Relevant bibliographies by topics / Cellular signal transduction

Contents

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

Academic literature on the topic 'Cellular signal transduction'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Cellular signal transduction"

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Bae, Yun Soo, and June Seung Lee. "Cellular Signal Transduction." Journal of the Korean Medical Association 44, no. 7 (2001): 716. http://dx.doi.org/10.5124/jkma.2001.44.7.716.

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Macara, I. G. "Oncogenes and cellular signal transduction." Physiological Reviews 69, no. 3 (July 1, 1989): 797–820. http://dx.doi.org/10.1152/physrev.1989.69.3.797.

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Ball, A. "Introduction to Cellular Signal Transduction." Cell Biology International 24, no. 11 (November 2000): 855. http://dx.doi.org/10.1006/cbir.2000.0590.

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Marks, F., and P. Angel. "Signal Transduction into the Nucleus: Fifth Colloquium on Cellular Signal Transduction." Journal of Cancer Research and Clinical Oncology 122, no. 10 (October 1996): 638–42. http://dx.doi.org/10.1007/bf01221198.

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Marks, F., and G. F�rstenberger. "Fourth colloquium on cellular signal transduction. Lipid mediators: signal transduction and transport." Journal of Cancer Research and Clinical Oncology 121, no. 7 (July 1995): 434–38. http://dx.doi.org/10.1007/bf01212952.

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Wurthner, Jens U., Amal K. Mukhopadhyay, and Claus-Jürgen Peimann. "A cellular automaton model of cellular signal transduction." Computers in Biology and Medicine 30, no. 1 (January 2000): 1–21. http://dx.doi.org/10.1016/s0010-4825(99)00020-7.

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Wetzel, C. H. "Cellular Mechanisms of Olfactory Signal Transduction." Chemical Senses 30, Supplement 1 (January 1, 2005): i321—i322. http://dx.doi.org/10.1093/chemse/bjh244.

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Schmidt-Ullrich, Rupert K., Paul Dent, Steven Grant, Ross B. Mikkelsen, and Kristoffer Valerie. "Signal Transduction and Cellular Radiation Responses." Radiation Research 153, no. 3 (March 2000): 245–57. http://dx.doi.org/10.1667/0033-7587(2000)153[0245:stacrr]2.0.co;2.

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Lin, James C. A., Jimmy K. Li, and Walter H. Chang. "Signal Transduction Pathway of Ultrasound Stimulation on Osteoblasts(Cellular & Tissue Engineering)." Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2004.1 (2004): 87–88. http://dx.doi.org/10.1299/jsmeapbio.2004.1.87.

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Mattson, Mark P. "Cerebral Signal Transduction." Journal of Molecular Neuroscience 14, no. 3 (2000): 206–8. http://dx.doi.org/10.1385/jmn:14:3:206.

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Dissertations / Theses on the topic "Cellular signal transduction"

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Pat, Betty Kila. "Signal transduction pathways in renal fibrosis /." St. Lucia, Qld, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17739.pdf.

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Haugh, Jason Michael 1972. "Cellular compartmentation effects in receptor-mediated signal transduction." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/85364.

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Leahy, Rachel A. "Signal Transduction and Cellular Differentiation in Airway Epithelium." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1352673026.

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Kim, Hyun Ji. "Development and signal transduction in Dictyostelium." Thesis, University of Oxford, 1999. http://ora.ox.ac.uk/objects/uuid:4ed80c6e-adc8-46d6-aeaf-c853cef7af77.

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Dictyostelium, is a simple eukaryote that multiplies as separate amoebae. However when nutrients are no longer available it embarks on a developmental programme in which the amoebae collect together by chemotaxis and the resulting aggregates eventually transform into fruiting bodies consisting of a cluster of spores held up on a cellular stalk. The entire process of development normally takes about 24 hours. However there are mutants, termed rapidly developing mutants (rde) which complete development in about two-thirds of this time. RdeA null mutants have been reported to have elevated levels of cyclic AMP that may lead to increased activity of the enzyme, cAMP dependent protein kinase (PKA). I started my work by measuring total cAMP levels in an rdeA mutant along with an aca-/rdeA- double mutant that is expected to have very low level of cAMP due to the absence of the adenylyl cyclase, AC A. Two Dictyostelium adenylyl cyclases were known at the beginning of my work; one is AC A the aggregative enzyme, and the other ACG, expressed only during spore germination. Contrary to expectation, I detected cAMP in aca-/rdeA cells. This raised the question of which enzyme was responsible for producing this cAMP. In collaboration with Dr.Pauline Schaap, I discovered a novel adenylyl cyclase that I initially detected in rdeA and regA mutants but not in wild-type cells. The product of the rdeA gene, RDEA was thought to be an H2-module histidine phosphotrasferase of the kind acting in multi-step phosphorelays. Similarly REGA was believed to be a response regulator associated with a cAMP-phosphodiesterase. It had been proposed that RDEA phosphorylates REGA in a multi-step phosphorelay and it had been shown that it is the phosphorylated form of REGA that is active as a cAMP-PDE. I therefore thought that cAMP produced by the novel AC could be protected in rdeA mutants by the absence of the REGA cAMP-PDE activity and this idea was supported by my finding that the enzyme activity could also be detected in wild-type (aca-) cells when REGA-PDE was inhibited by IBMX. In order to investigate further the proposed phosphorelay model, I tested for possible interaction between RDEA and REGA using the yeast two-hybrid system and also measured intracellular cAMP-phosphodiesterase activity in rdeA and regA mutants. I found that the interaction between RDEA and REGA appeared to be too transient to be detected in the two-hybrid system. In addition rdeA and regA mutants seemed to have levels of intracellular cAMP-phosphodiesterase activity similar to wild type. However REGA-PDE activity measured specifically by immuno-precipitation was completely absent in the regA mutant. It therefore appeared that there is another intracellular cAMP-phosphodiesterase, in addition to the REGA PDE, in Dictyostelium and that the latter cannot be easily detected in total cell lysates. One possible explanation is that the novel adenylyl cyclase exists together with REGA in a complex (that may also include PKA) and that REGA PDE preferentially destroys the cAMP made by the novel adenylyl cyclase. I conclude that rdeA and regA mutants may develop rapidly due to high PKA activity induced by the accumulation of cAMP made by the novel AC when the REGA cAMP-PDE activity is absent.
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Chang, Wen-Tsan. "Molecular studies of signal transduction and development." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360212.

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Brownlie, Zoe. "Regulation of signal transduction by RGS4." Connect to e-thesis, 2007. http://theses.gla.ac.uk/124/.

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Thesis (Ph.D.) - University of Glasgow, 2007.<br>Ph.D. thesis submitted to the Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, 2007. Includes bibliographical references.
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Gammon, Benjamin Matthew. "Signal transduction in the cellular slime mould Dictyostelium discoideum." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279872.

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Manne, Bhanu Kanth. "CLEC-2 SIGNAL TRANSDUCTION IN PLATELET ACTIVATION." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/340495.

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Physiology<br>Ph.D.<br>Platelets are involved in many processes ranging from fighting microbial infections and triggering inflammation to promoting tumor angiogenesis and metastasis. Nevertheless, the primary physiological function of platelets is to act as essential mediators in maintaining homeostasis of the circulatory system by forming hemostatic thrombi that prevent blood loss and maintain vascular integrity. CLEC-2 is a C-type lectin-like receptor that is highly expressed in platelets and lesser extent, in other cell types such as activated dendritic cells and B cells. Rhodocytin was the first ligand used to identify CLEC-2 receptor and it’s signaling on platelets. In the first chapter we identified a new agonist for CLEC-2 receptor. Fucoidan, a sulfated polysaccharide from fucus vesiculosus, decreases bleeding time and clotting time in hemophilia, possibly through inhibition of tissue factor pathway inhibitor. However, its effect on platelets and the receptor by which fucoidan induces cellular processes has not been elucidated. In this study, we demonstrate that fucoidan induces platelet activation in a concentration-dependent manner. Fucoidan-induced platelet activation was completely abolished by the pan-Src family kinase (SFK) inhibitor, PP2, or when Syk is inhibited. PP2 abolished phosphorylation of Syk and Phospholipase Cγ−2. Fucoidan-induced platelet activation had a lag phase, which is reminiscent of platelet activation by collagen and CLEC-2 receptor agonists. Platelet activation by fucoidan was only slightly inhibited in FcRγ chain null mice, indicating that fucoidan was not acting primarily through GPVI receptor. On the other hand, fucoidan-induced platelet activation was inhibited in platelet-specific CLEC-2 knock-out murine platelets revealing CLEC-2 as a physiological target of fucoidan. Thus, our data show fucoidan as a novel CLEC-2 receptor agonist that activates platelets through a SFK-dependent signaling pathway. Furthermore, the efficacy of fucoidan in hemophilia raises the possibility that decreased bleeding times could be achieved through activation of platelets. Lipid rafts are distinct areas of the plasma membrane implicated in the regulation of signaling in a variety of cells including platelets. A previous study C-type lectin like receptor 2 (CLEC-2) has been reported to activate platelets through a lipid raft-dependent manner. Secreted ADP potentiates CLEC-2-mediated platelet aggregation. We have investigated whether the decrease in CLEC-2-mediated platelet aggregation, previously reported in platelets with disrupted rafts, is a result of the loss of agonist potentiation by ADP. We disrupted platelet lipid rafts with methyl-β-cyclodextrin (MβCD) and measured signaling events downstream of CLEC-2 activation. Lipid raft disruption decreases platelet aggregation induced by CLEC-2 agonists. The inhibition of platelet aggregation by the disruption of lipid rafts was rescued by the exogenous addition of epinephrine but not 2-methylthioadenosine diphosphate (2MeSADP), which suggests that lipid raft disruption effects P2Y12-mediated Gi activation but not Gz. Phosphorylation of Syk (Y525/526) and PLCγ2 (Y759), were not affected by raft disruption in CLEC-2 agonist-stimulated platelets. Furthermore, tyrosine phosphorylation of the CLEC-2 hemi-ITAM was not effected when MβCD disrupts lipid rafts. Lipid rafts do not directly contribute to CLEC-2 receptor activation in platelets. The effects of disruption of lipid rafts in in vitro assays can be attributed to inhibition of ADP feedback that potentiates CLEC-2 signaling. Tyrosine kinase pathways are known to play an important role in the activation of platelets. In particular, the GPVI and CLEC-2 receptors are known to activate Syk upon tyrosine phosphorylation of an Immune Tyrosine Activation Motif (ITAM) and hemi-ITAM, respectively. However, unlike GPVI, the CLEC-2 receptor contains only one tyrosine motif in the intracellular domain. The mechanisms by which this receptor activates Syk are not completely understood. In chapter 3, we identified a novel signaling mechanism in CLEC-2-mediated Syk activation. CLEC-2-mediated, but not GPVI-mediated, platelet activation and Syk phosphorylation were abolished by inhibition of PI3-Kinase, which demonstrates that PI3-Kinase regulates Syk downstream of CLEC-2. Ibrutinib, a Tec family kinase inhibitor, also completely abolished CLEC-2-mediated aggregation and Syk phosphorylation in human and murine platelets. Furthermore, embryos lacking both Btk and Tec exhibited cutaneous edema associated with blood-filled vessels in a typical lymphatic pattern similar to CLEC-2 or Syk-deficient embryos. Thus our data show, for the first time, that PI3-Kinase and Tec family kinases play a crucial role in the regulation of platelet activation and Syk phosphorylation downstream of CLEC-2 receptor.<br>Temple University--Theses
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Hung, Hiu Wai. "Signal transduction mechanism in xenopus presynaptic differentiation /." View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202003%20HUNG.

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Gong, Yunchen 1965. "Analyses of alternative cell signal transduction pathways." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85552.

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Living cells keep sensing the changes in their environments, mostly, via cell surface receptors for different ligands. Attachment-dependent cells are sensitive to alterations in extracellular matrix (ECM). ECM is not only required for cell survival, but also prerequisite for epidermal growth factor (EGF) to stimulate cell proliferation. The receptors for the majority of ECM components are integrins and the receptor for EGF is EGF receptor (EGFR). When bound by their ligands, integrins and EGFR induce signal transduction cascades composed of alternative pathways. A quantitative assessment of relative contributions of alternative pathways to one final cell signaling will help understand designing principles of the network. Unfortunately, a methodology for such assessment is still not available, partly because of lack of relatively mature mathematical models. On the other hand, in most biochemical cascades, existence of alternative pathways increases the complexity and thus the robustness of networks. The relationships between the topology and robustness of large-scale biochemical networks have been studied intensively recently. In small-scale networks, while feedback has been revealed as an important contributor for adaptation and robustness, the quantitative correlation between the topology/pathway redundancy of small networks and their robustness remains unknown.<br>In this thesis, apoptosis of bovine mammary gland epithelial cells was demonstrated to be induced when fibronectin, one of the major components of ECM, was degraded by overexpressed tPA via two potential ways: deprivation of attachment and the effects of fibronectin fragments. Secondly, a mathematical model for EGFR activation of the MAPK cascade, in which alternative pathways exist, was explored and it was found that the Shc-dependent pathway is both redundant and dominant. We hypothesize that the Shc-dependent pathway is important for EGFR to compete with other receptors, which need Shc to transduce cell signals; and this pathway is not aimed to increase the robustness of the EGFR cascade. Finally, for the general importance of alternative pathways to the network topology and robustness, several concepts have been proposed to decompose and quantitatively characterize the networks. We demonstrate that the pathnet score is a better assessment for robustness than the molecular connectivity.
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Books on the topic "Cellular signal transduction"

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Sitaramayya, Ari, ed. Introduction to Cellular Signal Transduction. Boston, MA: Birkhäuser Boston, 1999. http://dx.doi.org/10.1007/978-1-4612-1990-3.

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Ari, Sitaramayya, ed. Introduction to cellular signal transduction. Boston: Birkhauser, 1999.

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Dennis, Edward A. Transduction mechanisms in cellular signaling. Amsterdam: Elsevier/AP, 2011.

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T, Leeds Dorothy, ed. Focus on cellular signalling. New York: Nova Science Publishers, 2006.

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Klaus, Palme, ed. Signals and signal transduction pathways in plants. Dordrecht: Kluwer Academic Publishers, 1994.

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Yehuda, Gutman, and Lazarovici Philip, eds. Toxins and signal transduction. Australia: Harwood Academic Pub., 1997.

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F, Greco Lorenzo, and Martino Alessandro L, eds. Signal transduction: New research. New York: Nova Science Publishers, 2008.

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R, Tatham Peter E., Kramer Ijsbrand M, Knovel (Firm), and ScienceDirect (Online service), eds. Signal transduction. 2nd ed. Amsterdam: Elsevier/Academic Press, 2009.

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J, Van Eldik Linda, and Watterson D. Martin, eds. Calmodulin and signal transduction. San Diego: Academic Press, 1998.

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Krauss, Gerhard. Biochemistry of signal transduction and regulation. 2nd ed. Weinheim: Wiley-VCH, 2001.

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Book chapters on the topic "Cellular signal transduction"

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Marks, Friedrich, Ursula Klingmüller, and Karin Müller-Decker. "Signal Transduction by Ions." In Cellular Signal Processing, 485–541. Second edition. | New York, NY: Garland Science, 2017.: Garland Science, 2017. http://dx.doi.org/10.4324/9781315165479-14.

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Park, Gyungsoon, Carol A. Jones, and Katherine A. Borkovich. "Signal Transduction Pathways." In Cellular and Molecular Biology of Filamentous Fungi, 50–59. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816636.ch5.

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Lee, Joanna Y., and Lina M. Obeid. "Ceramide, Aging and Cellular Senescence." In Sphingolipid-Mediated Signal Transduction, 61–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-22425-0_5.

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Marks, Friedrich, Ursula Klingmüller, and Karin Müller-Decker. "Signal Transduction by Proteolysis, and Programmed Cell Death." In Cellular Signal Processing, 453–83. Second edition. | New York, NY: Garland Science, 2017.: Garland Science, 2017. http://dx.doi.org/10.4324/9781315165479-13.

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Marks, Friedrich, Ursula Klingmüller, and Karin Müller-Decker. "Signal Transduction by Receptors with Seven Transmembrane Domains." In Cellular Signal Processing, 191–227. Second edition. | New York, NY: Garland Science, 2017.: Garland Science, 2017. http://dx.doi.org/10.4324/9781315165479-5.

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Marks, Friedrich, Ursula Klingmüller, and Karin Müller-Decker. "Signal Transduction by Serine/Threonine Kinase-Coupled Receptors." In Cellular Signal Processing, 229–47. Second edition. | New York, NY: Garland Science, 2017.: Garland Science, 2017. http://dx.doi.org/10.4324/9781315165479-6.

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Boyd, Jonathan W., Richard R. Neubig, Alice Han, and Maren Prediger. "Introduction to Cellular Signal Transduction." In Cellular Signal Transduction in Toxicology and Pharmacology, 1–19. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2019. http://dx.doi.org/10.1002/9781119060208.ch1.

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Neubig, Richard R., Jonathan W. Boyd, Julia A. Mouch, and Nicole Prince. "Mechanisms of Cellular Signal Transduction." In Cellular Signal Transduction in Toxicology and Pharmacology, 21–48. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2019. http://dx.doi.org/10.1002/9781119060208.ch2.

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Niederfellner, Gerhard. "Signal Transduction and Cellular Communication." In Biochemical Pathways, 286–324. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118657072.ch7.

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Ganey, Patricia E., and Sean A. Misek. "Signal Transduction in Disease." In Cellular Signal Transduction in Toxicology and Pharmacology, 73–111. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2019. http://dx.doi.org/10.1002/9781119060208.ch4.

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Conference papers on the topic "Cellular signal transduction"

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Liu, Yuan-Wei, and Chun-Liang Lin. "Idea of Control Design for Cellular Signal Transduction Pathway of Ras." In International Conference on Computational Intelligence and Multimedia Applications (ICCIMA 2007). IEEE, 2007. http://dx.doi.org/10.1109/iccima.2007.267.

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Uzgare, Rajneesh, Thomas Hundley, Dhanrajan Tiruchinapalli, Anna Solomon, Cheryl Horton, and Hao Chen. "Abstract 236: Characterizing cellular signal transduction cross-talk using in-cell kinase screen." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-236.

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Mednieks, M. I. "Secretory proteins characteristic of environmental changes in cellular signal transduction: Expression in oral fluid." In HADRONS AND NUCLEI: First International Symposium. AIP, 2000. http://dx.doi.org/10.1063/1.1302484.

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Rattanakul, Chontita, and Yongwimon Lenbury. "Cellular automata simulation of signal transduction and calcium dynamics with healthy and faulty receptor trafficking." In 2016 Annual IEEE Systems Conference (SysCon). IEEE, 2016. http://dx.doi.org/10.1109/syscon.2016.7490536.

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KYODA, KOJI M., MICHIKO MURAKI, and HIROAKI KITANO. "CONSTRUCTION OF A GENERALIZED SIMULATOR FOR MULTI-CELLULAR ORGANISMS AND ITS APPLICATION TO SMAD SIGNAL TRANSDUCTION." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814447331_0030.

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Takai, Erica, Clark T. Hung, Aurea Tucay, Djordje Djukic, Mary L. Linde, Kevin D. Costa, James T. Yardley, and X. Edward Guo. "Design of a Microfluidic System for 3D Culture of Osteocytes In Vitro." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33229.

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Bone adapts to its mechanical environment so that its form follows function, a mechanism known as Wolff’s law, or bone adaptation. Although the basic concepts of Wolff’s law have been generally accepted, the regulatory signals and the underlying cellular and molecular pathways, which mediate this adaptive process, are unknown. Failure of normal bone adaptation plays a significant role in the etiology of metabolic bone diseases such as osteoporosis and osteopetrosis, bone loss in space flight and failure of total joint replacements. During the past three decades, there have been extensive in vitro studies addressing mechano-signal transduction mechanisms in bone cells including osteoblasts, osteocytes, and osteoclasts [1–8].
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LeDuc, Philip. "Linking Molecular to Cellular Biomechanics With Nano- and Micro-Technology." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43987.

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The link between mechanics and biochemistry has been implicated in a myriad of scientific and medical problem, from orthopedics and cardiovascular medicine, to cell motility and division, to signal transduction and gene expression. Most of these studies have been focused on organ-level issues, yet cellular and molecular level research has become essential over the last decade in this field thanks to the revolutionary developments in genetics, molecular biology, fabrication processes, and biotechnology. Developing the link between molecular and cellular biomechanics through subcellular studies can help uncover the complex interactions requisite for understanding higher order macroscopic behavior. Here, we will explore the link between molecular and cellular research through novel systems of nano- and micro-technology. In this, I will discuss novel technologies that we have developed and are utilizing, which include magnetic needles, three-dimension cell stretching systems, and microfluidics to examine the link between mechanics and biochemistry (including structural regulation through the cytoskeleton). By combining these novel approaches between engineering and biology, this multidisciplinary research can make a tremendous impact on the studies of human health and diseases through advances in fields such as proteomics, tissue engineering, and medical diagnostics.
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HATTA-OHASHI, Y., T. TAKAHASHI, and H. SUZUKI. "VISUALIZATION OF SEQUENTIAL RESPONSE IN INTRA CELLULAR SIGNAL TRANSDUCTION CASCADE BY FLUORESCENCE AND LUMINESCENCE IMAGING IN THE SAME LIVING CELL." In Proceedings of the 15th International Symposium. WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812839589_0081.

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Yang, Jui-Ming, and Philip R. LeDuc. "Three-Dimensional Laminar Flow for Localized Cellular Stimulation." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61643.

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Stimulation of living mammalian cells is primarily accomplished by the delivery of chemical agents to single cells or cell populations. Due to the fast response time of diffusion for these agents over the small size scale of individual cells, localized stimulation is limited. Currently, there are alternate techniques that can produce localized gradients of chemical stimulants over single cells, but they lack the ability for long time scale events that are requisite for many cellular processes because of this diffusion limitation. We have developed a device that is able to create chemical agent separation in three dimensions along distinct boundaries that can be applied to cells. As many techniques are two-dimensionally constrained, this provides us with a more physiologically relevant system for investigating cellular signal transduction and can allow basal to apical activation separations. To accomplish this, multiple flow paths were introduced to manipulate spatiotemporally distinct regions inside a single capillary channel. Solutions that flow laminarly inside these fluidic channels deliver predefined chemicals to specific locations without turbulent mixing. Separation using this system under laminar flows created not only side by side domains in this capillary but also vertical as well. This device has multiple potential applications both in cell and molecular biology as well as in fluid dynamics and fabrication processes.
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Guilak, Farshid, and H. Ping Ting-Beall. "The Effects of Osmotic Pressure on the Viscoelastic and Physical Properties of Articular Chondrocytes." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0398.

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Abstract Mechanical stress is an important factor in the regulation of chondrocyte metabolism and the maintenance of the cartilage extracellular matrix. Previous studies have shown that compression of cartilage explants alters cellular metabolism in a time- and spatially-varying manner which is correlated with the mechanical environment within the extracellular matrix [1]. Furthermore, cellular response has been shown to be influenced by mechanical, electrical, and physicochemical events which are coupled to deformation of the cells and the extracellular matrix. Therefore, detailed information on the stress-strain and physicochemical environments of individual cells in response to mechanical and osmotic stresses would improve our understanding of the sequence of events involved in mechanical signal transduction [2–4]. The goal of this study was to quantify the osmotic and viscoelastic properties of isolated chondrocytes and to test the hypothesis that the mechanical properties of the chondrocyte are influenced by their physicochemical (osmotic) environment.
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Reports on the topic "Cellular signal transduction"

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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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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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4

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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Philosoph-Hadas, Sonia, Peter Kaufman, Shimon Meir, and Abraham Halevy. Signal Transduction Pathway of Hormonal Action in Control and Regulation of the Gravitropic Response of Cut Flowering Stems during Storage and Transport. United States Department of Agriculture, October 1999. http://dx.doi.org/10.32747/1999.7695838.bard.

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Original objectives: The basic goal of the present project was to increase our understanding of the cellular mechanisms operating during the gravitropic response of cut flowers, for solving their bending problem without affecting flower quality. Thus, several elements operating at the 3 levels o the gravity-induced signal transduction pathway, were proposed to be examined in snapdragon stems according to the following research goals: 1) Signaling: characterize the signal transduction pathway leading to the gravitropic response, regarding the involvement of [Ca2+]cyt as a mediator of IAA movement and sensitivity to auxin. 2) Transduction by plant hormones: a) Examine the involvement of auxin in the gravitropic response of flower stems with regard to: possible participation of auxin binding protein (ABP), auxin redistribution, auxin mechanism of action (activation of H+-ATPase) mediation by changes in [Ca2+]cyt and possible regulation of auxin-induced Ca2+ action b: calmodulin-activated or Ca2+-activated protein kinases (PK). b) Examine the involvement of ethylene in the gravitropic response of flower stems with regard to auxin-induced ethylene production and sensitivity of the tissue to ethylene. 3) Response: examine the effect of gravistimulation on invertase (associated with growth and elongation) activity and invertase gene expression. 4) Commercial practice: develop practical and simple treatments to prevent bending of cut flowers grown for export. Revisions: 1) Model systems: in addition to snapdragon (Antirrhinum majus L.), 3 other model shoe systems, consisting of oat (Avena sativa) pulvini, Ornithogalun 'Nova' cut flowers and Arabidopsis thaliana inflorescence, were targeted to confirm a more general mechanism for shoot gravitropism. 2 Research topics: the involvement of ABP, auxin action, PK and invertase in the gravitropic response of snapdragon stems could not be demonstrated. Alternatively, the involvement in the gravity signaling cascade of several other physiological mediators apart of [Ca2+]cyt such as: IP3, protein phosphorylation and actin cytoskeleton, was shown. Additional topics introduced: starch statolith reorientation, differential expression of early auxin responsive genes, and differential shoot growth. Background to the topic: The gravitropic bending response of flowering shoots occurring upon their horizontal placement during shipment exhibits a major horticultural problem. In spite of extensive studies in various aboveground organs, the gravitropic response was hardly investigated in flowering shoots. Being a complex multistep process that requires the participation of various cellular components acting in succession or in parallel, analysis of the negative gravitropic response of shoot includes investigation of signal transduction elements and various regulatory physiological mediators. Major achievements: 1) A correlative role for starch statoliths as gravireceptors in flowering shoot was initially established. 2) Differentially phosphorylated proteins and IP3 levels across the oat shoe pulvini, as well as a differential appearance of 2 early auxin-responsive genes in snapdragon stems were all detected within 5-30 minutes following gravistimulation. 3) Unlike in roots, involvement of actin cytoskeleton in early events of the gravitropic response of snapdragon shoots was established. 4) An asymmetric IAA distribution, followed by an asymmetric ethylene production across snapdragon stems was found following gravistimulation. 5) The gravity-induced differential growth in shoots of snapdragon was derived from initial shrinkage of the upper stem side and a subsequent elongation o the lower stem side. 6) Shoot bending could be successfully inhibited by Ca2+ antagonists (that serve as a basis for practical treatments), kinase and phosphatase inhibitors and actin-cytoskeleton modulators. All these agents did not affect vertical growth. The essential characterization of these key events and their sequence led us to the conclusion that blocking gravity perception may be the most powerful means to inhibit bending without hampering shoot and flower growth after harvest. Implications, scientific and agriculture: The innovative results of this project have provided some new insight in the basic understanding of gravitropism in flower stalks, that partially filled the gap in our knowledge, and established useful means for its control. Additionally, our analysis has advanced the understanding of important and fundamental physiological processes involved, thereby leading to new ideas for agriculture. Gravitropism has an important impact on agriculture, particularly for controlling the bending of various important agricultural products with economic value. So far, no safe control of the undesired bending problem of flower stalks has been established. Our results show for the first time that shoot bending of cut flowers can be inhibited without adverse effects by controlling the gravity perception step with Ca2+ antagonists and cytoskeleton modulators. Such a practical benefit resulting from this project is of great economic value for the floriculture industry.
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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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Olszewski, Neil, and David Weiss. Role of Serine/Threonine O-GlcNAc Modifications in Signaling Networks. United States Department of Agriculture, September 2010. http://dx.doi.org/10.32747/2010.7696544.bard.

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Significant evidence suggests that serine/threonine-O-linked N-acetyl glucosamine0-(GlcNAc) modifications play a central role in the regulation of plant signaling networks. Forexample, mutations in SPINDLY,) SPY (an O-GlcNAc transferase,) OGT (promote gibberellin GA) (signal transduction and inhibit cytokinin responses. In addition, mutating both Arabidopsis OGTsSEC (and SPY) causes embryo lethality. The long-term goal of this research is to elucidate the mechanism by which Arabidopsis OGTs regulate signaling networks. This project investigated the mechanisms of O-GlcNAc regulation of cytokinin and gibberellin signaling, identified additional processes regulated by this modification and investigated the regulation of SEC activity. Although SPY is a nucleocytoplasmic protein, its site of action and targets were unknown. Severalstudies suggested that SPY acted in the nucleus where it modified nuclear components such as the DELLA proteins. Using chimeric GFP-SPY fused to a nuclear-export signal or to a nuclear-import signal, we showed that cytosolic, but not nuclear SPY, regulated cytokinin and GA signaling. We also obtained evidence suggesting that GA and SPY affect cytokinin signaling via a DELLA-independent pathway. Although SEC and SPY were believed to have overlapping functions, the role of SEC in cytokinin and GA signaling was unclear. The role of SEC in cytokinin and GA responses was investigated by partially suppressing SPY expression in secplants using a synthetic Spymicro RNA miR(SPY). The possible contribution of SEC to the regulation of GA and cytokinin signaling wastest by determining the resistance of the miR spy secplants to the GA biosynthesis inhibitor paclobutrazol and to cytokinin. We found that the transgenic plants were resistant to paclobutrazol and to cytokinin, butonlyata level similar to spy. Moreover, expressing SEC under the 35S promoter in spy mutant did not complement the spy mutation. Therefore, we believe that SEC does not act with SPY to regulate GA or cytokinin responses. The cellular targets of Spy are largely unknown. We identified the transcription factor TCP15 in a two-hybrid screen for SPY-interacting proteins and showed that both TCP15 and its closely homolog TCP14 were O-GlcNAc modified by bacterially-produced SEC. The significance of the interaction between SPY and these TCPs was examined by over-expressing the minwild-type and spy-4plants. Overexpression of TCP14 or TCP15 in wild-type background produced phenotypes typical of plants with increased cytokinin and reduced GA signaling. TCP14 overexpression phenotypes were strongly suppressed in the spy background, suggesting that TCP14 and TCP15 affect cytokinin and GA signaling and that SPY activates them. In agreement with this hypothesis, we created a tcp14tcp15 double mutant and found that it has defects similar to spyplants. In animals, O-GlcNAc modification is proposed to regulate the activity of the nuclear pore. Therefore, after discovering that SEC modified a nucleoporinNUP) (that also interacts with SPY, we performed genetic experiments exploring the relationship between NUPs and SPY nupspy double mutants exhibited phenotypes consistent with SPY and NUPs functioning in common processes and nupseeds were resistant to GA biosynthesis inhibitors. All eukaryotic OGTs have a TPR domain. Deletion studies with bacterially-expressed SEC demonstrated SEC'sTPR domain inhibits SEC enzymatic activity. Since the TPR domain interacts with other proteins, we propose that regulatory proteins regulate OGT activity by binding and modulating the inhibitory activity of the TPR domain.
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