Relevant bibliographies by topics / MET signalling

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

Academic literature on the topic 'MET signalling'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "MET signalling"

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Comoglio, Paolo M. "Pathway specificity for Met signalling." Nature Cell Biology 3, no. 7 (July 2001): E161—E162. http://dx.doi.org/10.1038/35083116.

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Kermorgant, S., and P. J. Parker. "c-Met Signalling: Spatio-Temporal Decisions." Cell Cycle 4, no. 3 (February 2005): 352–55. http://dx.doi.org/10.4161/cc.4.3.1519.

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Bolanos-Garcia, Victor Martin. "MET meet adaptors: Functional and structural implications in downstream signalling mediated by the Met receptor." Molecular and Cellular Biochemistry 276, no. 1-2 (August 2005): 149–57. http://dx.doi.org/10.1007/s11010-005-3696-6.

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Skead, Garret, and Dhirendra Govender. "Gene of the month: MET." Journal of Clinical Pathology 68, no. 6 (April 22, 2015): 405–9. http://dx.doi.org/10.1136/jclinpath-2015-203050.

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The MET receptor tyrosine kinase and its ligand hepatocyte growth factor/scatter factor (HGF/SF) are potential therapeutic targets in many human malignancies, making this pathway an important focus of molecular and cancer research. MET mutations have been detected in various tumours. In addition, many tumour types demonstrate MET and HGF/SF overexpression and amplification. The MET signal transduction cascade is complex, and manifests in a broad spectrum of mitogenic and morphogenic functions, affecting cell proliferation, migration, differentiation, morphology and survival. Cancer cells commandeer the physiological functions of this signalling axis to facilitate invasion and metastasis. Significant progress has been made in the development of agents that inhibit MET-HGF/SF signalling. In this article, we outline the key features of the MET gene, its protein product and the ligand HGF/SF, to provide an overview of this important signalling pathway and offer a summary of the relevant pathological and clinical directions of research.
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Stakenborg, Michelle, Bram Verstockt, Elisa Meroni, Gera Goverse, Veronica De Simone, Sare Verstockt, Mario Di Matteo, et al. "Neutrophilic HGF-MET Signalling Exacerbates Intestinal Inflammation." Journal of Crohn's and Colitis 14, no. 12 (June 17, 2020): 1748–58. http://dx.doi.org/10.1093/ecco-jcc/jjaa121.

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Abstract Background and Aims Ulcerative colitis [UC] is associated with excessive neutrophil infiltration and collateral tissue damage, but the link is not yet completely understood. Since c-MET receptor tyrosine kinase [MET] is required for neutrophil chemoattraction and cytotoxicity in response to its ligand hepatocyte growth factor [HGF], we aimed to identify the function of HGF-MET signalling in neutrophils in UC patients and in mice during intestinal inflammation. Methods Serum and colonic biopsies from healthy controls and UC patients with active [Mayo endoscopic subscore 2–3] and inactive [Mayo endoscopic subscore 0–1] disease were collected to assess the level of serum and colonic HGF. Disease progression and immune cell infiltration were assessed during dextran sodium sulphate [DSS] colitis in wild-type and MRP8-Cre MET-LoxP mice. Results Increased mucosal HGF expression was detected in patients with active UC, and in mice during the inflammatory phase of DSS colitis. Similarly, serum HGF was significantly increased in active UC patients and positively correlated with C-reactive protein and blood neutrophil counts. Flow cytometric analysis also demonstrated an upregulation of colonic MET+ neutrophils during DSS colitis. Genetic ablation of MET in neutrophils reduced the severity of DSS-induced colitis. Concomitantly, there was a decreased number of TH17 cells, which could be due to a decreased production of IL-1β by MET-deficient neutrophils. Conclusions These data highlight the central role of neutrophilic HGF-MET signalling in exacerbating damage during intestinal inflammation. Hence, selective blockade of this pathway in neutrophils could be considered as a novel therapeutic approach in UC.
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Jeffers, M., S. Rong, and G. F. Vande Woude. "Enhanced tumorigenicity and invasion-metastasis by hepatocyte growth factor/scatter factor-met signalling in human cells concomitant with induction of the urokinase proteolysis network." Molecular and Cellular Biology 16, no. 3 (March 1996): 1115–25. http://dx.doi.org/10.1128/mcb.16.3.1115.

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Hepatocyte growth factor/scatter factor (HGF/SF) is a pleiotropic effector of cells expressing the Met tyrosine kinase receptor. Although HGF/SF is synthesized by mesenchymal cells and acts predominantly on epithelial cells, we have recently demonstrated that human sarcoma cell lines often inappropriately express high levels of Met and respond mitogenically to HGF/SF. In the present report we show that HGF/SF-Met signalling in the human leiomyosarcoma cell line SK-LMS-1 enhances its in vivo tumorigenicity, an effect for which the mitogenicity of this signalling pathway is likely to play a role. In addition, we found that HGF/SF-Met signalling dramatically induces the in vitro invasiveness and in vivo metastatic potential of these cells. We have studied the molecular basis by which HGFSF-Met signalling mediates the invasive phenotype. A strong correlation has previously been demonstrated between the activation of the urokinase plasminogen activator (uPA) proteolysis network and the acquisition of the invasive-metastatic phenotype, and we show here that HGF/SF-Met signalling significantly increases the protein levels of both uPA and its cellular receptor in SK-LMS-1 cells. This results in elevated levels of cell-associated uPA and enhanced plasmin-generating ability by these cells. These studies couple HGF/SF-Met signalling to the activation of proteases that mediate dissolution of the extracellular matrix-basement membrane, and important property for cellular invasion-metastasis.
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Badreldin, W., T. Powles, L. Menard, C. Ho-Yen, and S. Kermorgant. "Understanding and targeting Met signalling in bladder cancer." Annals of Oncology 28 (September 2017): v16. http://dx.doi.org/10.1093/annonc/mdx361.055.

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Cecchi, Fabiola, Daniel C. Rabe, and Donald P. Bottaro. "Targeting the HGF/Met signalling pathway in cancer." European Journal of Cancer 46, no. 7 (May 2010): 1260–70. http://dx.doi.org/10.1016/j.ejca.2010.02.028.

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Thayaparan, Thivyan, James F. Spicer, and John Maher. "The role of the HGF/Met axis in mesothelioma." Biochemical Society Transactions 44, no. 2 (April 11, 2016): 363–70. http://dx.doi.org/10.1042/bst20150252.

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Malignant mesothelioma is an asbestos-related cancer that occurs most commonly in the pleural space and is incurable. Increasing evidence suggests that aberrant receptor tyrosine kinase (RTK)-directed signalling plays a key role in the pathogenesis of this cancer. In the majority of mesotheliomas, up-regulated expression or signalling by Met, the receptor for hepatocyte growth factor (HGF) can be demonstrated. Following binding of ligand, Met relays signals that promote cell survival, proliferation, movement, invasiveness, branching morphogenesis and angiogenesis. Here we describe the HGF/Met axis and review the mechanisms that lead to the aberrant activation of this signalling system in mesothelioma. We also describe the cross-talk that occurs between HGF/Met and a number of other receptors, ligands and co-receptor systems. The prevalent occurrence of HGF/Met dysregulation in patients with mesothelioma sets the scene for the investigation of pharmaceutical inhibitors of this axis. In light of the inter-relationship between HGF/Met and other ligand receptor, combinatorial targeting strategies may provide opportunities for therapeutic advancement in this challenging tumour.
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Baird, A. M., M. Jarzabek, L. Shiels, S. Raeppel, S. Finn, S. Cuffe, H. I. Pass, I. Schmitt-Opitz, A. T. Byrne, and S. G. Gray. "Targeting the RON/MET/TAM signalling network in mesothelioma." Annals of Oncology 28 (April 2017): ii56. http://dx.doi.org/10.1093/annonc/mdx093.003.

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Dissertations / Theses on the topic "MET signalling"

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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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Carter, Stephanie. "Met receptor dynamics and signalling." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404701.

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Joffre, Carine. "Trafficking and signalling of oncogenic met." Thesis, Institute of Cancer Research (University Of London), 2010. http://qmro.qmul.ac.uk/jspui/handle/123456789/520.

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The Receptor Tyrosine Kinase (RTK) Met influences behaviour of several cancers by controlling growth, survival and metastasis. Recently, compartmentalisation of signals generated by RTKs, due to their endocytosis / trafficking, has emerged as a major determinant of various cell functions. The aim of my project was to study oncogenic Met signalling in relation to endosomal trafficking and to determine the consequences of such spatial changes on tumour cell growth and migration in vitro and in vivo. The model studied was NIH3T3 cells stably transfected with Wild type (Wt) Met or with three distinct mutants reported in human cancers. I found that two activating mutations in the kinase domain are highly tumorigenic in vivo. Using functional assays and tumour growth experiments, I demonstrated that one mutant is highly sensitive to Met specific tyrosine kinase inhibitors (TKI) while another is resistant. Such results suggested that therapeutical approaches to these mutants should be different. Furthermore, I demonstrated a direct link between endocytosis and tumorigenicity, suggesting a major role for Met endosomal signalling in cancer progression. Using confocal microscopy and quantitative biochemical assays, I demonstrated that Met mutants displayed an increased endocytosis and recycling and a decreased degradation profile. This led to an accumulation of phosphorylated Met on endosomes that induced activation of the GTPase Rac1, loss of stress fibres and increased cell migration. Blocking endocytosis by pharmacological and genetic 4 means inhibited mutants’ anchorage independent growth and, strikingly, tumorigenesis and experimental metastasis. Interestingly, the mutant resistant to TKI inhibition was sensitive to endocytosis inhibition. Taken together, these results suggest that Met localisation constitutes a major determinant in neoplastic development, while Met activation alone is insufficient to effect this change.
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Barrow, Rachel Jenny Mary. "Spatial signalling of Met in cancer." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/3364.

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Met, the receptor of Hepatocyte Growth Factor, is a receptor tyrosine kinase (RTK) overexpressed or mutated in cancer. RTKs have been increasingly recognised to signal post-endocytosis, possibly leading to unique consequences on cellular outcome due to the spatial and temporal activation of downstream signalling pathways. The objectives of my study were to investigate the role of Met “endosomal signalling” in cancer progression. I found, using four human breast cell lines, that the requirement of Met endocytosis for Met signalling as well as Met trafficking significantly vary with the cells’ aggressiveness, suggesting Met resides longer on endosomes in invasive cells. Furthermore Met endosomal localisation increases with the progression of breast cancer of human samples. Our study suggests that the endosomal location of Met is important in breast cancer progression. I used a model of Wt and two Met oncogenic mutants, M1268T and D1246N, expressed in NIH3T3 fibroblasts. I determined some mechanisms regulating the constitutive endocytosis and defect in degradation of the mutants. I established that targeting these mechanisms could be used to reduce Met mutants’ tumourigenicity. Thus impairing c-Cbl or Grb2 expression and/or binding to Met mutant or restoring Met mutant degradation through inhibiting the chaperone protein HSP90, greatly reduced the transforming capacities of the mutants in vitro and in vivo, including the D1246N that I show to be resistant to small molecule Met inhibitors.
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Paliouras, Grigorios. "Regulation of met receptor tyrosine kinase signalling and biology." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86661.

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Growth factor receptor tyrosine kinases (RTKs) are critical initiators of signal transduction pathways necessary for cell growth, differentiation, migration and survival. Many of these signals are coordinated through scaffold proteins that are phosphorylated upon their recruitment to the activated receptor complex. This provides binding sites for multiple proteins to activate and generate distinct biological responses. The amplitude and duration of a signal is regulated via dephosphorylation and degradation of target proteins. Signal regulation in this manner acts to promote the formation and disassembly of multi-protein complexes and diversify and localize signals downstream from RTKs.
The Met RTK and its ligand, hepatocyte growth factor (HGF), are positive regulators of epithelial morphogenesis, scatter, and survival. However little was known regarding the proteins responsible for attenuating Met receptor activation. In Chapter II, I demonstrated that the Met receptor was hyperphopshorylated in PTP1B-null mice in response to Fas-induced liver damage. Inhibition of Met signaling with PHA665752, removed protection from liver failure in PTP1B-null hepatocytes, demonstrating that PTP1B was a negative regulator of the Met RTK and its removal promoted cell survival against Fas-induced hepatic failure.
In response to Met receptor stimulation, the Gab1 scaffold protein is the prominent protein recruited and phosphorylated downstream from Met and is critical in mediating Met-dependent biological responses. In chapters III and IV, I identified the serine/threonine kinase Pak4 and the microtubule-bound guanine nucleotide exchange factor GEF-H1 as novel proteins recruited to Gab1 following Met receptor activation. I demonstrate that Gab1 and Pak4 synergize to enhance migration and invasion following HGF stimulation. Furthermore, the recruitment of Pak4 to Gab1 is important for its subcellular localization to lamellipodia and critical for epithelial cell dispersal and morphogenesis downstream from Met. In addition, GEF-H1 is important in focal adhesion formation and turnover and this correlates with the ability of GEF-H1 to promote epithelial migration and invasion downstream from Met.
Overall, these studies investigate molecular mechanisms regulating Met-dependent signals and demonstrate for the first time that the Met receptor is a substrate for PTP1B and identify Pak4 and GEF-H1 as key integrators of Met dependent cellular migration and invasion.
Les récepteurs tyrosine kinase aux facteurs de croissance sont des initiateurs critiques des voies de signalisation nécessaires à la croissance, la différentiation, la migration et la survie cellulaire. Beaucoup de ces signaux sont coordonnés par des protéines d'échafaudage qui sont phosphorylées au cours de leur recrutement au complexe de récepteurs activés. Ceci fournit des sites de liaison à de multiples protéines permettant l'activation et la génération de différentes réponses biologiques. L'amplitude et la durée d'un signal est régulée via la déphosphorylation et la dégradation des protéines cibles. De cette façon, la régulation du signal agit pour promouvoir la formation et le désassemblage de complexes protéiques et pour diversifier et localiser les signaux en aval des récepteurs tyrosine kinase.
Le récepteur Met et son ligand HGF (Hepatocyte Growth Factor) sont des régulateurs de la morphogenèse, la dispersion et la survie des cellules épithéliales. Toutefois, peu d'informations sont disponibles sur les protéines responsables de l'extinction des signaux issus du récepteur Met. Dans le chapitre II, je démontre que le récepteur Met est hyperphosphorylé dans les souris knock-out pour PTP1B en réponse aux dommages induits par Fas. L'inhibition par le composé PHA665752 de la signalisation par Met, relève la protection contre les crises hépatiques dans les souris KO pour PTP1B. Ceci démontre que PTP1B est un régulateur négatif de Met et son retrait permet la survie cellulaire contre les crises hépatiques induites par Fas.
En réponse à la stimulation du récepteur Met, la protéine d'échafaudage Gab1 est la plus importante des protéines recrutées et phosphorylées en aval de Met et cette protéine est critique dans la médiation des réponses biologiques dépendantes de Met. Dans les chapitres III et IV, j'ai identifié la kinase Ser/Thr Pak4 et le facteur d'échange de guanine lié aux microtubules (GEF-H1) en tant que nouvelles protéines recrutées à Gab1 suite à l'activation de Met. Je démontre que Gab1 et Pak4 agissent de façon synergique pour promouvoir la migration et l'invasion suite à la stimulation par HGF. De plus, le recrutement de Pak4 à Gab1 est important pour sa localisation cellulaire dans les lamellipodes et est critique pour la dispersion et la morphogenèse des cellules épithéliales en aval de Met. En outre, GEF-H1 est important pour la formation et le roulement des points d'adhésion focaux ce qui est en corrélation avec la capacité de GEF-H1 de promouvoir la migration et l'invasion épithéliale en aval de Met.
Ces études ont pour but d'investiguer les mécanismes moléculaires régulant les signaux dépendants de Met et démontrent pour la première fois que le récepteur Met est un substrat pour PTP1B. Finalement, Pak4 et GEF-H1 sont identifiés comme des intégrateurs clés de la migration et l'invasion cellulaire dépendante de Met.
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Moore, Amy Elizabeth. "The role of HGF/Met signalling in colorectal tumorigenesis." Thesis, University of Bristol, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544331.

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Webb, Craig Paul. "C-MET signalling in MDCK cells and a non-scattering variant." Thesis, University of East Anglia, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294659.

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Fournier, Tanya M. "The role of signalling pathways downstream from the Grb2 adaptor protein in Met receptor and Tpr-Met oncoprotein biological activities /." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36925.

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Activation of the Met receptor tyrosine kinase by its ligand, Hepatocyte Growth Factor (HGF), leads to mitogenesis, cell motility, morphogenesis, and angiogenesis. Mutational analysis has demonstrated the requirement of a single tyrosine within the carboxy-terminus (Y1356) of the Met receptor for the recruitment and activation of all Met-dependent signalling pathways and for the transformation of fibroblasts by the Tpr-Met oncogene. The selective abolishment of Grb2 from the Tpr-Met oncoprotein, by generating an asparagine to histidine mutation two amino acids downstream from Y1356 (N1358H), led to a reduction in Tpr-Met-mediated transformation of fibroblasts. Moreover, Met receptor studies demonstrate that while a Grb2 binding site is not required for epithelial cell motility, it is critical for the formation of branching tubules when cells are suspended in a collagen matrix. This suggests that Grb2-dependent pathways are involved in the organization and polarization of epithelial cells following Met receptor stimulation.
Grb2 associated molecules, Gab1 and Cbl, are highly phosphorylated following stimulation of the Met receptor. Moreover, signaling pathways associated with Gab1 are critical for branching tubulogenesis in epithelial cells. Expression of a constitutively active version of Cbl, 70z-Cbl, results in an epithelial-mesenchymal transition, leading to the breakdown of cellular junctions and reorganization of the actin cytoskeleton. The amino-terminal SH2 domain is the minimal region required to induce morphological changes, which may be mediated through its interaction with the Met receptor, and/or an unidentified protein of 150 kDa.
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Lai, Andrea. "Characterization of oncogenic signalling and mechanisms of resistance to inhibitors of Met in Gastric Cancer." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121360.

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Receptor tyrosine kinases (RTKs) are transmembrane cellular receptors that respond to growth factor stimulation and promote cellular proliferation in normal biological processes, such embryogenesis and wound healing. RTK activation and signalling are tightly regulated processes; their dysregulation promotes unrestrained cellular proliferation and is associated with cancer initiation and progression. As such, RTKs are targets of many therapeutic strategies for the treatment of cancer. However, despite initial success, both innate and acquired resistance hinders the efficacy of many of these inhibitors. Active signalling by the Met RTK plays a role in melanomas, osteosarcomas, breast carcinomas, gliomas, non-small cell lung cancers (NSCLC), and cancers of the gastro-intestinal (GI) tract. Multiple mechanisms of Met oncogenic activation have been identified, including autocrine/paracrine stimulation, Met overexpression, genomic amplification, point mutation and alternative splicing. Inhibitors of Met are currently in all phases of clinical trials for multiple tumour types, thus there exists a need to better understand the mechanisms through which Met promotes tumourigenesis, and how cells respond to Met inhibitors, and how resistance can occur.In my thesis, I establish that in four different MET-amplified gastric cancer cells there is a Met-dependent loss of its negative regulator, the E3 ligase, Cbl. I utilized structure-function analysis to demonstrate that this loss of Cbl levels requires Met kinase activity, Cbl E3 ligase activity, and recruitment of Cbl to Met. Where Met is active, Cbl is recruited and subsequently ubiquitinated, and degraded through the proteasome. I also observed that EGFR, which is also negatively regulated by Cbl, is less efficiently degraded upon stimulation in the presence of active Met and low Cbl levels. Thus, I demonstrate that Met-driven Cbl loss not only promotes dysregulation of Met, but of other Cbl target proteins as well.As much of what is known with respect to Met signalling has been identified in the context of activation by its ligand, hepatocyte growth factor (HGF), I investigated the Met-dependent pathways and transcriptional program in gastric cancer cells where Met is chronically active via amplification. I observed that activation of the Ras/Mek/Erk, PI3K/AKT and STAT3 pathways all require Met kinase activity, with STAT3 signalling required for Met-dependent cell proliferation. Interestingly, upon treatment with Met inhibitor, Erk becomes reactivated at later time points (16-24h) in 2/4 cell lines tested. This correlated with loss of Erk negative regulators, DUSP4 and DUSP6, upon Met inhibition. Dual inhibition of Met and Mek decreased cell viability as compared to inhibition of either alone. Hence loss of Erk negative regulators upon Met inhibition, allows for reactivated Erk to promote cell survival and may contribute to innate resistance to targeted Met therapeutics. Next, I established Met inhibitor-resistant cells and utilized gene and protein expression arrays to identify the mechanisms of resistance. I observed that resistant cells were still MET-amplified, but Met kinase activity remained inhibited. Met-independent cell proliferation is, in part, mediated by Erk signalling. Further, I also provide evidence that cell survival signals, in the presence of Met inhibition, may be mediated by a mesenchymal-to-epithelial transition. Altogether, the reactivation of Erk signalling under conditions of innate and acquired resistance to Met inhibitors suggests that combinatorial therapy targeting both Met and Mek may lead to better efficacy and response.
Les récepteurs à activité kinase (RTK) sont des protéines transmembranaires situées à la surface des cellules qui, une fois activés par des facteurs de croissance, induisent la prolifération cellulaire durant des processus biologiques normaux. La signalisation par les RTKs est un processus devant être hautement régulé étant donné qu'une signalisation aberrante des RTKs induit une prolifération cellulaire incontrôlée typique au développement et à la progression de tumeurs. Les RTKs constituent donc une cible thérapeutique de choix pour le traitement du cancer et plusieurs inhibiteurs de RTKs sont maintenant utilisés en clinique. Par contre, malgré des résultats initiaux prometteurs, il appert que de multiples tumeurs développent des mécanismes de résistance aux inhibiteurs de RTKs. Le RTK Met joue un rôle important dans de multiples cancers. Plusieurs mécanismes d'activation oncogénique du récepteur Met ont été identifiés. Des inhibiteurs de Met sont présentement testés en essais cliniques pour le traitements du cancers. Il est donc essentiel de mieux comprendre comment le RTK Met promeut la formation de tumeurs, comment les cellules cancéreuses répondent aux traitements ainsi que les mécanismes de développement de résistance aux inhibiteurs. Dans cette thèse, j'établis que dans des lignées de cellules cancéreuses gastriques où le gène MET est amplifié, il y a une perte de la protéine ligase E3 Cbl qui est un inhibiteur de Met. À l'aide d'une analyse structurelle et fonctionnelle, je démontre que cette perte de Cbl requière l'activité kinase de Met, l'activité ligase de Cbl et le recrutement de Cbl à Met. L'activation de Met mène au recrutement de Cbl, à son ubiquitination et sa dégradation via le protéasome. J'ai observé que le RTK EGFR, qui est aussi régulé négativement par Cbl, est moins efficacement dégradé suite à sa stimulation en présence d'un récepteur Met actif et de bas niveaux de Cbl. Ainsi, je démontre que la perte de Cbl suite à l'activation de Met mène à la dérégulation de Met, ainsi que d'autres cibles de Cbl.Étant donné que la majorité de ce qui est connu concernant la signalisation en aval de Met a été étudiée dans le contexte de l'activation du RTK par son ligand, le facteur de croissance hépatocytaire HGF, j'ai décidé d'étudier les signaux et programmes de transcription activés en aval de Met quand le récepteur est activé de manière chronique, suite à son amplification. J'ai observé que l'activation des voies de signalisation Erk, AKT et STAT3 requièrent toutes l'activité kinase Met, la signalisation par STAT3 contribuant à la prolifération cellulaire. Curieusement, suite au traitement des cellules cancéreuses avec un inhibiteur de Met, Erk devient réactivé à des temps subséquents (16-24h) dans deux des quatre lignées cellulaires analysées. Ceci corrobore avec la perte des régulateurs négatifs de Erk, DUSP4 et DUSP6, suite à l'inhibition de Met. L'inhibition combinée de Met et Mek diminue la viabilité cellulaire comparée à l'inhibition de Met ou Mek seulement. Par conséquent, la perte des régulateurs négatifs d'Erk suite à l'inhibition de Met permet la réactivation d'Erk et la survie des cellules, et peut contribuer à la résistance innée de certaines cellules cancéreuses aux inhibiteurs de Met.Suite à ces résultats, j'ai établi des lignées cellulaires résistantes à un inhibiteur de Met et analysé l'expression des gènes et protéines à l'aide de matrices pour identifier les mécanismes de résistances. J'ai observé que le gène MET est toujours amplifié dans les cellules résistantes, mais que l'activité kinase reste inhibée en présence de l'inhibiteur. La prolifération cellulaire indépendante de Met est en partie assurée par Erk. Sur la base de ces résultats, la réactivation de la voie de signalisation Erk dans des conditions de résistance innée ou acquise aux inhibiteurs de Met implique qu'une thérapie combinatoire ciblant Met et Mek puisse être plus efficace que les monothérapies.
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Villalobos, Hernandez Alberto. "Role of suppressor of cytokine signalling 1 (SOCS1) in the pathogenesis of prostate cancer." Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/11618.

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Le cancer de la prostate (PCa) est le deuxième cancer le plus courant chez les hommes au niveau mondial. Le suppresseur de la signalisation des cytokines 1 (SOCS1) est considéré comme un suppresseur de tumeur en raison de la fréquente répression épigénétique de ce gène dans de nombreux cancers. Il a été reporté que SOCS1 inhibait l’activation de STAT3 induite par l’IL-6, ainsi que les cyclines et les kinases dépendantes des cyclines dans les cellules malignes de la prostate. D’autre part, il a été montré que SOCS1 n’était pas essentiel lors du contrôle de la signalisation de l’IL-6 dans les hépatocytes dépourvus de cette protéine, cependant elle est essentielle pour atténuer la signalisation du facteur de croissance des hépatocytes (HGF) via son récepteur MET. MET est un récepteur de tyrosine kinases qui est surexprimé dans le PCa agressif et métastatique. Notre hypothèse de recherche propose que la répression de SOCS1 par méthylation du promoteur et la dérégulation de l’expression de MET et de sa signalisation, sont des mécanismes pathogéniques liés au développement et à la progression du PCa. Nous avons généré des lignées de cellules PC3 et DU145 stables exprimant SOCS1. Les cellules ont été stimulées avec HGF et l’activation des voies de signalisation a été évaluée par immunobuvardage. Des essais in vitro de migration, de prolifération et d’invasion ont été effectués en présence de HGF. Des gènes de transition épithélio-mésenchymateuse ont été évalués par PCR quantitatif en présence ou non du facteur de croissance. Les cellules du PCa transfectées ou pas avec SOCS1 ont été inoculées dans des souris NOD SCID gamma de façon sous-cutanée ou orthoptique afin d’évaluer respectivement la croissance tumorale et la formation de métastases. Les tumeurs reséquées ont été analysées histologiquement et biochimiquement. Nos résultats montrent que SOCS1 atténue l'activation de MET induite par HGF et la phosphorylation d’ERK dans les cellules PC3, ainsi que la phosphorylation d’ERK et d’AKT dans les cellules DU145. SOCS1 inhibe également la prolifération cellulaire induite par HGF, ainsi que la migration et l’invasion in vitro. De plus, SOCS1 réduit l’expression des gènes de transition épithélio-mésenchymateuse impliqués dans la dégradation des composants de la matrice extracellulaire dans les cellules DU145 mais pas dans les cellules PC3. La surexpression de SOCS1 a stimulé l’augmentation de déposition de collagène, in vivo. Les tumeurs formées par les cellules exprimant SOCS1 étaient de taille significativement plus petites avec une réduction de la prolifération comparé aux tumeurs provenant des cellules contrôles. En outre, SOCS1 a inhibé la formation de métastases à distance dans un modèle orthotopique. En conclusion, nous suggérons que SOCS1 est un suppresseur de tumeur indispensable de la prostate, et qu’au moins une partie de sa fonction a lieu via la régulation négative de la signalisation du récepteur MET.
Abstract : Prostate cancer (PCa) is the second most common cancer among men worldwide. Suppressor of cytokine signaling 1 (SOCS1) is considered a tumor suppressor due to frequent epigenetic repression of the SOCS1 gene in several human malignancies. Inactivation of SOCS1 also occurs in PCa by gene methylation and micro-RNA-mediated repression. SOCS1 has been reported to inhibit IL-6-induced STAT3 activation and down-regulates cyclins and cyclin-dependent kinases in PCa cells. It has been shown that SOCS1 is not required to control IL-6 signaling in SOCS1-deficient hepatocytes, but is essential to attenuate hepatocyte growth factor (HGF) signaling via its receptor MET. This protein is a receptor tyrosine kinase (RTK), overexpressed in aggressive and metastatic PCa. Thus we hypothesized that the repression of SOCS1 via promoter methylation and deregulated MET expression and signaling are inter-related pathogenic mechanisms in PCa development and progression. We generated stable SOCS1-expressing PCa cell lines (PC3 and DU145) using lentiviral transduction followed by clonal selection via limiting dilution. Cells were stimulated with HGF and downstream signaling events were assessed by Western blot. Proliferation, migration and invasion assays were also conducted in the presence of HGF in vitro. Epithelial mesenchymal transition genes were evaluated by qPCR in the presence or absence of the growth factor. The PCa cells transfected with SOCS1 and non-transfected controls were inoculated into NOD SCID gamma mice as xenografts or as orthotopic tumors to assess tumor growth and metastasis formation, respectively. Resected tumors were further analyzed histologically and biochemically. Our results showed that SOCS1 attenuates HGF-induced MET activation and ERK phosphorylation in PC3 and DU145 PCa cell lines. SOCS1 inhibited HGF induced cell proliferation, migration and invasion in vitro. Additionally, SOCS1 decreased epithelial mesenchymal transition genes involved in the degradation of extracellular matrix components in DU145 cells but not in PC3. In vivo, SOCS1 overexpression leads to an increase of collagen deposition. Tumors formed by SOCS1 expressing cells were significantly smaller in size with reduced cell proliferation compared to tumors arising from control cells. Furthermore, SOCS1 inhibited distant metastasis formation in the orthotopic model. Overall our results suggest that SOCS1 has a tumor suppressor role in PCa evolution and part of this function is mediated by the negative regulation of MET receptor signalling and down-regulation of genes supporting migration and invasion processes such as matrix metalloproteinases.
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Books on the topic "MET signalling"

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Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B3 (niacin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0009.

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Niacin (as nicotinamide) is a component of coenzyme systems that function in the reductive biosynthesis of fatty acids and steroids, including cholesterol, and are involved in cell signalling. Niacin deficiency is rare, as the daily requirement can usually be met by food sources, and also via synthesis from tryptophan, which is present in dietary proteins. The prevalence of niacin deficiency is higher in populations consuming mainly corn or sorghum as a dietary staple. Corn contains niacin, but only in a bound form that is nutritionally unavailable. The additional needs for niacin during pregnancy are mirrored by the increased energy intake needs, and dietary supplementation is only necessary in cases of overall poor nutritional intake.
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D’Amato, Gaetano, Guillermo Luxán, and José Luis de la Pompa. Defining cardiac domains from the inside: NOTCH in endocardial–myocardial interactions. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0011.

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In this chapter we illustrate the signalling interactions of the endocardium with the other cardiac tissues to coordinate cardiac development. First, we describe the developmental origins of the endocardium. Then we focus on the Notch pathway because of its unique signalling activity in the endocardium, and briefly describe the elements of this signalling mechanism and the key cardiogenic processes that require endocardial Notch signalling: patterning of the early embryonic endocardium into prospective territories for valves and ventricular chambers, early valve formation, ventricular trabeculation, and compaction. Finally, we discuss how Notch dysfunction in the endocardium results in cardiac structural malformations that can lead to congenital heart disease.
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Monaco, Claudia, and Giuseppina Caligiuri. Molecular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0014.

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The development of the atherosclerotic plaque relies on specific cognate interactions between ligands and receptors with the ability to regulate cell recruitment, inflammatory signalling, and the production of powerful inflammatory and bioactive lipid mediators. This chapter describes how signalling is engaged by cell-cell surface interactions when the endothelium interacts with platelets and leukocytes enhancing leukocyte recruitment during atherogenesis. It also exemplifies intracellular signalling pathways induced by the activation of innate immune receptors, the most potent activators of inflammation in physiology and disease. Differences are highlighted in innate signalling pathways in metabolic diseases such as atherosclerosis compared to canonical immunological responses. Finally, the key lipid mediators whose production can affect endothelial function, inflammation, and atherosclerosis development are summarized. This Chapter will take you through these fundamental steps in the development of the atherosclerotic plaque by summarizing very recent knowledge in the field and highlighting recent or ongoing clinical trials that may enrich our ability to target cardiovascular disease in the future.
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Zaffran, Stéphane. Cardiac growth II: Cardiomyocyte polarization. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0010.

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During vertebrate embryogenesis, the planar cell polarity (PCP) signalling pathway is responsible for cell movements essential for convergent extension during gastrulation, neural tube closure, neural crest cell migration, and heart morphogenesis. In the heart, the non-canonical Wnt/PCP pathway regulates cell polarity, cell shape, and cell dynamics during formation of the cardiac crescent and deployment of second heart field cardiac progenitors to the poles of the heart tube. PCP signalling is also essential for the establishment of left–right patterning in the early embryo. This chapter reviews our current understanding of PCP signalling in heart morphogenesis and how it affects the pathogenesis of congenital heart diseases.
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Alves, Ines Teles, Jan Trapman, and Guido Jenster. Molecular biology of prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0059.

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Prostate cancer is a heterogeneous disease that arises through the acquisition of key malignant hallmarks. At the molecular level, prostate tumours are dependent upon the androgen receptor pathway, which affects cell function, growth, and behaviour through downstream androgen-regulated genes. Prostate cancer requires this activity and manipulates the AR pathway to maintain signalling. For example, mutation of the AR (to bind ligands other than androgens) or amplification/duplication of the AR allows signalling to continue in the absence of testosterone. Around 50% of prostate cancers have a gene fusion between the androgen-regulated component of the TMPRSS2 gene and a transcription factor (e.g. ETS family members ERG and ETV1). This results in aberrant androgen stimulated cell growth. Current research is using molecular knowledge to identify biomarkers, such as PCA3, and new therapies, such as enzalutamide or abiraterone acetate.
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Cahill, Thomas J., and Paul R. Riley. Epicardial and coronary vascular development. Edited by Miguel Torres. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0009.

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The coronary circulation is essential for human life. In embryonic development, abnormal formation of the coronary vasculature can cause death in utero or after birth. In adulthood, atherosclerosis of the coronary arteries is the commonest cause of death worldwide. The last decade has witnessed significant strides forward in our understanding of coronary development. Multiple sources of coronary endothelial cells have been identified using genetic tools for fate mapping. The epicardium, the outermost layer of the developing heart, has emerged as both a source of cell progenitors and key signalling mediators. Knowledge of the specific genes underlying formation, function, and heterogeneity of the epicardium is expanding. Significant challenges remain, however, in understanding the spatiotemporal signalling patterns required for organized migration, differentiation, and patterning of the vasculature. In addition, dissecting how coronary development is perturbed in patients with congenital coronary anomalies is a major ongoing focus of research.
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Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. The pancreas. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0046.

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Congenital anomalies 326Pancreatitis 328Pancreatic insufficiency 335These are rare. Most anomalies are sporadic. Only the gene coding for the homeodomain protein PDX1 is clearly demonstrated to be causal of pancreatic agenesis. Inactivation or inhibition of signalling molecule sonic hedgehog (Shh) could potentially lead to annular pancreas, pancreatic divisum, and pancreatic ectopia....
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Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.

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Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
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Rammah, Mayyasa, Francesca Rochais, and Robert G. Kelly. Incorporation of myocardial progenitors at the arterial pole of the heart. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0007.

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The arterial pole of the heart is a hotspot for life-threatening forms of congenital heart defects (CHDs). It is formed by progressive addition of myocardium from epithelial progenitor cells in the second heart field (SHF). SHF cells contribute successively to the right ventricle and proximal and distal outflow tract myocardial walls which, after neural crest influx and cardiac septation, give rise to myocardium at the base of the aorta and pulmonary trunk. SHF cells are characterized by continued proliferation and differentiation delay controlled by an array of transcriptional regulators and signalling pathways which define the SHF progenitor cell niche in pharyngeal mesoderm. Failure of normal SHF deployment leads to a shortened outflow tract and failure of ventriculo-arterial alignment, resulting in a spectrum of conotruncal CHD. We discuss the origins of the SHF in cardiopharyngeal mesoderm and focus on the mechanisms driving SHF deployment, summarizing current understanding of critical signalling pathways and transcription factors.
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Book chapters on the topic "MET signalling"

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Hammond, D. E., S. Carter, and M. J. Clague. "Met Receptor Dynamics and Signalling." In Current Topics in Microbiology and Immunology, 21–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-69494-6_2.

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Zambelli, Alberto, Giuseppe Biamonti, and Angela Amato. "HGF/c-Met Signalling in the Tumor Microenvironment." In Advances in Experimental Medicine and Biology, 31–44. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-47189-7_2.

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Lokker, Nathalie A., Melanie R. Mark, and Paul J. Godowski. "Structure-Function Analysis of Hepatocyte Growth Factor and its Tyrosine-Kinase Receptor c-Met." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling, 99–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78247-3_8.

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Rodrigues, Gerard A., and Morag Park. "Oncogenic Activation of the Met/HGF Receptor Tyrosine Kinase is Promoted by Leucine Zipper Mediated Dimerization." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling, 103–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78247-3_9.

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Joffre, Carine, Rachel Barrow, Ludovic Ménard, and Stéphanie Kermorgant. "RTKs as Models for Trafficking Regulation: c-Met/HGF Receptor-c-Met Signalling in Cancer—Location Counts." In Vesicle Trafficking in Cancer, 261–77. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6528-7_13.

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Plíhal, Ondřej. "Cytokinin Signalling and Mechanism of Action of Meta-Topolin and Its Derivatives." In Meta-topolin: A Growth Regulator for Plant Biotechnology and Agriculture, 39–48. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-9046-7_5.

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Mussabbir, Qazi Bouland, and Thomas Owens. "IEEE802.21 Assisted Fast Re-Authentication Scheme over GSABA." In IT Policy and Ethics, 539–61. IGI Global, 2013. http://dx.doi.org/10.4018/978-1-4666-2919-6.ch025.

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To satisfy customer demand for a high performance “global” mobility service, network operators are facing the need to evolve to a converged “all-IP” centric heterogeneous access infrastructure. However, the integration of such heterogeneous access networks brings major mobility issues. Dynamic service bootstrapping and authorization mechanisms must be in place to efficiently deploy a mobility service, which will allow only legitimate users to access the service. Authentication, access, and accounting based authentication mechanisms like Extensible Authentication Protocol (EAP) incur signalling overheads due to large Round Trip Times (RTTs). As a result, overall handover latency also increases. A fast re-authentication scheme is presented in this chapter, which utilizes IEEE802.21 Media Independent Handover (MIH) services to minimize the EAP authentication process delays and reduce the overall handover latency. In this way, it is shown that the demands mobility places on availability can broadly be met, leaving only the generic issues of Internet availability.
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Mussabbir, Qazi Bouland, and Thomas Owens. "IEEE802.21 Assisted Fast Re-Authentication Scheme over GSABA." In Situational Awareness in Computer Network Defense, 221–43. IGI Global, 2012. http://dx.doi.org/10.4018/978-1-4666-0104-8.ch013.

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To satisfy customer demand for a high performance “global” mobility service, network operators are facing the need to evolve to a converged “all-IP” centric heterogeneous access infrastructure. However, the integration of such heterogeneous access networks brings major mobility issues. Dynamic service bootstrapping and authorization mechanisms must be in place to efficiently deploy a mobility service, which will allow only legitimate users to access the service. Authentication, access, and accounting based authentication mechanisms like Extensible Authentication Protocol (EAP) incur signalling overheads due to large Round Trip Times (RTTs). As a result, overall handover latency also increases. A fast re-authentication scheme is presented in this chapter, which utilizes IEEE802.21 Media Independent Handover (MIH) services to minimize the EAP authentication process delays and reduce the overall handover latency. In this way, it is shown that the demands mobility places on availability can broadly be met, leaving only the generic issues of Internet availability.
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Floto, R. Andres. "Intracellular signalling." In Oxford Textbook of Medicine, edited by John D. Firth, Christopher P. Conlon, and Timothy M. Cox, 256–65. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0033.

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This chapter outlines the general principles of intracellular signalling. Focusing on cell surface receptors, the requirements for effective transmission of information across the plasma membrane are outlined. The principal mechanisms utilized in mammalian signal transduction are described. For each, the pathological consequences of aberrant signalling and means by which pathways can be pharmacologically targeted are described in molecular terms. Intracellular signalling pathways permit the transmission and integration of information within cells. Mammalian receptor signalling relies on only a small number of distinct molecular processes which interact to determine cellular responses. Rapid advances in our knowledge of the mechanisms of intracellular signalling has greatly increased understanding of how cells function physiologically, how they malfunction pathologically, and how their behaviour might be manipulated therapeutically.
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Floto, R. Andres. "Intracellular signalling." In Oxford Textbook of Medicine, 169–76. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.0405.

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This section outlines the general principles of intracellular signalling. Focusing on cell surface receptors, the requirements for effective transmission of information across the plasma membrane are outlined. The principal mechanisms utilized in mammalian signal transduction are described. For each, the pathological consequences of aberrant signalling and means by which pathways can be pharmacologically targeted are described in molecular terms....
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Conference papers on the topic "MET signalling"

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Topel, H., D. Comez, and N. Atabey. "PO-144 HGF/c-met signalling pathway downregulates lncRNA HOTAIR to induce adhesion independent growth in HCC by increasing caveolin-1 expression." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.667.

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Edwards, C., D. G. Waddington, and D. Hutchison. "Meta-signalling for open network control." In 1999 IEEE Second Conference on Open Architectures and Network Programming. Proceedings. OPENARCH '99 (Cat. No.99EX252). IEEE, 1999. http://dx.doi.org/10.1109/opnarc.1999.758435.

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He, Xiaoping, R. Tafazolli, and B. Evans. "An optimised signalling architecture for a MEO/ICO satellite system." In 16th International Communications Satellite Systems Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1996. http://dx.doi.org/10.2514/6.1996-1040.

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Deshpande, Saniya, Jean-Phillip Paquette, Mehrnoosh Vahidpour, Michael Selvanayagam, Rob Lion, Michael Pelstring, Shane Caldwell, Matthew Reagor, and Damon Russell. "Integrating High-Density Microwave Signalling and Packaging With Superconducting Qubits." In 2019 IEEE/MTT-S International Microwave Symposium - IMS 2019. IEEE, 2019. http://dx.doi.org/10.1109/mwsym.2019.8701125.

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Zhan, T., G. Ambrosi, AM Wandmacher, B. Rauscher, J. Betge, N. Rindtorff, RS Häussler, et al. "MEK inhibitors activate Wnt signalling and induce stem cell plasticity in colorectal cancer." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695401.

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Chowdhury, Md Abdullah Al Harun Khan. "Design of an Intelligent Remote Monitoring and Control of Bangladesh Railway Transport System Using Information and Communication Technologies (ICTs)." In IEEE/ASME/ASCE 2008 Joint Rail Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/jrc2008-63009.

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In Bangladesh, transport sectors are developing rapidly to meet the increasing demand for transporting passengers and freight inside and outside the country. But there is not such development in railway transport system. The Bangladesh Railway transport system is still using an old technology to monitor and control signalling, scheduling, operations etc. This paper describes various problems in the existing systems and also solutions have been provided considering the existing railway transport systems of Bangladesh. A new system has been developed to control and monitor the total railway transport system from remote locations. While designing the system, various sensors and actuators have been introduced and also Information and Communication Technologies (ICTs) have been applied in the field of railway transport. So a Machatronics aspect of system has been designed to ensure a collision free, safe and efficient operation and management of railway transport system. This system is not only for monitoring and controlling of railway transport but also ensures efficient asset management. As a result face-to-face accidents, cross-road accidents and accidents due to railway line displacements or breakage can be avoided and there will be no loss of assets and valuable human lives.
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Mendez-Villalon, Armando, David W. P. Thomas, and Steve Greedy. "Performance study of ZigBee networks in a rail environment for signalling systems." In 2017 5th IEEE International Conference on Models and Technologies for Intelligent Transportation Systems (MT-ITS). IEEE, 2017. http://dx.doi.org/10.1109/mtits.2017.8005641.

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Kandolf Sekulović, Lidija. "TOXICITIES OF TARGETED THERAPY AND IMMUNE-RELATED ADVERSE DRUG REACTIONS OF IMMUNOTHERAPY IN THE TREATMENT OF METASTATIC MELANOMA." In Okrugli sto s međunarodnim učešćem "Melanom". Akademija nauka i umjetnosti Bosne i Hercegovine, 2018. http://dx.doi.org/10.5644/pi2019.180.04.

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Targeted therapy and immunotherapy changed the treatment landscape for metastatic melanoma, which is chemotherapy resistant cancer. In pre-innovation era, the overall survival of patients with metastatic melanoma was 6 months, while today 5-year overall survival rate of 34% (and 50% in good prognostic groups) is evident. However, both treatments have their side effects, and cutaneous are the most frequent. Treating physicians in oncology centres, but also primary care specialists, need to be aware of their spectrum which differs for each class of drug: BRAF inhibitors, MEK inhibitors and immunotherapy with anti-PD1 and anti-CTLA4. While BRAF inhibitors have the most prominent adverse effects which are class specific, there are also drug-specific adverse effects. For example, vemurafenib causes photosensitivity, which is not specific for dabrafenib, while dabrafenib induces pyrexia, that occurs much less frequently with other BRAF inhibitors. Cutaneous rash and cutaneous neoplasms which develop due to paradoxical activation of RAS signalling are described with BRAF inhibitor monotherapy. These side-effects are much less common in combination therapy with BRAF and MEK inhibitor, but MEK inhibitor itself causes characteristic acneiform eruption, and serous retinopathy. Immune related adverse drug reactions are a hallmark of the immune checkpoint inhibitor immunotherapy, which can affect every organ system, and most commonly skin, lungs and gastrointestinal system, with differential frequencies recorded with anti-CTLA4 therapy and anti PD-1 therapy. Skin reactions most frequently include pruritus and eczematous reactions, as well as vitiligo-like hypopigmentation, which is linked Melanom 45 to the better response to treatment. In this review, frequent and rare side effects are presented, as well as the current algorithms for their treatment.
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Talwelkar, S., A. Nagaraj, J. Devlin, A. Hemmes, S. Potdar, E. Kiss, K. Salmenkivi, M. Mäyränpää, K. Wennerberg, and E. Verschuren. "PO-489 Tumour-specific oncogenic signalling activities define sensitivity to combinatorial MEK inhibition and stratify Kras-driven lung cancer." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.506.

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Carvajal-Carreno, William, Asuncion P. Cucala Garcia, Antonio Fernandez-Cardador, and Lennart Soder. "Efficient driving algorithms for non-disturbed and disturbed trains with the CBTC signalling system." In 2015 International Conference on Models and Technologies for Intelligent Transportation Systems (MT-ITS). IEEE, 2015. http://dx.doi.org/10.1109/mtits.2015.7223289.

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