Journal articles: 'SIGNALLING MECHANISM'

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BILLESTRUP, NILS, JOHNNY A. HANSEN, LONE H. HANSEN, ANNETTE H. MOLDRUP, ELISABETH D. GALSGAARD, and JENS H. NIELSEN. "Molecular Mechanism of Growth Hormone Signalling." Endocrine Journal 45, Suppl (1998): S41—S45. http://dx.doi.org/10.1507/endocrj.45.suppl_s41.

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Villalobos-Labra, Roberto, Luis Silva, Mario Subiabre, Joaquín Araos, Rocío Salsoso, Bárbara Fuenzalida, Tamara Sáez, et al. "Akt/mTOR Role in Human Foetoplacental Vascular Insulin Resistance in Diseases of Pregnancy." Journal of Diabetes Research 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/5947859.

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Insulin resistance is characteristic of pregnancies where the mother shows metabolic alterations, such as preeclampsia (PE) and gestational diabetes mellitus (GDM), or abnormal maternal conditions such as pregestational maternal obesity (PGMO). Insulin signalling includes activation of insulin receptor substrates 1 and 2 (IRS1/2) as well as Src homology 2 domain-containing transforming protein 1, leading to activation of 44 and 42 kDa mitogen-activated protein kinases and protein kinase B/Akt (Akt) signalling cascades in the human foetoplacental vasculature. PE, GDM, and PGMO are abnormal conditions coursing with reduced insulin signalling, but the possibility of the involvement of similar cell signalling mechanisms is not addressed. This review aimed to determine whether reduced insulin signalling in PE, GDM, and PGMO shares a common mechanism in the human foetoplacental vasculature. Insulin resistance in these pathological conditions results from reduced Akt activation mainly due to inhibition of IRS1/2, likely due to the increased activity of the mammalian target of rapamycin (mTOR) resulting from lower activity of adenosine monophosphate kinase. Thus, a defective signalling via Akt/mTOR in response to insulin is a central and common mechanism of insulin resistance in these diseases of pregnancy. In this review, we summarise the cell signalling mechanisms behind the insulin resistance state in PE, GDM, and PGMO focused in the Akt/mTOR signalling pathway in the human foetoplacental endothelium.

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Laurinen, P. I., and L. A. Olzak. "Functional Aspects of Border-Signalling Mechanisms." Perception 25, no. 1_suppl (August 1996): 92. http://dx.doi.org/10.1068/v96l1208.

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Multiple border-signalling mechanisms have been proposed in some models of object segregation. We investigated whether distinct functions of different border mechanisms could be isolated in human psychophysical tasks. The display was a low-spatial-frequency (1.5 cycles deg−1) sinusoidal grating. Two types of centre-surround stimuli were produced by (i) increasing or decreasing the mean luminance of a central patch of the grating to create a signed luminance border (LB), or (ii) by shifting the grating within the central patch 180° to create a sign-reversing border (PSB) without a change in mean luminance. Grating contrast was kept constant at 20%. Observers performed a spatial 2AFC task in each condition. The PSB stimulus served as the comparison stimulus. Test stimuli were either LB or PSB+LB. The mean luminance of the central test patches varied over trials to create border contrasts of −15% to 15% Michelson contrast. In separate sessions, subjects made four types of comparisons: which of the two central areas appeared (1) to differ more in depth from its surround; (2) to have greater modulation contrast of the sinusoid; (3) lighter/darker, (4) to have higher border contrast. Results depended strongly upon test border type and suggested that the mechanism responding to each has a distinct and different perceptual function, and the two may interact. Our results support the hypothesis that surface lightness is calculated by a sign-preserving mechanism, whereas a phase-insensitive mechanism is involved in percepts relating to segregation in depth.

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Pagliaro, P., and C. Penna. "Redox signalling and cardioprotection: translatability and mechanism." British Journal of Pharmacology 172, no. 8 (January 12, 2015): 1974–95. http://dx.doi.org/10.1111/bph.12975.

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Ye, Hong, Joseph R. Arron, Betty Lamothe, Maurizio Cirilli, Takashi Kobayashi, Nirupama K. Shevde, Deena Segal, et al. "Distinct molecular mechanism for initiating TRAF6 signalling." Nature 418, no. 6896 (July 2002): 443–47. http://dx.doi.org/10.1038/nature00888.

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ROBBINS, EDWARD HENRY, and JOHN D. SCHATZBERG. "Callable Bonds: A Risk-Reducing Signalling Mechanism." Journal of Finance 41, no. 4 (September 1986): 935–49. http://dx.doi.org/10.1111/j.1540-6261.1986.tb04558.x.

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Broz, Petr, and Vishva M. Dixit. "Inflammasomes: mechanism of assembly, regulation and signalling." Nature Reviews Immunology 16, no. 7 (June 13, 2016): 407–20. http://dx.doi.org/10.1038/nri.2016.58.

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García-Padilla, Carlos, Estefanía Lozano-Velasco, Carmen López-Sánchez, Virginio Garcia-Martínez, Amelia Aranega, and Diego Franco. "Non-Coding RNAs in Retinoic Acid as Differentiation and Disease Drivers." Non-Coding RNA 7, no. 1 (February 17, 2021): 13. http://dx.doi.org/10.3390/ncrna7010013.

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All-trans retinoic acid (RA) is the most active metabolite of vitamin A. Several studies have described a pivotal role for RA signalling in different biological processes such as cell growth and differentiation, embryonic development and organogenesis. Since RA signalling is highly dose-dependent, a fine-tuning regulatory mechanism is required. Thus, RA signalling deregulation has a major impact, both in development and disease, related in many cases to oncogenic processes. In this review, we focus on the impact of ncRNA post-transcriptional regulatory mechanisms, especially those of microRNAs and lncRNAs, in RA signalling pathways during differentiation and disease.

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Winterbourn, Christine C. "Hydrogen peroxide reactivity and specificity in thiol-based cell signalling." Biochemical Society Transactions 48, no. 3 (May 15, 2020): 745–54. http://dx.doi.org/10.1042/bst20190049.

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Reversible oxidation of thiol proteins is an important cell signalling mechanism. In many cases, this involves generation or exposure of the cells to H2O2, and oxidation of proteins that are not particularly H2O2-reactive. There is a conundrum as to how these proteins are oxidised when other highly reactive proteins such as peroxiredoxins are present. This article discusses potential mechanisms, focussing on recent evidence for oxidation being localised within the cell, redox relays involving peroxiredoxins operating in some signalling pathways, and mechanisms for facilitated or directed oxidation of specific targets. These findings help define conditions that enable redox signalling but there is still much to learn regarding mechanisms.

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Tsydenova, Irina A., Daria S. Dolgasheva, Ksenia A. Gaptulbarova, Marina K. Ibragimova, Matvei M. Tsyganov, Ekaterina A. Kravtsova, Anna A. Nushtaeva, and Nikolai V. Litviakov. "WNT-Conditioned Mechanism of Exit from Postchemotherapy Shock of Differentiated Tumour Cells." Cancers 15, no. 10 (May 15, 2023): 2765. http://dx.doi.org/10.3390/cancers15102765.

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Background: the present study aims to prove or disprove the hypothesis that the state of copy number aberration (CNA) activation of WNT signalling pathway genes accounts for the ability of differentiated tumour cells to emerge from postchemotherapy shock. Methods: In the first step, the CNA genetic landscape of breast cancer cell lines BT-474, BT-549, MDA-MB-231, MDA-MD-468, MCF7, SK-BR-3 and T47D, which were obtained from ATCC, was examined to rank cell cultures according to the degree of ectopic activation of the WNT signalling pathway. Then two lines of T47D with ectopic activation and BT-474 without activation were selected. The differentiated EpCAM+CD44-CD24-/+ cells of these lines were subjected to IL6 de-differentiation with formation of mammospheres on the background of cisplatin and WNT signalling inhibitor ICG-001. Results: it was found that T47D cells with ectopic WNT signalling activation after cisplatin exposure were dedifferentiated to form mammospheres while BT-474 cells without ectopic WNT-signalling activation did not form mammospheres. The dedifferentiation of T47D cells after cisplatin exposure was completely suppressed by the WNT signalling inhibitor ICG-001. Separately, ICG-001 reduced, but did not abolish, the ability to dedifferentiate in both cell lines. Conclusions: these data support the hypothesis that the emergence of differentiated tumour cells from postchemotherapy shock after chemotherapy is due to ectopic activation of WNT signalling pathway genes.

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Kalderon, D. "The mechanism of hedgehog signal transduction." Biochemical Society Transactions 33, no. 6 (October 26, 2005): 1509–12. http://dx.doi.org/10.1042/bst0331509.

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Hedgehog (Hh) proteins are one of a small number of families of secreted signalling proteins that are responsible for cell interactions during development in many animals. As such, Hh signals produce many different responses at different times and in different cells. As for other multifunctional ligands, this requires regulated patterns of expression, special mechanisms for ligand movement between cells and ligand destruction, and mechanisms for integrating a generic signalling state (on or off) with the status of responding cells in order to produce an appropriate cell-specific response. Here I discuss what is known about the biochemical mechanisms by which an Hh signal is transduced in order to change the patterns of gene transcription.

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Cordeiro, Aline, Luana Lopes Souza, Marcelo Einicker-Lamas, and Carmen Cabanelas Pazos-Moura. "Non-classic thyroid hormone signalling involved in hepatic lipid metabolism." Journal of Endocrinology 216, no. 3 (January 7, 2013): R47—R57. http://dx.doi.org/10.1530/joe-12-0542.

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Thyroid hormones are important modulators of lipid metabolism because the liver is a primary hormonal target. The hypolipidaemic effects of thyroid hormones result from the balance between direct and indirect actions resulting in stimulation of lipid synthesis and lipid oxidation, which favours degradation pathways. Originally, it was believed that thyroid hormone activity was only transduced by alteration of gene transcription mediated by the nuclear receptor thyroid hormone receptors, comprising the classic action of thyroid hormone. However, the discovery of other effects independent of this classic mechanism characterised a new model of thyroid hormone action, the non-classic mechanism that involves other signalling pathways. To date, this mechanism and its relevance have been intensively described. Considering the increasing evidence for non-classic signalling of thyroid hormones and the major influence of these hormones in the regulation of lipid metabolism, we reviewed the role of thyroid hormone in cytosolic signalling cascades, focusing on the regulation of second messengers, and the activity of effector proteins and the implication of these mechanisms on the control of hepatic lipid metabolism.

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Hu, Z. Y., and J. Liu. "Mechanism of Cardiac Preconditioning with Volatile Anaesthetics." Anaesthesia and Intensive Care 37, no. 4 (July 2009): 532–38. http://dx.doi.org/10.1177/0310057x0903700402.

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In recent years, there has been increased interest in the mechanisms involved in anaesthetic-induced cardioprotection. It is not thoroughly understood how volatile anaesthetics protect the myocardium from ischaemia or reperfusion injury, but the overall mechanism is likely to be multifactorial. This review examines the recent experimental and clinical research underlying the cellular and molecular mechanisms involved in anaesthetic-induced preconditioning. A variety of intracellular signalling pathways have been implicated in the protective phenomenon. Ischaemic preconditioning and anaesthetic-induced preconditioning share similar molecular mechanisms, including activation of guanine nucleotide-binding proteins, triggering of second messenger pathways, activation of multiple kinases, mediation of nitric oxide formation and reactive oxygen species release, maintenance of intracellular and/or mitochondrial Ca2+ homeostasis and moderation of the opening of adenosine-triphosphate-sensitive potassium channels. A more thorough understanding of the multiple signalling steps and the ultimate cytoprotective mechanisms underlying anaesthetic-induced preconditioning may lead to improvements in the management of ischaemia and/or reperfusion injury.

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Lund, I. K., J. A. Hansen, H. S. Andersen, N. P. H. Møller, and N. Billestrup. "Mechanism of protein tyrosine phosphatase 1B-mediated inhibition of leptin signalling." Journal of Molecular Endocrinology 34, no. 2 (April 2005): 339–51. http://dx.doi.org/10.1677/jme.1.01694.

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Upon leptin binding, the leptin receptor is activated, leading to stimulation of the JAK/STAT signal transduction cascade. The transient character of the tyrosine phosphorylation of JAK2 and STAT3 suggests the involvement of protein tyrosine phosphatases (PTPs) as negative regulators of this signalling pathway. Specifically, recent evidence has suggested that PTP1B might be a key regulator of leptin signalling, based on the resistance to diet-induced obesity and increased leptin signalling observed in PTP1B-deficient mice. The present study was undertaken to investigate the mechanism by which PTP1B mediates the cessation of the leptin signal transduction. Leptin-induced activation of a STAT3 responsive reporter was dose-dependently inhibited by co-transfection with PTP1B. No inhibition was observed when a catalytically inactive mutant of PTP1B was used or when other PTPs were co-transfected. PTP1B was able to dephosphorylate activated JAK2 and STAT3 in vitro, whereas either no or a minimal effect was observed with cluster of differentiation 45 (CD45), PTPα and leukocyte antigen-related (LAR). By utilisation of a selective PTP1B inhibitor, the leptin-induced STAT3 activation was enhanced in cells. In conclusion, these results suggested that the negative regulatory role of PTP1B on leptin signalling is mediated through a direct and selective dephosphorylation of the two signalling molecules, JAK2 and STAT3.

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Juillot, Samuel, Hannes M. Beyer, Josef Madl, Wilfried Weber, Matias D. Zurbriggen, and Winfried Römer. "Signalling to the nucleus under the control of light and small molecules." Molecular BioSystems 12, no. 2 (2016): 345–49. http://dx.doi.org/10.1039/c5mb00763a.

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One major regulatory mechanism in cell signalling is the spatio-temporal control of the localization of signalling molecules. We synthetically designed an entire cell signalling pathway, which allows controlling the transport of signalling molecules from the plasma membrane to the nucleus, by using light and small molecules.

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Hirose, Munetaka, J. A. Jeevendra Martyn, Yoshihiro Kuroda, Yoshinori Marunaka, and Yoshifumi Tanaka. "Mechanism of suppression of insulin signalling with lignocaine." British Journal of Pharmacology 136, no. 1 (May 2002): 76–80. http://dx.doi.org/10.1038/sj.bjp.0704691.

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Smith, Steven P., and Gary S. Shaw. "A change-in-hand mechanism for S100 signalling." Biochemistry and Cell Biology 76, no. 2-3 (May 1, 1998): 324–33. http://dx.doi.org/10.1139/o98-062.

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S100 proteins are a group of small dimeric calcium-binding proteins making up a large subclass of the EF-hand family of calcium-binding proteins. Members of this family of proteins have been proposed to act as intracellular calcium modulatory proteins in a fashion analogous to that of the EF-hand sensor proteins troponin-C and calmodulin. Recently, NMR spectroscopy has provided the three-dimensional structures of the S100 family members S100A6 and S100B in both the apo- and calcium-bound forms. These structures have allowed for the identification of a novel calcium-induced conformational change termed the change-in-hand mechanism. Helix III of the C-terminal calcium-binding loop changes its helix-helix interactions (or handness) with the remainder of the molecule primarily owing to the reorientation of the backbone in an effort to coordinate the calcium ion. This reorientation of helix III exposes several residues in the C-terminus and linker regions of S100B resulting in the formation of a hydrophobic patch surrounded be a number of acidic residues. This site is the proposed region for protein-protein recognition.Key words: S100, calcium-binding protein, EF-hand, conformational change.

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Wong, D. L., and T. C. Tai. "444. Phenylethanolamine N-methyltransferase gene: neural signalling mechanism." Biological Psychiatry 47, no. 8 (April 2000): S136. http://dx.doi.org/10.1016/s0006-3223(00)00714-9.

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Peso, Marianne, Mark A. Elgar, and Andrew B. Barron. "Pheromonal control: reconciling physiological mechanism with signalling theory." Biological Reviews 90, no. 2 (June 13, 2014): 542–59. http://dx.doi.org/10.1111/brv.12123.

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Shiva, Sruti, Doug Moellering, Anup Ramachandran, Anna-Liisa Levonen, Aimee Landar, Aparna Venkatraman, Erin Ceaser, et al. "Redox signalling: from nitric oxide to oxidized lipids." Biochemical Society Symposia 71 (March 1, 2004): 107–20. http://dx.doi.org/10.1042/bss0710107.

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Cellular redox signalling is mediated by the post-translational modification of proteins in signal-transduction pathways by ROS/RNS (reactive oxygen species/reactive nitrogen species) or the products derived from their reactions. NO is perhaps the best understood in this regard with two important modifications of proteins known to induce conformational changes leading to modulation of function. The first is the addition of NO to haem groups as shown for soluble guanylate cyclase and the newly discovered NO/cytochrome c oxidase signalling pathway in mitochondria. The second mechanism is through the modification of thiols by NO to form an S-nitrosated species. Other ROS/RNS can also modify signalling proteins although the mechanisms are not as clearly defined. For example, electrophilic lipids, formed as the reaction products of oxidation reactions, orchestrate adaptive responses in the vasculature by reacting with nucleophilic cysteine residues. In modifying signalling proteins ROS/RNS appear to change the overall activity of signalling pathways in a process that we have termed 'redox tone'. In this review, we discuss these different mechanisms of redox cell signalling, and give specific examples of ROS/RNS participation in signal transduction.

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Carr, Richard, and Jeffrey L. Benovic. "From biased signalling to polypharmacology: unlocking unique intracellular signalling using pepducins." Biochemical Society Transactions 44, no. 2 (April 11, 2016): 555–61. http://dx.doi.org/10.1042/bst20150230.

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For over a decade, pepducins have been utilized to develop unique pharmacological profiles that have been particularly challenging for traditional drug discovery methods. It is becoming increasingly clear that these cell-penetrating lipopeptides can access receptor conformations that are currently not accessible through orthosteric targeting. This review addresses the emerging concepts in the development of pepducins including the elicitation of biased signalling, pepducin polypharmacology and recent insight into their mechanism of action.

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Sancak, Yasemin, and David M. Sabatini. "Rag proteins regulate amino-acid-induced mTORC1 signalling." Biochemical Society Transactions 37, no. 1 (January 20, 2009): 289–90. http://dx.doi.org/10.1042/bst0370289.

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The serum- and nutrient-sensitive protein kinase mTOR (mammalian target of rapamycin) is a master regulator of cell growth and survival. The mechanisms through which nutrients regulate mTOR have been one of the major unanswered questions in the mTOR field. Identification of the Rag (Ras-related GTPase) family of GTPases as mediators of amino acid signalling to mTOR is an important step towards our understanding of this mechanism.

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Zampieri, N., and M. V. Chao. "Mechanisms of neurotrophin receptor signalling." Biochemical Society Transactions 34, no. 4 (July 21, 2006): 607–11. http://dx.doi.org/10.1042/bst0340607.

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Regulation of cell survival decisions and neuronal plasticity by neurotrophins are mediated by two classes of receptors, Trks (tropomyosin receptor kinases) and p75, the first discovered member of the tumour necrosis factor receptor superfamily. The p75 receptor participates with the TrkA receptor in the formation of high-affinity nerve growth factor-binding sites to promote survival under limiting concentrations of neurotrophins. Activation of Trk receptors leads to increased phosphorylation of Shc (Src homology and collagen homology), phospholipase C-γ and novel adaptor molecules, such as the ARMS (ankyrin-rich membrane spanning)/Kidins220 protein. Small ligands that interact with G-protein-coupled receptors can also activate Trk receptor kinase activity. Transactivation of Trk receptors and their downstream signalling pathways raise the possibility of using small molecules to elicit neuroprotective effects for the treatment of neurodegenerative diseases. Like amyloid precursor protein and Notch, p75 is a substrate for γ-secretase cleavage. The p75 receptor undergoes an α-secretase-mediated release of the extracellular domain followed by a γ-secretase-mediated intramembrane cleavage. Cleavage of p75 may represent a general mechanism for transmitting signals as an independent receptor and as a co-receptor for other signalling systems.

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Murray, P. J. "STAT3-mediated anti-inflammatory signalling." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1028–31. http://dx.doi.org/10.1042/bst0341028.

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IL-1O (interleukin-10) negatively regulates inflammation through a mechanism that blocks the expression of pro-inflammatory genes encoding cytokines, chemokines, cell-surface molecules and other molecules required for the full activation of the innate and adaptive immune responses. The signalling pathway used by the IL-10 receptor to generate the anti-inflammatory response requires STAT3 (signal transducer and activator of transcription 3) and is indirect. Thus STAT3 activates other genes whose task is to selectively control transcription of inflammatory targets. Here, I summarize current knowledge of the key features of IL-10 signalling and make predictions concerning the mechanism of IL-10 at the level of inflammatory genes. Understanding IL-10 signalling should be a gateway to the development of broadly acting anti-inflammatory agents.

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Pfannschmidt, Thomas, Matthew J. Terry, Olivier Van Aken, and Pedro M. Quiros. "Retrograde signals from endosymbiotic organelles: a common control principle in eukaryotic cells." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1801 (May 4, 2020): 20190396. http://dx.doi.org/10.1098/rstb.2019.0396.

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Endosymbiotic organelles of eukaryotic cells, the plastids, including chloroplasts and mitochondria, are highly integrated into cellular signalling networks. In both heterotrophic and autotrophic organisms, plastids and/or mitochondria require extensive organelle-to-nucleus communication in order to establish a coordinated expression of their own genomes with the nuclear genome, which encodes the majority of the components of these organelles. This goal is achieved by the use of a variety of signals that inform the cell nucleus about the number and developmental status of the organelles and their reaction to changing external environments. Such signals have been identified in both photosynthetic and non-photosynthetic eukaryotes (known as retrograde signalling and retrograde response, respectively) and, therefore, appear to be universal mechanisms acting in eukaryotes of all kingdoms. In particular, chloroplasts and mitochondria both harbour crucial redox reactions that are the basis of eukaryotic life and are, therefore, especially susceptible to stress from the environment, which they signal to the rest of the cell. These signals are crucial for cell survival, lifespan and environmental adjustment, and regulate quality control and targeted degradation of dysfunctional organelles, metabolic adjustments, and developmental signalling, as well as induction of apoptosis. The functional similarities between retrograde signalling pathways in autotrophic and non-autotrophic organisms are striking, suggesting the existence of common principles in signalling mechanisms or similarities in their evolution. Here, we provide a survey for the newcomers to this field of research and discuss the importance of retrograde signalling in the context of eukaryotic evolution. Furthermore, we discuss commonalities and differences in retrograde signalling mechanisms and propose retrograde signalling as a general signalling mechanism in eukaryotic cells that will be also of interest for the specialist. This article is part of the theme issue ‘Retrograde signalling from endosymbiotic organelles’.

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Mahmood, Sanabil A. "Proposed a WebRTC Data Communication Using Effective Signalling Protocol." Technium: Romanian Journal of Applied Sciences and Technology 4, no. 10 (December 6, 2022): 83–96. http://dx.doi.org/10.47577/technium.v4i10.7956.

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Web Real-Time Communication (WebRTC) is designed to permit the co-occurrence of audio, video, and data communications. However, an effective signalling mechanism that setup, establish and end communication between peers has not been specified in WebRTC. This paper designs and implements an effective WebRTC signalling mechanism for data communication compared with the common existing applications and current reviews. Moreover, it focuses on the limitations of multi-browsers communication and data. As long as no elaboration specifies how the signalling mechanism can be used in WebRTC because it does not understand the concept of sessions but rather that of streams, which create and consumes media flows. In addition, this research will elaborate on the related work and analyse the communication quality of data communications, such as data, audio, and video. Keywords: Web Real-time Communication (WebRTC); Signalling Protocols.

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Hadjivasiliou, Zena, Ginger L. Hunter, and Buzz Baum. "A new mechanism for spatial pattern formation via lateral and protrusion-mediated lateral signalling." Journal of The Royal Society Interface 13, no. 124 (November 2016): 20160484. http://dx.doi.org/10.1098/rsif.2016.0484.

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Tissue organization and patterning are critical during development when genetically identical cells take on different fates. Lateral signalling plays an important role in this process by helping to generate self-organized spatial patterns in an otherwise uniform collection of cells. Recent data suggest that lateral signalling can be mediated both by junctional contacts between neighbouring cells and via cellular protrusions that allow non-neighbouring cells to interact with one another at a distance. However, it remains unclear precisely how signalling mediated by these distinct types of cell–cell contact can physically contribute to the generation of complex patterns without the assistance of diffusible morphogens or pre-patterns. To explore this question, in this work we develop a model of lateral signalling based on a single receptor/ligand pair as exemplified by Notch and Delta. We show that allowing the signalling kinetics to differ at junctional versus protrusion-mediated contacts, an assumption inspired by recent data which show that the cleavage of Notch in several systems requires both Delta binding and the application of mechanical force, permits individual cells to act to promote both lateral activation and lateral inhibition. Strikingly, under this model, in which Delta can sequester Notch, a variety of patterns resembling those typical of reaction–diffusion systems is observed, together with more unusual patterns that arise when we consider changes in signalling kinetics, and in the length and distribution of protrusions. Importantly, these patterns are self-organizing—so that local interactions drive tissue-scale patterning. Together, these data show that protrusions can, in principle, generate different types of patterns in addition to contributing to long-range signalling and to pattern refinement.

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Biernaskie, Jay M., Alan Grafen, and Jennifer C. Perry. "The evolution of index signals to avoid the cost of dishonesty." Proceedings of the Royal Society B: Biological Sciences 281, no. 1790 (September 7, 2014): 20140876. http://dx.doi.org/10.1098/rspb.2014.0876.

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Animals often convey useful information, despite a conflict of interest between the signaller and receiver. There are two major explanations for such ‘honest’ signalling, particularly when the size or intensity of signals reliably indicates the underlying quality of the signaller. Costly signalling theory (including the handicap principle) predicts that dishonest signals are too costly to fake, whereas the index hypothesis predicts that dishonest signals cannot be faked. Recent evidence of a highly conserved causal link between individual quality and signal growth appears to bolster the index hypothesis. However, it is not clear that this also diminishes costly signalling theory, as is often suggested. Here, by incorporating a mechanism of signal growth into costly signalling theory, we show that index signals can actually be favoured owing to the cost of dishonesty. We conclude that costly signalling theory provides the ultimate, adaptive rationale for honest signalling, whereas the index hypothesis describes one proximate (and potentially very general) mechanism for achieving honesty.

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Jeon, Tae-Il, Young-Kyo Seo, and Timothy F. Osborne. "Gut bitter taste receptor signalling induces ABCB1 through a mechanism involving CCK." Biochemical Journal 438, no. 1 (July 27, 2011): 33–37. http://dx.doi.org/10.1042/bj20110009.

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T2Rs (bitter taste-sensing type 2 receptors) are expressed in the oral cavity to prevent ingestion of dietary toxins through taste avoidance. They are also expressed in other cell types, including gut enteroendocrine cells, where their physiological role is enigmatic. Previously, we proposed that T2R-dependent CCK (cholecystokinin) secretion from enteroendocrine cells limits absorption of dietary toxins, but an active mechanism was lacking. In the present study we show that T2R signalling activates ABCB1 (ATP-binding cassette B1) in intestinal cells through a CCK signalling mechanism. PTC (phenylthiocarbamide), an agonist for the T2R38 bitter receptor, increased ABCB1 expression in both intestinal cells and mouse intestine. PTC induction of ABCB1 was decreased by either T2R38 siRNA (small interfering RNA) or treatment with YM022, a gastrin receptor antagonist. Thus gut ABCB1 is regulated through signalling by CCK/gastrin released in response to PTC stimulation of T2R38 on enteroendocrine cells. We also show that PTC increases the efflux activity of ABCB1, suggesting that T2R signalling limits the absorption of bitter tasting/toxic substances through modulation of gut efflux membrane transporters.

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Imajo, Masamichi, Koichi Miyatake, Akira Iimura, Atsumu Miyamoto, and Eisuke Nishida. "A molecular mechanism that links Hippo signalling to the inhibition of Wnt/β-catenin signalling." EMBO Journal 31, no. 5 (January 10, 2012): 1109–22. http://dx.doi.org/10.1038/emboj.2011.487.

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WERRY, Tim D., Graeme F. WILKINSON, and Gary B. WILLARS. "Mechanisms of cross-talk between G-protein-coupled receptors resulting in enhanced release of intracellular Ca2+." Biochemical Journal 374, no. 2 (September 1, 2003): 281–96. http://dx.doi.org/10.1042/bj20030312.

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Alteration in [Ca2+]i (the intracellular concentration of Ca2+) is a key regulator of many cellular processes. To allow precise regulation of [Ca2+]i and a diversity of signalling by this ion, cells possess many mechanisms by which they are able to control [Ca2+]i both globally and at the subcellular level. Among these are many members of the superfamily of GPCRs (G-protein-coupled receptors), which are characterized by the presence of seven transmembrane domains. Typically, those receptors able to activate PLC (phospholipase C) enzymes cause release of Ca2+ from intracellular stores and influence Ca2+ entry across the plasma membrane. It has been well documented that Ca2+ signalling by one type of GPCR can be influenced by stimulation of a different type of GPCR. Indeed, many studies have demonstrated heterologous desensitization between two different PLC-coupled GPCRs. This is not surprising, given our current understanding of negative-feedback regulation and the likely shared components of the signalling pathway. However, there are also many documented examples of interactions between GPCRs, often coupling preferentially to different signalling pathways, which result in a potentiation of Ca2+ signalling. Such interactions have important implications for both the control of cell function and the interpretation of in vitro cell-based assays. However, there is currently no single mechanism that adequately accounts for all examples of this type of cross-talk. Indeed, many studies either have not addressed this issue or have been unable to determine the mechanism(s) involved. This review seeks to explore a range of possible mechanisms to convey their potential diversity and to provide a basis for further experimental investigation.

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Šrámek, Jan, Vlasta Němcová-Fürstová, and Jan Kovář. "Molecular Mechanisms of Apoptosis Induction and Its Regulation by Fatty Acids in Pancreatic β-Cells." International Journal of Molecular Sciences 22, no. 8 (April 20, 2021): 4285. http://dx.doi.org/10.3390/ijms22084285.

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Pancreatic β-cell failure and death contribute significantly to the pathogenesis of type 2 diabetes. One of the main factors responsible for β-cell dysfunction and subsequent cell death is chronic exposure to increased concentrations of FAs (fatty acids). The effect of FAs seems to depend particularly on the degree of their saturation. Saturated FAs induce apoptosis in pancreatic β-cells, whereas unsaturated FAs are well tolerated and are even capable of inhibiting the pro-apoptotic effect of saturated FAs. Molecular mechanisms of apoptosis induction by saturated FAs in β-cells are not completely elucidated. Saturated FAs induce ER stress, which in turn leads to activation of all ER stress pathways. When ER stress is severe or prolonged, apoptosis is induced. The main mediator seems to be the CHOP transcription factor. Via regulation of expression/activity of pro- and anti-apoptotic Bcl-2 family members, and potentially also through the increase in ROS production, CHOP switches on the mitochondrial pathway of apoptosis induction. ER stress signalling also possibly leads to autophagy signalling, which may activate caspase-8. Saturated FAs activate or inhibit various signalling pathways, i.e., p38 MAPK signalling, ERK signalling, ceramide signalling, Akt signalling and PKCδ signalling. This may lead to the activation of the mitochondrial pathway of apoptosis, as well. Particularly, the inhibition of the pro-survival Akt signalling seems to play an important role. This inhibition may be mediated by multiple pathways (e.g., ER stress signalling, PKCδ and ceramide) and could also consequence in autophagy signalling. Experimental evidence indicates the involvement of certain miRNAs in mechanisms of FA-induced β-cell apoptosis, as well. In the rather rare situations when unsaturated FAs are also shown to be pro-apoptotic, the mechanisms mediating this effect in β-cells seem to be the same as for saturated FAs. To conclude, FA-induced apoptosis rather appears to be preceded by complex cross talks of multiple signalling pathways. Some of these pathways may be regulated by decreased membrane fluidity due to saturated FA incorporation. Few data are available concerning molecular mechanisms mediating the protective effect of unsaturated FAs on the effect of saturated FAs. It seems that the main possible mechanism represents a rather inhibitory intervention into saturated FA-induced pro-apoptotic signalling than activation of some pro-survival signalling pathway(s) or metabolic interference in β-cells. This inhibitory intervention may be due to an increase of membrane fluidity.

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Gorvin, Caroline M. "Insights into calcium-sensing receptor trafficking and biased signalling by studies of calcium homeostasis." Journal of Molecular Endocrinology 61, no. 1 (July 2018): R1—R12. http://dx.doi.org/10.1530/jme-18-0049.

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The calcium-sensing receptor (CASR) is a class C G-protein-coupled receptor (GPCR) that detects extracellular calcium concentrations, and modulates parathyroid hormone secretion and urinary calcium excretion to maintain calcium homeostasis. The CASR utilises multiple heterotrimeric G-proteins to mediate signalling effects including activation of intracellular calcium release; mitogen-activated protein kinase (MAPK) pathways; membrane ruffling; and inhibition of cAMP production. By studying germline mutations in the CASR and proteins within its signalling pathway that cause hyper- and hypocalcaemic disorders, novel mechanisms governing GPCR signalling and trafficking have been elucidated. This review focusses on two recently described pathways that provide novel insights into CASR signalling and trafficking mechanisms. The first, identified by studying a CASR gain-of-function mutation that causes autosomal dominant hypocalcaemia (ADH), demonstrated a structural motif located between the third transmembrane domain and the second extracellular loop of the CASR that mediates biased signalling by activating a novel β-arrestin-mediated G-protein-independent pathway. The second, in which the mechanism by which adaptor protein-2 σ-subunit (AP2σ) mutations cause familial hypocalciuric hypercalcaemia (FHH) was investigated, demonstrated that AP2σ mutations impair CASR internalisation and reduce multiple CASR-mediated signalling pathways. Furthermore, these studies showed that the CASR can signal from the cell surface using multiple G-protein pathways, whilst sustained signalling is mediated only by the Gq/11 pathway. Thus, studies of FHH- and ADH-associated mutations have revealed novel steps by which CASR mediates signalling and compartmental bias, and these pathways could provide new targets for therapies for patients with calcaemic disorders.

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Machesky, Laura, and Gary Burd. "Cytoskeleton signalling: 7 November 2001." Biochemist 24, no. 1 (February 1, 2002): 32. http://dx.doi.org/10.1042/bio02401032.

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Laura Machesky was invited by the University of Leicester to present a seminar at a meeting sponsored by the Biochemical Society in November. “Laura was involved in discovering actin-related proteins (Arps)”, says host Jim Norman introducing her achievements. “She also elucidated the key mechanism by which actin polymerization is controlled.”

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Pearce, Andrew C., Gemma L. J. Fuller, Katsue Suzuki-Inoue, Michael G. Tomlinson, and Steve P. Watson. "Signalling by the Platelet C-Type Lectin Receptor CLEC-2 Is Mediated by a Novel Mechanism Involving Syk and a Single YxxL Motif." Blood 106, no. 11 (November 16, 2005): 381. http://dx.doi.org/10.1182/blood.v106.11.381.381.

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Abstract We have recently identified the C-type lectin-like receptor CLEC-2 as a novel receptor for the snake toxin rhodocytin on platelets. CLEC-2 is a 32 kDa type II transmembrane protein with a single cytoplasmic tyrosine residue in a YxxL consensus sequence. It is the first C-type lectin receptor that has been shown to activate platelets. The aim of the present study was to investigate the mechanism of signalling by CLEC-2 using model cell lines and to establish the role of the YxxL motif in this process. We have expressed CLEC-2 in wild type DT40 B cells and Jurkat T cells and in mutant derivatives of these cell lines that lack key signalling proteins. We have assayed PLCγ activation using an NFAT-luciferase reporter assay. Site directed mutagenesis of the cytoplasmic tyrosine residue of CLEC-2 has been used to assess its role in CLEC-2 signalling. We have compared the signalling pathway of CLEC-2 with that of the ITAM-coupled collagen receptor GPVI by expressing GPVI in the mutant cell lines and monitoring responses to the GPVI specific agonist convulxin as above. Cells transfected with CLEC-2 respond to rhodocytin. Mutation of the CLEC-2 YxxL motif to FxxL abrogates CLEC-2 signalling. CLEC-2 signalling is abrogated in cells deficient in Src or Syk family kinases or PLCγ . CLEC-2 signalling is partially dependent on Tec family kinases and the adaptors LAT and SLP-76/BLNK. Interestingly, GPVI signalling and CLEC-2 signalling show a differential requirement for the SLP-76 family adaptor proteins SLP-76 or Blnk; GPVI signalling is entirely dependent on SLP-76/Blnk, whereas CLEC-2 signalling is only partially dependent on these proteins. These observations are consistent with a model whereby CLEC-2 recruits Syk via its YxxL motif and initiates a signalling cascade similar to the major platelet glycoproteins GPVI and integrin α IIbβ 3. CLEC-2 is the first platelet receptor shown to regulate Syk through a single YxxL motif. Importantly, despite the similarity in the signalling proteins involved in signalling by the ITAM receptor, the integrin receptor and the C-type lectin receptor, the signalling pathways are organised and initiated differently.

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WALL, LARRY D. "Callable Bonds: A Risk-Reducing Signalling Mechanism-A Comment." Journal of Finance 43, no. 4 (September 1988): 1057–65. http://dx.doi.org/10.1111/j.1540-6261.1988.tb02624.x.

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ROBBINS, EDWARD HENRY, and JOHN D. SCHATZBERG. "Callable Bonds: A Risk-Reducing Signalling Mechanism-A Reply." Journal of Finance 43, no. 4 (September 1988): 1067–73. http://dx.doi.org/10.1111/j.1540-6261.1988.tb02625.x.

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Ksionda, Olga, Alexander Saveliev, Robert Köchl, Jonathan Rapley, Mustapha Faroudi, Jennifer E. Smith-Garvin, Christoph Wülfing, Katrin Rittinger, Tom Carter, and Victor L. J. Tybulewicz. "Mechanism and function of Vav1 localisation in TCR signalling." Journal of Cell Science 125, no. 22 (September 6, 2012): 5302–14. http://dx.doi.org/10.1242/jcs.105148.

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Michiels, Nico K., Nils Anthes, Nathan S. Hart, Jürgen Herler, Alfred J. Meixner, Frank Schleifenbaum, Gregor Schulte, Ulrike E. Siebeck, Dennis Sprenger, and Matthias F. Wucherer. "Red fluorescence in reef fish: A novel signalling mechanism?" BMC Ecology 8, no. 1 (2008): 16. http://dx.doi.org/10.1186/1472-6785-8-16.

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del Álamo, David, Hervé Rouault, and François Schweisguth. "Mechanism and Significance of cis-Inhibition in Notch Signalling." Current Biology 21, no. 1 (January 2011): R40—R47. http://dx.doi.org/10.1016/j.cub.2010.10.034.

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NOMURA, Yasuyuki. "Recent advances in molecular pharmacology of cellular signalling mechanism." Folia Pharmacologica Japonica 93, no. 6 (1989): 321–31. http://dx.doi.org/10.1254/fpj.93.321.

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Balakumar, Pitchai, Mandeep Kumar Arora, Jayarami Reddy, and Madhu B. Anand-Srivastava. "Pathophysiology of Diabetic Nephropathy: Involvement of Multifaceted Signalling Mechanism." Journal of Cardiovascular Pharmacology 54, no. 2 (August 2009): 129–38. http://dx.doi.org/10.1097/fjc.0b013e3181ad2190.

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Suetsugu, Noriyuki, and Masamitsu Wada. "Signalling mechanism of phototropin-mediated chloroplast movement in Arabidopsis." Journal of Plant Biochemistry and Biotechnology 29, no. 4 (September 25, 2020): 580–89. http://dx.doi.org/10.1007/s13562-020-00594-5.

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Rexin, Daniel, Christian Meyer, Christophe Robaglia, and Bruce Veit. "TOR signalling in plants." Biochemical Journal 470, no. 1 (August 6, 2015): 1–14. http://dx.doi.org/10.1042/bj20150505.

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Although the eukaryotic TOR (target of rapamycin) kinase signalling pathway has emerged as a key player for integrating nutrient-, energy- and stress-related cues with growth and metabolic outputs, relatively little is known of how this ancient regulatory mechanism has been adapted in higher plants. Drawing comparisons with the substantial knowledge base around TOR kinase signalling in fungal and animal systems, functional aspects of this pathway in plants are reviewed. Both conserved and divergent elements are discussed in relation to unique aspects associated with an autotrophic mode of nutrition and adaptive strategies for multicellular development exhibited by plants.

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Richter, Erik A., Jakob N. Nielsen, Sebastian B. Jørgensen, Christian Frøsig, Jesper B. Birk, and Jørgen F. P. Wojtaszewski. "Exercise signalling to glucose transport in skeletal muscle." Proceedings of the Nutrition Society 63, no. 2 (May 2004): 211–16. http://dx.doi.org/10.1079/pns2004343.

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Contraction-induced glucose uptake in skeletal muscle is mediated by an insulin-independent mechanism that leads to translocation of the GLUT4 glucose transporter to the muscle surface membrane from an intracellular storage site. Although the signalling events that increase glucose transport in response to muscle contraction are not fully elucidated, the aim of the present review is to briefly present the current understanding of the molecular signalling mechanisms involved. Glucose uptake may be regulated by Ca2+-sensitive contraction-related mechanisms, possibly involving Ca2+/calmodulin-dependent protein kinase II and some isoforms of protein kinase C. In addition, glucose transport may be regulated by mechanisms that reflect the metabolic status of the muscle, probably involving the 5′AMP-activated protein kinase. Furthermore, the p38 mitogen-activated protein kinase may be involved in activating the GLUT4 translocated to the surface membrane. Nevertheless, the picture is incomplete, and fibre type differences also seem to be involved.

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Ma, Chen-Yu, Yu-Qian Ma, and Min Deng. "Mechanism of Zhen Wu Decoction in the Treatment of Heart Failure Based on Network Pharmacology and Molecular Docking." Evidence-Based Complementary and Alternative Medicine 2022 (March 15, 2022): 1–10. http://dx.doi.org/10.1155/2022/4877920.

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Heart failure (HF) is a serious manifestation or advanced stage of various cardiovascular diseases, and its mortality and rehospitalization rate are still on the rise in China. Based on the network pharmacology method, 59 components of Zhen Wu decoction (ZWD) and 83 target genes related to HF were obtained. Through the PPI network, four potential therapeutic targets were identified: AKT1, IL6, JUN, and MAPK8. The beneficial components of ZWD might intervene HF through the AGE-RAGE signalling pathway in the diabetes component, fluid shear stress and atherosclerosis, the TNF signalling pathway, TB, and Kaposi sarcoma related herpesvirus infection, according to a KEGG enrichment study. The protein interaction network of candidate targets was constructed by the STRING database, and the protein interaction network was clustered by MEODE software. GO and KEGG enrichment analyses were performed on the core modules obtained by clustering. Finally, AutoDock Vina software was used for molecular docking verification of key targets and active ingredients. The result was that 75 active ingredients and 109 genes were screened as potential active ingredients and potential targets of Shengjie Tongyu decoction for CHF treatment. The main active components were quercetin, luteolin, kaempferol, dehydrated icariin, isorhamnetin, formononetin, and other flavonoids. Il-6, MAPK1, MAPK8, AKT1, VEGFA, and JUN were selected as the core targets. Molecular docking showed that the key components were well connected with the target. GO enrichment analysis showed that Shengjie Tongyu decoction could play a role through multiple biological pathways including angiogenesis, regulation of endothelial cell proliferation, binding of cytokine receptors, negative regulation of apoptotic signalling pathways, regulation of nitric oxide synthase activity, and reactive oxygen metabolism. Key pathways mainly focus on the toll-like receptor signalling pathway, nod-like receptor signalling pathway, MAPK signalling pathway, mTOR signalling pathway, JAK-STAT signalling pathway, VEGF signalling pathway, and other pathways. Through molecular docking technology, it was found that a variety of effective components in ZWD, such as kaempferol. Molecular docking technology has preliminatively verified the network pharmacology and laid a foundation for the follow-up pharmacological research.

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Jeynes-Smith, Cailan, and Robyn P. Araujo. "Ultrasensitivity and bistability in covalent-modification cycles with positive autoregulation." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 477, no. 2252 (August 2021): 20210069. http://dx.doi.org/10.1098/rspa.2021.0069.

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Switch-like behaviours in biochemical networks are of fundamental significance in biological signal processing, and exist as two distinct types: ultra-sensitivity and bistability. Here we propose two new models of a reversible covalent-modification cycle with positive autoregulation (PAR), a motif structure that is thought to be capable of both ultrasensitivity and bistability in different parameter regimes. These new models appeal to a modelling framework that we call complex-complete , which accounts fully for the molecular complexities of the underlying signalling mechanisms. Each of the two new models encodes a specific molecular mechanism for PAR. We demonstrate that the modelling simplifications for PAR models that have been used in previous work, which rely on Michaelian approximations, are unable to accurately recapitulate the qualitative signalling responses supported by our detailed models. Strikingly, we show that complex-complete PAR models are capable of new qualitative responses such as one-way switches and a ‘prozone’ effect, depending on the specific PAR-encoding mechanism, which are not supported by Michaelian simplifications. Our results highlight the critical importance of accurately representing the molecular details of biochemical signalling mechanisms, and strongly suggest that the Michaelian approximation is inadequate for predictive models of enzyme-mediated chemical reactions with added regulations such as PAR.

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Mihail, Sandra M., Andi Wangzhou, Kumud K. Kunjilwar, Jamie K. Moy, Gregory Dussor, Edgar T. Walters, and Theodore J. Price. "MNK-eIF4E signalling is a highly conserved mechanism for sensory neuron axonal plasticity: evidence from Aplysia californica." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1785 (September 23, 2019): 20190289. http://dx.doi.org/10.1098/rstb.2019.0289.

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Injury to sensory neurons causes an increase in the excitability of these cells leading to enhanced action potential generation and a lowering of spike threshold. This type of sensory neuron plasticity occurs across vertebrate and invertebrate species and has been linked to the development of both acute and persistent pain. Injury-induced plasticity in sensory neurons relies on localized changes in gene expression that occur at the level of mRNA translation. Many different translation regulation signalling events have been defined and these signalling events are thought to selectively target subsets of mRNAs. Recent evidence from mice suggests that the key signalling event for nociceptor plasticity is mitogen-activated protein kinase-interacting kinase (MNK) -mediated phosphorylation of eukaryotic translation initiation factor (eIF) 4E. To test the degree to which this is conserved in other species, we used a previously described sensory neuron plasticity model in Aplysia californica . We find, using a variety of pharmacological tools, that MNK signalling is crucial for axonal hyperexcitability in sensory neurons from Aplysia . We propose that MNK-eIF4E signalling is a core, evolutionarily conserved, signalling module that controls nociceptor plasticity. This finding has important implications for the therapeutic potential of this target, and it provides interesting clues about the evolutionary origins of mechanisms important for pain-related plasticity. This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.

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Ghaleb, Safwan M., Shamala Subramaniam, Mukhtar Ghaleb, and Ali Mohamed E. Ejmaa. "An Efficient Group-Based Control Signalling within Proxy Mobile IPv6 Protocol." Computers 8, no. 4 (October 4, 2019): 75. http://dx.doi.org/10.3390/computers8040075.

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Providing a seamless handover in the Internet of Thing (IoT) applications with minimal efforts is a big challenge in mobility management protocols. Several research efforts have been attempted to maintain the connectivity of nodes while performing mobility-related signalling, in order to enhance the system performance. However, these studies still fall short at the presence of short-term continuous movements of mobile nodes within the same network, which is a requirement in several applications. In this paper, we propose an efficient group-based handoff scheme for the Mobile Nodes (MNs) in order to reduce the nodes handover during their roaming. This scheme is named Enhanced Cluster Sensor Proxy Mobile IPv6 (E-CSPMIPv6). E-CSPMIPv6 introduces a fast handover scheme by implementing two mechanisms. In the first mechanism, we cluster mobile nodes that are moving as a group in order to register them at a prior time of their actual handoff. In the second mechanism, we manipulate the mobility-related signalling of the MNs triggering their handover signalling simultaneously. The efficiency of the proposed scheme is validated through extensive simulation experiments and numerical analyses in comparison to the state-of-the-art mobility management protocols under different scenarios and operation conditions. The results demonstrate that the E-CSPMIPv6 scheme significantly improves the overall system performance, by reducing handover delay, signalling cost and end-to-end delay.

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Edan, Naktal, and Enas Y. Abdullah. "Design and implementation of a novel secured and wide WebRTC signalling mechanism for multimedia over internet." International Journal of Electrical and Computer Engineering (IJECE) 10, no. 5 (October 1, 2020): 5430. http://dx.doi.org/10.11591/ijece.v10i5.pp5430-5435.

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A modern and free technology called web real-time communication (WebRTC) was enhanced to allow browser-to-browser multimedia communication without plugins. In contract, WebRTC has not categorised a specific signalling mechanism to set, establish and end communication between browsers. The primary target of this application is to produce and implement a novel WebRTC signalling mechanism for multimedia communication between different users over the Internet without plugins. Furthermore, it has been applied over different browsers, such as Explorer, Safari, Google Chrome, Firefox and Opera without any downloading or fees. This application designed using JavaScript language under ASP.net and C# language. Moreover, to prevent irrelevant users from accessing or attacking the session, user-id for initiating and joining the course using encryption technique was done. This system has been employed in real implementation among various users; therefore, an evaluation of bandwidth consumption, CPU, and quality of experience (QoE) was accomplished. The results show an original signalling mechanism which applied to different browsers, multiple users, and diverse networks such as Ethernet and Wireless. Besides, it sets session initiator, saves the communication efficient even if the initiator leaves, and communicating new participator with existing participants, etc. This studying focuses on the creation of a new signalling mechanism, the limitations of resources for WebRTC video conferencing.

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Journal articles on the topic 'SIGNALLING MECHANISM'

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