlk-likeusing CRISPR/Cas9 increased EIX- induced ethylene production and SlACSgene expression in tomato. Co-expression of SlRLK-like with different RLPs and RLKs led to their degradation, apparently through an endoplasmic reticulum-associated degradation process. We provided new knowledge and expertise relevant to expression of specific be exploited to enhance immunity in crops enabling the development of novel environmentally friendly disease control strategies.
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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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Or, Etti, David Galbraith, and Anne Fennell. Exploring mechanisms involved in grape bud dormancy: Large-scale analysis of expression reprogramming following controlled dormancy induction and dormancy release. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7587232.bard.

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The timing of dormancy induction and release is very important to the economic production of table grape. Advances in manipulation of dormancy induction and dormancy release are dependent on the establishment of a comprehensive understanding of biological mechanisms involved in bud dormancy. To gain insight into these mechanisms we initiated the research that had two main objectives: A. Analyzing the expression profiles of large subsets of genes, following controlled dormancy induction and dormancy release, and assessing the role of known metabolic pathways, known regulatory genes and novel sequences involved in these processes B. Comparing expression profiles following the perception of various artificial as well as natural signals known to induce dormancy release, and searching for gene showing similar expression patterns, as candidates for further study of pathways having potential to play a central role in dormancy release. We first created targeted EST collections from V. vinifera and V. riparia mature buds. Clones were randomly selected from cDNA libraries prepared following controlled dormancy release and controlled dormancy induction and from respective controls. The entire collection (7920 vinifera and 1194 riparia clones) was sequenced and subjected to bioinformatics analysis, including clustering, annotations and GO classifications. PCR products from the entire collection were used for printing of cDNA microarrays. Bud tissue in general, and the dormant bud in particular, are under-represented within the grape EST database. Accordingly, 59% of the our vinifera EST collection, composed of 5516 unigenes, are not included within the current Vitis TIGR collection and about 22% of these transcripts bear no resemblance to any known plant transcript, corroborating the current need for our targeted EST collection and the bud specific cDNA array. Analysis of the V. riparia sequences yielded 814 unigenes, of which 140 are unique (keilin et al., manuscript, Appendix B). Results from computational expression profiling of the vinifera collection suggest that oxidative stress, calcium signaling, intracellular vesicle trafficking and anaerobic mode of carbohydrate metabolism play a role in the regulation and execution of grape-bud dormancy release. A comprehensive analysis confirmed the induction of transcription from several calcium–signaling related genes following HC treatment, and detected an inhibiting effect of calcium channel blocker and calcium chelator on HC-induced and chilling-induced bud break. It also detected the existence of HC-induced and calcium dependent protein phosphorylation activity. These data suggest, for the first time, that calcium signaling is involved in the mechanism of dormancy release (Pang et al., in preparation). We compared the effects of heat shock (HS) to those detected in buds following HC application and found that HS lead to earlier and higher bud break. We also demonstrated similar temporary reduction in catalase expression and temporary induction of ascorbate peroxidase, glutathione reductase, thioredoxin and glutathione S transferase expression following both treatments. These findings further support the assumption that temporary oxidative stress is part of the mechanism leading to bud break. The temporary induction of sucrose syntase, pyruvate decarboxylase and alcohol dehydrogenase indicate that temporary respiratory stress is developed and suggest that mitochondrial function may be of central importance for that mechanism. These finding, suggesting triggering of identical mechanisms by HS and HC, justified the comparison of expression profiles of HC and HS treated buds, as a tool for the identification of pathways with a central role in dormancy release (Halaly et al., in preparation). RNA samples from buds treated with HS, HC and water were hybridized with the cDNA arrays in an interconnected loop design. Differentially expressed genes from the were selected using R-language package from Bioconductor project called LIMMA and clones showing a significant change following both HS and HC treatments, compared to control, were selected for further analysis. A total of 1541 clones show significant induction, of which 37% have no hit or unknown function and the rest represent 661 genes with identified function. Similarly, out of 1452 clones showing significant reduction, only 53% of the clones have identified function and they represent 573 genes. The 661 induced genes are involved in 445 different molecular functions. About 90% of those functions were classified to 20 categories based on careful survey of the literature. Among other things, it appears that carbohydrate metabolism and mitochondrial function may be of central importance in the mechanism of dormancy release and studies in this direction are ongoing. Analysis of the reduced function is ongoing (Appendix A). A second set of hybridizations was carried out with RNA samples from buds exposed to short photoperiod, leading to induction of bud dormancy, and long photoperiod treatment, as control. Analysis indicated that 42 genes were significant difference between LD and SD and 11 of these were unique.
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