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Thematische Bibliographien / Signalling

Auswahl der wissenschaftlichen Literatur zum Thema „Signalling“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 6. September 2023

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Inhaltsverzeichnis

Zeitschriftenartikel
Dissertationen
Bücher
Buchteile
Konferenzberichte
Berichte der Organisationen

Zeitschriftenartikel zum Thema "Signalling":

1

Wheeler, Glen, Katherine Helliwell und Colin Brownlee. „Calcium signalling in algae“. Perspectives in Phycology 6, Nr. 1-2 (01.07.2019): 1–10. http://dx.doi.org/10.1127/pip/2018/0082.

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2

Kharor, Neeraj, und J. S. Dhanda. „Periplasmic Proteins: Signalling, Kinetics, Thermodynamics and Expression“. Journal of Advances and Scholarly Researches in Allied Education 15, Nr. 7 (01.09.2018): 138–46. http://dx.doi.org/10.29070/15/57842.

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3

ROBINS, P. M. „SIGNALLING.“ Proceedings of the Institution of Civil Engineers - Civil Engineering 108, Nr. 6 (November 1995): 49–53. http://dx.doi.org/10.1680/icien.1995.28049.

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4

Sun, Shan, Michal Johanis und Jan Rychtář. „Costly signalling theory and dishonest signalling“. Theoretical Ecology 13, Nr. 1 (04.05.2019): 85–92. http://dx.doi.org/10.1007/s12080-019-0429-0.

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5

Lafont, Elodie. „Stress Management: Death Receptor Signalling and Cross-Talks with the Unfolded Protein Response in Cancer“. Cancers 12, Nr. 5 (29.04.2020): 1113. http://dx.doi.org/10.3390/cancers12051113.

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Throughout tumour progression, tumour cells are exposed to various intense cellular stress conditions owing to intrinsic and extrinsic cues, to which some cells are remarkably able to adapt. Death Receptor (DR) signalling and the Unfolded Protein Response (UPR) are two stress responses that both regulate a plethora of outcomes, ranging from proliferation, differentiation, migration, cytokine production to the induction of cell death. Both signallings are major modulators of physiological tissue homeostasis and their dysregulation is involved in tumorigenesis and the metastastic process. The molecular determinants of the control between the different cellular outcomes induced by DR signalling and the UPR in tumour cells and their stroma and their consequences on tumorigenesis are starting to be unravelled. Herein, I summarize the main steps of DR signalling in relation to its cellular and pathophysiological roles in cancer. I then highlight how the UPR and DR signalling control common cellular outcomes and also cross-talk, providing potential opportunities to further understand the development of malignancies.

6

Omerovic, Jasminka, und Ian A. Prior. „Compartmentalized signalling: Ras proteins and signalling nanoclusters“. FEBS Journal 276, Nr. 7 (23.02.2009): 1817–25. http://dx.doi.org/10.1111/j.1742-4658.2009.06928.x.

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7

PÉREZ, A. CUÉLLAR, und A. GOOSSENS. „Jasmonate signalling: a copycat of auxin signalling?“ Plant, Cell & Environment 36, Nr. 12 (14.05.2013): 2071–84. http://dx.doi.org/10.1111/pce.12121.

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8

Huang, Dashun, Xiaojiao Li, Li Sun, Ping Huang, Hao Ying, Hui Wang, Jiarui Wu und Haiyun Song. „Regulation of Hippo signalling by p38 signalling“. Journal of Molecular Cell Biology 8, Nr. 4 (August 2016): 328–37. http://dx.doi.org/10.1093/jmcb/mjw036.

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9

Turrigiano, G. „Signalling mechanisms, Signalling development, survival, and plasticity“. Current Opinion in Neurobiology 12, Nr. 3 (01.06.2002): 241–43. http://dx.doi.org/10.1016/s0959-4388(02)00332-x.

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10

Kiselyov, Kirill, Dong Min Shin und Shmuel Muallem. „Signalling specificity in GPCR-dependent Ca2+ signalling“. Cellular Signalling 15, Nr. 3 (März 2003): 243–53. http://dx.doi.org/10.1016/s0898-6568(02)00074-8.

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Dissertationen zum Thema "Signalling":

1

Schelfaut, Roselien. „Integrin Signalling“. Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6265.

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Integrins are receptors presented on most cells. By binding ligand they can generate signalling pathways inside the cell. Those pathways are a linkage to proteins in the cytosol. It is known that tumor cells can survive and proliferate in the absence of a solid support while normal cells need to be bound to ligand. To understand why tumour cells act that way, we first have to know how ligand-binding to integrins affect the cell. This research field includes studies on activation of proteins by integrins and the following protein-protein interactions.

The part of the research that I did, focused on the activation of PI3K by integrins and the question whether Ras is included in that pathway. I also studied the conformation changes of the integrins and tried to identify factors which regulate these changes.

Known is that Ras can activate PI3K. But we wanted to know if this is a step in the activation of PI3K by integrins. So if this would be a fact then Ras must be activated by integrins.

To see if integrins could activate Ras I did a pull down assay. GTP loaded Ras was isolated through its affinity for Raf. Only when Ras is in its activated state then it is GTP loaded, otherwise it is GDP loaded. In the experiment we also compared the β1A and the β1B splice variants. As result we could see that both splice variants probably can activate Ras. By blotting with anti-PI3K antibody we looked if PI3K had bound to Ras but no clear result could be obtained.

Integrins presented on blood cells are mostly in the inactive state while adherent cells have integrins which are mostly in the active state. PI3K has been shown, for blood cells, to be involved in the conformation regulation of integrins. Possibly, there is a positive circle that for blood cells just has to be switched on. It could be that the integrins in adherent cells are active because the cells are adhesive. By being adhesive, PI3K is activated. PI3K may then activate the integrins, through which the integrins stay in the active state. This circle could be broken at two points: we could inhibit PI3K or we could make the cells un-adhesive. I analysed this in cell attachment assay and by binding of conformation-specific integrin antibodies in FACScan. From the results we could not find any evidence that the whole idea around the positive circle is correct. Surprisingly we saw that the integrin value at the surface decrease if you add PI3K inhibitor. This could be due to distribute recirculation of integrins from the cytoplasm to the cell surface.

β1- and β3-integrins are both widely spread, but no functional difference could be shown already. Previous results suggest that there is a difference between migrations of those two types. To ensure this suggestion I did a wound assay. Hereby I compared the migration of different cell types, with different integrins on their surface and on different ligands.

2

Demuth, Dirk Geoffrey. „Cannabinoid signalling“. Thesis, University of Hertfordshire, 2004. http://hdl.handle.net/2299/14229.

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The general aim of the study was to investigate the signalling pathways utilised by cannabinoids. Cannabinoid CB1 receptor stimulation in DDT, MF-2 smooth muscle cells induces a rise in [Ca2], which is dependent on extracellular Cat' and modulated by thapsigargin-sensitive stores and MAP kinase suggesting capacitative Ca2+ entry (CCE). Non-capacitative calcium entry (NCCE) stimulated by arachidonic acid (AA) partly mediates histamine Hl receptor-evoked increases in [Ca2+]; in DDTI MF-2 cells. In the current study both Ca 2+ entry mechanisms and a possible link between MAP kinase activation and increasing [Ca2+];, were investigated. In the whole-cell patch clamp configuration, the cannabinoid receptor agonist CP 55,940 evoked a transient Cat+-dependent K+ current, which was not blocked by inhibitors of CCE, 2-APB and SKF 96365, although SKF 96365 did inhibit the outward current evoked by the refilling component of the response to histamine. AA but not its metabolites evoked a transient outward current and inhibited the response to CP 55,940 in a concentration-dependent manner. CP 55,940 induced a concentration-dependent release of AA, which was inhibited by the CB1 receptor antagonist SR 141716A. The non-specific Ca2+ channel blockers, La3+ and Gd3+, inhibited the CP 55,940-induced current at concentrations that had no effect on thapsigargin-evoked CCE. La3+ also inhibited AA-mediated currents. The effect of CP 55,940 on AA release was abolished by phospholipase A2 inhibition with quinacrine. This compound also inhibited outward currents mediated by CP 55,940. The data supports the possibility that in DDT, MF-2 cells AA is an integral component of the CBI receptor signalling pathway, upstream of NCCE and, via PLA2, downstream of MAP kinase. In a parallel line of work the present study aimed to identify the signalling events that might mediate a cannabinoid-induced inhibition of neurotransmission in the myenteric plexus, leading to a reduction in intestinal motility. Myenteric neurons were grown in primary culture enabling electrophysiological recordings to be made from individual cells to study the effects of cannabinoids on ion conductance. Immunohistochemistry validated these neurons as a model for those in situ, demonstrating that all CB1 receptor-positive cells express the cholinergic marker choline acetyltransferase. CP 55,940 was not shown to activate G-protein inwardly rectifying K+ channels but did inhibit evoked Ca2+ currents in myenteric cultures, a signalling mechanism that may underlie the CB1 receptor-mediated inhibition of neurotransmitter release from presynaptic sites. Nicotinic ACh (nACh) receptors are also expressed on cultured myenteric neurons. Stimulation of these receptors by nicotine evoked a transient inward current, which was inhibited by CP 55,940 and the endogenous cannabinoid anandamide, in an SR 14716A-insensitive manner. In fact, SR 141716A alone inhibited currents mediated by nACh receptors. PEA, a cannabinoid ligand whose effects are thought to occur independently of CB1/ CB2 receptor activation, also inhibited nicotine-induced currents. Pertussis toxin, a Gil,, inhibitor, did not reverse the cannabinoid-induced inhibition of nicotinic currents. In addition, CP 55,940 inhibited the sustained inward current evoked by 5-11T application in cultured myenteric neurons. The results suggest that cannabinoids inhibit nACh channels through a CB1 receptor-independent pathway in myenteric neurons, which would lead to a reduction in excitatory neurotransmission in the intact myenteric plexus. The inhibitory effect on the 5-HTinduced sustained inward current also suggests a cannabinoid-evoked inhibition of currents possibly mediated by the 5-HT1p receptor.

3

Potter, Timothy James. „Transmembrane signalling“. Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275041.

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4

O'Byrne, Declan. „CD28 and associated signalling elements of T lymphocyte signalling“. Thesis, University of Bath, 1998. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266468.

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5

Shivdasani, Anish Anil. „Hedgehog signalling, TGF-Î² signalling and spermatogenesis in Drosophila melanogaster“. Thesis, University of Sheffield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408836.

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6

Jordan, Lindsay. „Signalling Towards IRES“. Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19946.

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XIAP and Bcl-xL are critical anti-apoptotic molecules that directly inhibit caspases and block mitochondrial membrane permeabilization, respectively. In addition to preventing apoptosis, both XIAP and Bcl-xL can be generated by cap-independent translation via the utilization of an IRES in the 5'-UTR of their mRNAs. In recent years it has been shown that activation of S6K2 induces the translational upregulation of these two apoptotic regulators. Here I have determined that activation of S6K2 enhances IRES-mediated translation of XIAP and Bcl-xL by inducing the degradation of PDCD4, which I have identified as a novel regulator of XIAP and Bcl-xL IRES elements. Furthermore, I have shown that PDCD4 is a positive modulator of the Apaf-1 IRES element. The concurrent regulation of XIAP, Bcl-xL and Apaf-1 by PDCD4 suggests a model in which the level of PDCD4 expression alters the apoptotic threshold by specifically impacting IRES-mediated translation of the XIAP, Bcl-xL and Apaf-1 mRNAs.

7

Anderson, Ian Paul. „Met receptor signalling“. Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526784.

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8

Clynes, David Alexander. „Signalling to chromatin“. Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496840.

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9

Samuels, Michael L. „Yeast stress signalling“. Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368116.

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Is'Harc, Hayaatun. „JAK/STAT signalling“. Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272414.

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Bücher zum Thema "Signalling":

1

Manterfield, Richard J. Telecommunications signalling. London: Institution of Electrical Engineers, 1999.

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2

Hancock, John T. Cell signalling. 3. Aufl. Oxford: Oxford University Press, 2010.

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3

Hancock, John T. Cell signalling. 2. Aufl. Oxford: Oxford University Press, 2005.

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4

Khan, Mohd Tanveer Alam, Mohammad Yusuf, Fariduddin Qazi und Aqeel Ahmad, Hrsg. Brassinosteroids Signalling. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-5743-6.

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5

Raffaello, Anna, und Denis Vecellio Reane, Hrsg. Calcium Signalling. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9018-4.

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6

Kaestner, Lars. Calcium signalling. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-34617-0.

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7

Hancock, John T. Cell signalling. 3. Aufl. Oxford: Oxford University Press, 2010.

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8

1954-, Parker Peter J., und Pawson T, Hrsg. Cell signalling. Plainview, NY: Cold Spring Harbor Laboratory Press, 1996.

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9

Hancock, John T. Cell signalling. Harlow: Longman, 1997.

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10

Bowles. Cell Signalling. London: Portland Press, 1998.

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Buchteile zum Thema "Signalling":

1

Bannier, Christina E. „Signalling“. In Physica-Lehrbuch, 147–59. Heidelberg: Physica-Verlag HD, 2005. http://dx.doi.org/10.1007/3-7908-1632-9_16.

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2

Lindner, Ines. „Signalling“. In Encyclopedia of Law and Economics, 1904–11. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-7753-2_439.

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3

Lindner, Ines. „Signalling“. In Encyclopedia of Law and Economics, 1–8. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7883-6_439-1.

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4

Adlung, Lorenz. „Signalling“. In Cell and Molecular Biology for Non-Biologists, 61–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-65357-9_6.

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5

Riley, John G. „Signalling“. In The New Palgrave Dictionary of Economics, 1–6. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1057/978-1-349-95121-5_1557-1.

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6

Riley, John G. „Signalling“. In The New Palgrave Dictionary of Economics, 12309–14. London: Palgrave Macmillan UK, 2018. http://dx.doi.org/10.1057/978-1-349-95189-5_1557.

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Riley, John G. „Signalling“. In Allocation, Information and Markets, 287–94. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-20215-7_29.

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8

Salih, Saif, und Charles Patrick Case. „Barrier Signalling“. In Nanomedicine and Nanotoxicology, 245–58. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-55139-3_14.

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9

Brusse, Carl. „Animal Signalling“. In Encyclopedia of Evolutionary Psychological Science, 1–4. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-16999-6_2146-1.

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10

Adriaensen, Johan. „Signalling Control“. In National Administrations in EU Trade Policy, 63–85. London: Palgrave Macmillan UK, 2016. http://dx.doi.org/10.1057/978-1-137-54767-5_4.

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Konferenzberichte zum Thema "Signalling":

1

Fenner, D. „Railway signalling“. In 3rd IET Professional Development Course on Railway Electrification Infrastructure and Systems. IET, 2007. http://dx.doi.org/10.1049/ic.2007.1649.

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Fenner, D. „Railway signalling“. In 4th IET Professional Development Course on Railway Electrification Infrastructure & Systems (REIS). IET, 2009. http://dx.doi.org/10.1049/ic.2009.0011.

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Fenner, D. „Railway signalling“. In 5th IET Professional Development Course on Railway Electrification Infrastructure and Systems (REIS 2011). IET, 2011. http://dx.doi.org/10.1049/ic.2011.0183.

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4

Manohar, Rajit, und Yoram Moses. „Asynchronous Signalling Processes“. In 2019 25th IEEE International Symposium on Asynchronous Circuits and Systems (ASYNC). IEEE, 2019. http://dx.doi.org/10.1109/async.2019.00018.

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5

Rahman, M. „Signalling power supplies“. In IET Seminar on Signalling and Power Distribution. IEE, 2006. http://dx.doi.org/10.1049/ic:20060627.

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6

Nicholson, T. J. „Trainborne signalling equipment“. In 11th IET Professional Development Course on Railway Signalling and Control Systems. Institution of Engineering and Technology, 2006. http://dx.doi.org/10.1049/ic.2006.0687.

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7

Mitchell, I. H. „Mainline signalling control“. In 11th IET Professional Development Course on Railway Signalling and Control Systems. Institution of Engineering and Technology, 2006. http://dx.doi.org/10.1049/ic.2006.0693.

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How, F. „Signalling the future“. In IET Professional Development Course on Railway Signalling and Control Systems (RSCS 2012). IET, 2012. http://dx.doi.org/10.1049/ic.2012.0039.

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Christmas, G. „Signalling system requirements“. In IET Seminar on Power Distribution for Signalling Systems. IEE, 2007. http://dx.doi.org/10.1049/ic:20070003.

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10

Spiers, I. „The future of signalling“. In IEE Colloquium on Signalling for Broadband. IEE, 1995. http://dx.doi.org/10.1049/ic:19951583.

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Berichte der Organisationen zum Thema "Signalling":

1

Maher, M. ATM Signalling Support for IP over ATM - UNI Signalling 4.0 Update. RFC Editor, April 1998. http://dx.doi.org/10.17487/rfc2331.

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Williams, A., K. Gross, R. van Brandenburg und H. Stokking. RTP Clock Source Signalling. RFC Editor, Juni 2014. http://dx.doi.org/10.17487/rfc7273.

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Schulzrinne, H., und R. Hancock. GIST: General Internet Signalling Transport. RFC Editor, Oktober 2010. http://dx.doi.org/10.17487/rfc5971.

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Boss, W. Cell signalling and phospholipid metabolism. Office of Scientific and Technical Information (OSTI), Januar 1989. http://dx.doi.org/10.2172/5943691.

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Boss, W. F. Cell signalling and phospholipid metabolism. Office of Scientific and Technical Information (OSTI), Januar 1990. http://dx.doi.org/10.2172/7045128.

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6

Library, Spring. Where Does Current Quorum Sensing Research Stand. Spring Library, Dezember 2020. http://dx.doi.org/10.47496/sl.blog.16.

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Quorum quenching is achieved by inactivating signalling enzymes, by introducing molecules that mimic signalling molecules and block their receptors, by degrading signalling molecules themselves, or by a modification of the quorum sensing signals due to an enzyme activity.

7

Boss, W. F. Cell signalling and phospholipid metabolism. Final report. Office of Scientific and Technical Information (OSTI), Dezember 1990. http://dx.doi.org/10.2172/10168282.

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8

Caselli, Francesco, Thomas Cunningham, Massimo Morelli und Inés Moreno de Barreda. Signalling, Incumbency Advantage, and Optimal Reelection Thresholds. Cambridge, MA: National Bureau of Economic Research, Februar 2012. http://dx.doi.org/10.3386/w17833.

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9

Persson, Torsten, und Sweder van Wijnbergen. Signalling, Wage Controls and Monetary Disinflation Policy. Cambridge, MA: National Bureau of Economic Research, April 1989. http://dx.doi.org/10.3386/w2939.

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10

Trostle, Jonathan T. The Serial Product of Controlled Signalling Systems. Fort Belvoir, VA: Defense Technical Information Center, Dezember 1991. http://dx.doi.org/10.21236/ada244576.

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