Relevant bibliographies by topics / Signalling pathway

Academic literature on the topic 'Signalling pathway'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Signalling pathway"

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Lojk, Jasna, and Janja Marc. "Roles of Non-Canonical Wnt Signalling Pathways in Bone Biology." International Journal of Molecular Sciences 22, no. 19 (October 7, 2021): 10840. http://dx.doi.org/10.3390/ijms221910840.

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The Wnt signalling pathway is one of the central signalling pathways in bone development, homeostasis and regulation of bone mineral density. It consists of numerous Wnt ligands, receptors and co-receptors, which ensure tight spatiotemporal regulation of Wnt signalling pathway activity and thus tight regulation of bone tissue homeostasis. This enables maintenance of optimal mineral density, tissue healing and adaptation to changes in bone loading. While the role of the canonical/β-catenin Wnt signalling pathway in bone homeostasis is relatively well researched, Wnt ligands can also activate several non-canonical, β-catenin independent signalling pathways with important effects on bone tissue. In this review, we will provide a thorough overview of the current knowledge on different non-canonical Wnt signalling pathways involved in bone biology, focusing especially on the pathways that affect bone cell differentiation, maturation and function, processes involved in bone tissue structure regulation. We will describe the role of the two most known non-canonical pathways (Wnt/planar cell polarity pathways and Wnt/Ca2+ pathway), as well as other signalling pathways with a strong role in bone biology that communicate with the Wnt signalling pathway through non-canonical Wnt signalling. Our goal is to bring additional attention to these still not well researched but important pathways in the regulation of bone biology in the hope of prompting additional research in the area of non-canonical Wnt signalling pathways.
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Sanz-Ezquerro, Juan José, and Ana Cuenda. "p38 Signalling Pathway." International Journal of Molecular Sciences 22, no. 3 (January 20, 2021): 1003. http://dx.doi.org/10.3390/ijms22031003.

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p38 Mitogen activated protein kinases (p38MAPK) are a highly evolutionary conserved group of protein kinases, which are central for cell adaptation to environmental changes as well as for immune response, inflammation, tissue regeneration, and tumour formation [...]
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Gomi, Kenji, and Makoto Matsuoka. "Gibberellin signalling pathway." Current Opinion in Plant Biology 6, no. 5 (October 2003): 489–93. http://dx.doi.org/10.1016/s1369-5266(03)00079-7.

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Wang, Lin-Qing, Jing-Cai Liu, Chun-Lei Chen, Shun-Feng Cheng, Xiao-Feng Sun, Yong Zhao, Shen Yin, et al. "Regulation of primordial follicle recruitment by cross-talk between the Notch and phosphatase and tensin homologue (PTEN)/AKT pathways." Reproduction, Fertility and Development 28, no. 6 (2016): 700. http://dx.doi.org/10.1071/rd14212.

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The growth of oocytes and the development of follicles require certain pathways involved in cell proliferation and survival, such as the phosphatidylinositol 3-kinase (PI3K) pathway and the Notch signalling pathway. The aim of the present study was to investigate the interaction between Notch and the PI3K/AKT signalling pathways and their effects on primordial follicle recruitment. When the Notch pathway was inhibited by L-685,458 or N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycinet-butyl ester (DAPT) in vitro, the expression of genes in the pathway and the percentage of oocytes in growing follicles decreased significantly in mouse ovaries. By 2 days postpartum, ovaries exposed to DAPT, short interference (si) RNA against Notch1 or siRNA against Hairy and enhancer of split-1 (Hes1) had significantly decreased expression of HES1, the target protein of the Notch signalling pathway. In contrast, expression of phosphatase and tensin homologue (Pten), a negative regulator of the AKT signalling pathway, was increased significantly. Co immunoprecipitation (Co-IP) revealed an interaction between HES1 and PTEN. In addition, inhibition of the Notch signalling pathway suppressed AKT phosphorylation and the proliferation of granulosa cells. In conclusion, the recruitment of primordial follicles was affected by the proliferation of granulosa cells and regulation of the interaction between the Notch and PI3K/AKT signalling pathways.
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Jarnæss, E., and K. Taskén. "Spatiotemporal control of cAMP signalling processes by anchored signalling complexes." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 931–37. http://dx.doi.org/10.1042/bst0350931.

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Ligand-induced changes in cAMP concentration vary in duration, amplitude and extension into the cell. cAMP microdomains are shaped by adenylate cyclases that form cAMP as well as PDEs (phosphodiesterases) that degrade cAMP. Various extracellular signals converge on the cAMP/PKA (protein kinase A) pathway through ligand binding to GPCRs (G-protein-coupled receptors) and the cAMP/PKA pathway is therefore tightly regulated on several levels to maintain specificity in the multitude of signal inputs. AKAPs (A-kinase-anchoring proteins) target PKA to specific substrates and distinct subcellular compartments, providing spatial and temporal specificity for mediation of biological effects channelled through the cAMP/PKA pathway. AKAPs also serve as scaffolding proteins that assemble PKA together with signal terminators such as phosphoprotein phosphatases and cAMP-specific PDEs as well as components of other signalling pathways into multiprotein signalling complexes.
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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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Hülsken, Jörg, and Jürgen Behrens. "The Wnt signalling pathway." Journal of Cell Science 113, no. 20 (January 1, 2000): 3545. http://dx.doi.org/10.1242/jcs.113.20.3545.

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Huelsken, J. "The Wnt signalling pathway." Journal of Cell Science 115, no. 21 (November 1, 2002): 3977–78. http://dx.doi.org/10.1242/jcs.00089.

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CARTER-SU, CHRISTIN, ANTHONY PJ KING, LAWRENCE S. ARGETSINGER, LISA S. SMIT, JOYCE VANDERKUUR, and GEORGE S. CAMPBELL. "Signalling Pathway of GH." Endocrine Journal 43, Suppl (1996): S65—S70. http://dx.doi.org/10.1507/endocrj.43.suppl_s65.

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Lizcano, Jose M., and Dario R. Alessi. "The insulin signalling pathway." Current Biology 12, no. 7 (April 2002): R236—R238. http://dx.doi.org/10.1016/s0960-9822(02)00777-7.

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Dissertations / Theses on the topic "Signalling pathway"

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Baumann, Fabrizio. "Cell signalling through the Wnt pathway /." [S.l.] : [s.n.], 2004. http://www.zb.unibe.ch/download/eldiss/04baumann_f.pdf.

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Ng, Ming-him. "Ras signalling pathway and MLL-rearranged leukaemias." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B3643419X.

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Buchanan, V. S. "Components of the Ret oncogene signalling pathway." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597050.

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The Multiple Endocrine Neoplasia type 2 syndromes are dominantly inherited cancer syndromes of tumour formation (affecting the thyroid C-cells, the adrenal chromaffin cells and the parathyroids) and developmental abnormalities. Germline activating mutations in the ret proto-oncogene, encoding a receptor tyrosine kinase (RTK), have previously been shown to predispose to MEN 2. In order to understand how Ret mutations cause MEN 2, it is important to understand the biology of Ret, including the signal transduction pathways recruited by both the normal and mutant Ret receptors. I have attempted to identify signalling proteins activated by Ret using two approaches. Firstly, the yeast 2-hybrid system was used to screen an expression library with the intracellular domains of both wild-type and MEN 2B Ret, in order to identify interacting proteins. The unreliability of the screen may have resulted from the Ret fusion proteins used being capable of weak activation of the 2-hybrid reporter genes in the absence of an interacting partner. Secondly, protein tyrosine phosphatases (PTPs) were chosen as candidates to interact with Ret. The population of PTPs expressed in tissues affected by MEN 2 (adrenal gland and a C-cell tumour cell line) was examined by degenerate RT-PCR of conserved phosphate domains. Five PTPs (PTPγ, LAR, PTPβ, SHP1 and SHP2) whose expression were detected were chosen as potential modulators of Ret and studied further. SHP1 and Ret expression studies on neural cell lines indicated that the PC12, Neuro 2A and SH-SY-5Y cell lines might be suitable for further signalling studies on SHP1 and Ret. NT cells would also be suitable if an efficient method of transfection could be found.
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Ng, Ming-him, and 吳明謙. "Ras signalling pathway and MLL-rearranged leukaemias." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37238656.

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Horton, Caroline Alison. "Computational modelling of cell signalling pathway dynamics." Thesis, University of Liverpool, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433816.

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Pogson, Mark. "Modelling the intracellular NF-κB signalling pathway." Thesis, University of Sheffield, 2006. http://etheses.whiterose.ac.uk/10353/.

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NF-κB is a transcription factor which is central to the regulation of genes involved in inflammatory and immune responses. Understanding the operation of NF-κB and its associated intracellular signalling pathway is essential in order to control a wide range of chronic inflammatory diseases, including asthma and rheumatoid arthritis. Abnormalities in the pathway are present in a variety of human cancers and may also affect the pathogenesis of Alzheimer's disease. Computational modelling of the signalling pathway is necessary to overcome the practical limitations of biological experiments and to facilitate a more comprehensive understanding of the system. The thesis begins by outlining existing understanding of the NF-κB signalling pathway, which in conjunction with a review of modelling methods is used to inform a different approach to model the pathway, using computational agents to represent individual molecules and receptors. The agent-based model is tested with well-understood chemical reactions before being used to describe the pathway. This provides a good appreciation of the system as a whole, offering a detailed description of events at every step in the pathway and allowing investigation of stochastic, spatial and structural parameters. The modelling process and simulation help to provide a prediction about the role of actin filaments of the cytoskeleton in regulating the unstimulated pathway; this is quantitatively validated by biological experiment. The effect of cell shape on the pathway is also investigated.
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Annavarapu, Srinivas Rao. "Characterisation of Wnt signalling pathway in rhabdomyosarcoma." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3009225/.

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Introduction: Rhabdomyosarcoma (RMS) remains one of the most challenging tumours in paediatric oncology, accounting for around 5% of all malignant paediatric tumours. Of the two major subtypes of RMS, embryonal and alveolar, the latter portends a poorer clinical outcome. Canonical Wnt signalling pathway is an important evolutionarily conserved signalling pathway that is required for muscle development and embryonal somite patterning. β-Catenin is a potent nuclear transcriptional activator and is the central effector of the canonical Wnt signalling pathway. Interestingly, constitutional activation of Wnt signalling also promotes tissue invasion and metastasis in various tumours. Aims: This study aims to characterise the canonical Wnt/β-catenin signalling in paediatric RMS to assess its functional relevance to the tumourigenesis of RMS and to investigate if modulation of this pathway could provide a therapeutic target for RMS. Results: When we evaluated the immunohistochemical expression of β-catenin in the paraffin-embedded tissues derived from 44 RMS patients, we found positive expression in 26 cases. There was positive expression of β-catenin in the cytoplasm or the cell membrane of alveolar (9/14) and embryonal RMS (15/30); nuclear staining was only seen in two embryonal RMS cases. Next, we assessed β-catenin expression by immunoblot analysis in four RMS cell lines - RD and RD18 (embryonal); Rh4 and Rh30 (alveolar). We were able to demonstrate expression of major canonical Wnt proteins in all cell lines that included: β-catenin, glycogen synthase kinase-3β, disheveled, axin-1, naked and LRP-6. To assess the functional significance of these proteins, we incubated the RMS cell lines with human recombinant Wnt3a to stimulate the Wnt signalling pathway. Thereafter, by using cellular fractionation and immunofluorescence experiments, we demonstrated change in the phosphorylation status of β-catenin, stabilisation of its active form and its nuclear translocation. By employing a TOP/FOP flash reporter gene assay, we showed a T-cell factor/lymphoid-enhancing factor (TCF/LEF)-mediated transactivation. In addition, we found a significant decrease in the proliferation rate of the alveolar RMS cells after Wnt3a stimulation. This decrease in proliferation rate was thought to be due to the concomitant activation of myodifferentiation as seen by the immunoblot expression of myogenin, MyoD1 and myf5. Our data indicates that the major regulatory proteins of the canonical Wnt/β-catenin signalling are expressed in RMS and that functional activation of this pathway, at least in a subset of RMS, may represent a novel therapeutic target.
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Brightman, Frances A. "Computer simulation of a growth factor signal transduction pathway." Thesis, Oxford Brookes University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340868.

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Filippi, Marta Cristina. "Signalling pathway in appressorium formation in Magnaporthe grisea." Texas A&M University, 2004. http://hdl.handle.net/1969.1/1109.

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We identified a synthetic hexapeptide that blocks Magnaporthe grisea appressorium formation, in artificial hydrophobic surface. The results suggest that peptides interfere with surface recognition. M. grisea non pathogenic pth1 mutants were complemented by N. crassa orthologous gene suggesting that the biochemical function of pth1 has not evolved specifically to play a role in appressorium development.
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Hardcastle, Zoe. "The Sonic Hedgehog signalling pathway in tooth development." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368160.

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Books on the topic "Signalling pathway"

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Bhimani, Munsif Ali. Detecting mediators of the Flk-1 signalling pathway by mRNA differential display. Ottawa: National Library of Canada, 1998.

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Nguyen, Melody Hong Hanh. TEL-Jak2 chromosomal translocations and the PI3' kinase and PKB signalling pathway. Ottawa: National Library of Canada, 2000.

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Rizza, Annalisa. Identification of components in the BBX24 light signalling pathway in Arabidopsis thaliana. [S.I: s.n.], 2013.

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1943-, Lavin Martin, and Watters Dianne 1952-, eds. Signalling pathways in apoptosis. Amsterdam: Harwood Academic, 1999.

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O, Pickens Charles, ed. Cell apoptotic signalling pathways. New York: Nova Biomedical Books, 2007.

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Chadwick, Derek J., and Jamie Goode, eds. Signalling Pathways in Acute Oxygen Sensing. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/9780470035009.

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Symposium on Signalling Pathways in Acute Oxygen Sensing (2005 Novartis Foundation). Signalling pathways in acute oxygen sensing. Chichester, UK: John Wiley, 2006.

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Foundation, Novartis. Signalling Pathways in Acute Oxygen Sensing. New York: John Wiley & Sons, Ltd., 2006.

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Tuominen-Gustafsson, Helena Birgitta. Calcium signalling pathways in human neutrophils. Åbo: Åbo Akademis Förlag, 1998.

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Dua, Kamal, Raimar Löbenberg, Ângela Cristina Malheiros Luzo, Shakti Shukla, and Saurabh Satija, eds. Targeting Cellular Signalling Pathways in Lung Diseases. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6827-9.

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Book chapters on the topic "Signalling pathway"

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Robert, Jacques. "Cytokines Pathway." In Textbook of Cell Signalling in Cancer, 55–65. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_4.

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Robert, Jacques. "TGFβ Pathway." In Textbook of Cell Signalling in Cancer, 67–76. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_5.

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Robert, Jacques. "Wnt Pathway." In Textbook of Cell Signalling in Cancer, 93–100. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_7.

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Robert, Jacques. "Notch Pathway." In Textbook of Cell Signalling in Cancer, 101–7. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_8.

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Robert, Jacques. "Hedgehog Pathway." In Textbook of Cell Signalling in Cancer, 109–15. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_9.

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Bashri, Gausiya, Abreeq Fatima, Shikha Singh, and Sheo Mohan Prasad. "Interplay of Brassinosteroids and Auxin for Understanding of Signaling Pathway." In Brassinosteroids Signalling, 137–54. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-5743-6_8.

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Robert, Jacques. "MAP Kinase Pathway." In Textbook of Cell Signalling in Cancer, 27–41. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_2.

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Toni, Tina, Juliane Liepe, and Michael P. H. Stumpf. "Inference of Signalling Pathway Models." In Handbook of Statistical Systems Biology, 417–39. Chichester, UK: John Wiley & Sons, Ltd, 2011. http://dx.doi.org/10.1002/9781119970606.ch21.

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Robert, Jacques. "Phosphatidylinositol 3-Kinase Pathway." In Textbook of Cell Signalling in Cancer, 43–54. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14340-8_3.

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Holik, Aliaksei, and Alan R. Clarke. "Targeting Wnt Signalling in Cancer." In Targeting the Wnt Pathway in Cancer, 165–82. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-8023-6_8.

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Conference papers on the topic "Signalling pathway"

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Spirina, L. V., Y. A. Usynin, I. V. Kondakova, Z. A. Yurmazov, E. M. Slonimskaya, and E. S. Kolegova. "The AKT-mTOR signalling pathway in kidney cancer tissues." In NEW OPERATIONAL TECHNOLOGIES (NEWOT’2015): Proceedings of the 5th International Scientific Conference «New Operational Technologies». AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4936067.

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Simone Clement, Michelle, Boe Sandahl Sorensen, Sinead Cuffe, Stephen Finn, and Kathy Gately. "Targeting STAT3 pathway signalling in EGFR TKI resistant NSCLC." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.330.

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Woodcock, Hannah, Simon Peace, Carmel Nanthakumar, Toby Maher, Paul Mercer, and Rachel Chamers. "mTOR signalling is an essential pathway for TGF-β1induced collagen synthesis." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa935.

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Tournier, Laurent, and Madalena Chaves. "Operational interactions in genetic networks: Application to an apoptosis signalling pathway." In 2009 European Control Conference (ECC). IEEE, 2009. http://dx.doi.org/10.23919/ecc.2009.7074679.

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Van der Ploeg, P., W. Verhaegh, J. De Hullu, A. Van der Stolpe, and J. Piek. "PO-138 Hedgehog signalling pathway activity in high-grade serous ovarian carcinoma." 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-eacr25.662.

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O'Toole, DP, PD Hassett, AM Leo, BD Higgins, and JG Laffey. "Molecular Effects of Hypercapnic Acidosis on the NF-κB Intracellular Signalling Pathway." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1931.

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Tung, C. H., J. M. Hsu, M. C. Lu, and N. S. Lai. "AB0055 Hydroxychloroquine inhibits soluble cd154 production through ca2+ and pkc signalling pathway." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3172.

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Seaton, Daniel D., and J. Krishnan. "Modelling the Influence of Allostery on Crosstalk in the Phosphatidylinositol Signalling Pathway." In Intelligent Systems and Control. Calgary,AB,Canada: ACTAPRESS, 2011. http://dx.doi.org/10.2316/p.2011.742-046.

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Williams, Richard A., Jon Timmis, and Eva E. Qwarnstrom. "Investigating IKK dynamics in the NF-κB signalling pathway using X-Machines." In 2017 IEEE Congress on Evolutionary Computation (CEC). IEEE, 2017. http://dx.doi.org/10.1109/cec.2017.7969320.

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Chou, JC, PS Wang, SW Wang, and H. Lin. "PO-183 Prolactin activation of JAK2/STAT3 signalling pathway through GHR in NSCLC." 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-eacr25.704.

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Reports on the topic "Signalling pathway"

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Friedman, Haya, Julia Vrebalov, James Giovannoni, and Edna Pesis. Unravelling the Mode of Action of Ripening-Specific MADS-box Genes for Development of Tools to Improve Banana Fruit Shelf-life and Quality. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592116.bard.

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Fruit deterioration is a consequence of a genetically-determined fruit ripening and senescence programs, in which developmental factors lead to a climacteric rise of ethylene production in ethylene-sensitive fruits such as tomato and banana. Breeding of tomato with extended fruit shelf life involves the incorporation of a mutation in RIN, a MADS-box transcription factor participating in developmental control signalling of ripening. The RIN mode of action is not fully understood, and it may be predicted to interact with other MADS-box genes to execute its effects. The overall goal of this study was to demonstrate conservation of ripening control functions between banana and tomato and thus, the potential to genetically extend shelf-life in banana based on tools developed in tomato. The specific objectives were: 1. To increase the collection of potential RIN-like genes from banana; 2. To verify their action as developmental regulators; 3. To elucidate MADS-box gene mode of action in ripening control; 4. To create transgenic banana plants that express low levels of endogenous Le-RIN- like, MaMADS- gene(s). We have conducted experiments in banana as well as in tomato. In tomato we have carried out the transformation of the tomato rin mutant with the MaMADS1 and MaMADS2 banana genes. We have also developed a number of domain swap constructs to functionally examine the ripening-specific aspects of the RIN gene. Our results show the RIN-C terminal region is essential for the gene to function in the ripening signalling pathway. We have further explored the tomato genome databases and recovered an additional MADS-box gene necessary for fruit ripening. This gene has been previously termed TAGL1 but has not been functionally characterized in transgenic plants. TAGL1 is induced during ripening and we have shown via RNAi repression that it is necessary for both fleshy fruit expansion and subsequent ripening. In banana we have cloned the full length of six MaMADS box genes from banana and determined their spatial and temporal expression patterns. We have created antibodies to MaMADS2 and initiated ChI assay. We have created four types of transgenic banana plants designed to reduce the levels of two of the MaMADS box genes. Our results show that the MaMADS-box genes expression in banana is dynamically changing after harvest and most of them are induced at the onset of the climacteric peak. Most likely, different MaMADS box genes are active in the pulp and peel and they are differently affected by ethylene. Only the MaMADS2 box gene expression is not affected by ethylene indicating that this gene might act upstream to the ethylene response pathway. The complementation analysis in tomato revealed that neither MaMADS1 nor MaMADS2 complement the rin mutation suggesting that they have functionally diverged sufficiently to not be able to interact in the context of the tomato ripening regulatory machinery. The developmental signalling pathways controlling ripening in banana and tomato are not identical and/or have diverged through evolution. Nevertheless, at least the genes MaMADS1 and MaMADS2 constitute part of the developmental control of ripening in banana, since transgenic banana plants with reduced levels of these genes are delayed in ripening. The detailed effect on peel and pulp, of these transgenic plants is underway. So far, these transgenic bananas can respond to exogenous ethylene, and they seem to ripen normally. The response to ethylene suggest that in banana the developmental pathway of ripening is different than that in tomato, because rin tomatoes do not ripen in response to exogenous ethylene, although they harbor the ethylene response capability This study has a major contribution both in scientific and agricultural aspects. Scientifically, it establishes the role of MaMADS box genes in a different crop-the banana. The developmental ripening pathway in banana is similar, but yet different from that of the model plant tomato and one of the major differences is related to ethylene effect on this pathway in banana. In addition, we have shown that different components of the MaMADS-box genes are employed in peel and pulp. The transgenic banana plants created can help to further study the ripening control in banana. An important and practical outcome of this project is that we have created several banana transgenic plants with fruit of extended shelf life. These bananas clearly demonstrate the potential of MaMADS gene control for extending shelf-life, enhancing fruit quality, increasing yield in export systems and for improving food security in areas where Musaspecies are staple food crops.
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2

Wagner, D. Ry, Eliezer Lifschitz, and Steve A. Kay. Molecular Genetic Analysis of Flowering in Arabidopsis and Tomato. United States Department of Agriculture, May 2002. http://dx.doi.org/10.32747/2002.7585198.bard.

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The primary objectives for the US lab included: the characterization of ELF3 transcription and translation; the creation and characterization of various transgenic lines that misexpress ELF3; defining genetic pathways related to ELF3 function regulating floral initiation in Arabidopsis; and the identification of genes that either interact with or are regulated by ELF3. Light quality, photoperiod, and temperature often act as important and, for some species, essential environmental cues for the initiation of flowering. However, there is relatively little information on the molecular mechanisms that directly regulate the developmental pathway from the reception of the inductive light signals to the onset of flowering and the initiation of floral meristems. The ELF3 gene was identified as possibly having a role in light-mediated floral regulation since elj3 mutants not only flower early, but exhibit light-dependent circadian defects. We began investigating ELF3's role in light signalling and flowering by cloning the ELF3 gene. ELF3 is a novel gene only present in plant species; however, there is an ELF3 homolog within Arabidopsis. The Arabidopsis elj3 mutation causes arrhythmic circadian output in continuous light; however, we show conclusively normal circadian function with no alteration of period length in elj3 mutants in dark conditions and that the light-dependent arrhythmia observed in elj3 mutants is pleiotropic on multiple outputs regardless of phase. Plants overexpressing ELF3 have an increased period length in constant light and flower late in long-days; furthermore, etiolated ELF3-overexpressing seedlings exhibit a decreased acute CAB2 response after a red light pulse, whereas the null mutant is hypersensitive to acute induction. This finding suggests that ELF3 negatively regulates light input to both the clock and its outputs. To determine whether ELF3's action is phase dependent, we examined clock resetting by light pulses and constructed phase response curves. Absence of ELF3 activity causes a significant alteration of the phase response curve during the subjective night, and overexpression of ELF3 results in decreased sensitivity to the resetting stimulus, suggesting that ELF3 antagonizes light input to the clock during the night. Indeed, the ELF3 protein interacts with the photoreceptor PHYB in the yeast two-hybrid assay and in vitro. The phase ofELF3 function correlates with its peak expression levels of transcript and protein in the subjective night. ELF3 action, therefore, represents a mechanism by which the oscillator modulates light resetting. Furthermore, flowering time is dependent upon proper expression ofELF3. Scientifically, we've made a big leap in the understanding of the circadian system and how it is coupled so tightly with light reception in terms of period length and clock resetting. Agriculturally, understanding more about the way in which the clock perceives and relays temporal information to pathways such as those involved in the floral transition can lead to increased crop yields by enabling plants to be grown in suboptimal conditions.
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3

Miller, Gad, and Jeffrey F. Harper. Pollen fertility and the role of ROS and Ca signaling in heat stress tolerance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598150.bard.

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The long-term goal of this research is to understand how pollen cope with stress, and identify genes that can be manipulated in crop plants to improve reproductive success during heat stress. The specific aims were to: 1) Compare heat stress dependent changes in gene expression between wild type pollen, and mutants in which pollen are heat sensitive (cngc16) or heat tolerant (apx2-1). 2) Compare cngc16 and apx2 mutants for differences in heat-stress triggered changes in ROS, cNMP, and Ca²⁺ transients. 3) Expand a mutant screen for pollen with increased or decreased thermo-tolerance. These aims were designed to provide novel and fundamental advances to our understanding of stress tolerance in pollen reproductive development, and enable research aimed at improving crop plants to be more productive under conditions of heat stress. Background: Each year crop yields are severely impacted by a variety of stress conditions, including heat, cold, drought, hypoxia, and salt. Reproductive development in flowering plants is highly sensitive to hot or cold temperatures, with even a single hot day or cold night sometimes being fatal to reproductive success. In many plants, pollen tube development and fertilization is often the weakest link. Current speculation about global climate change is that most agricultural regions will experience more extreme environmental fluctuations. With the human food supply largely dependent on seeds, it is critical that we consider ways to improve stress tolerance during fertilization. The heat stress response (HSR) has been intensively studied in vegetative tissues, but is poorly understood during reproductive development. A general paradigm is that HS is accompanied by increased production of reactive oxygen species (ROS) and induction of ROS-scavenging enzymes to protect cells from excess oxidative damage. The activation of the HSR has been linked to cytosolic Ca²⁺ signals, and transcriptional and translational responses, including the increased expression of heat shock proteins (HSPs) and antioxidative pathways. The focus of the proposed research was on two mutations, which have been discovered in a collaboration between the Harper and Miller labs, that either increase or decrease reproductive stress tolerance in a model plant, Arabidopsis thaliana (i.e., cngc16--cyclic nucleotide gated channel 16, apx2-1--ascorbate peroxidase 2,). Major conclusions, solutions, achievements. Using RNA-seq technology, the expression profiles of cngc16 and apx2 pollen grains were independently compared to wild type under favourable conditions and following HS. In comparison to a wild type HSR, there were 2,776 differences in the transcriptome response in cngc16 pollen, consistent with a model in which this heat-sensitive mutant fails to enact or maintain a normal wild-type HSR. In a comparison with apx2 pollen, there were 900 differences in the HSR. Some portion of these 900 differences might contribute to an improved HSR in apx2 pollen. Twenty-seven and 42 transcription factor changes, in cngc16 and apx2-1, respectively, were identified that could provide unique contributions to a pollen HSR. While we found that the functional HS-dependent reprogramming of the pollen transcriptome requires specific activity of CNGC16, we identified in apx2 specific activation of flavonol-biosynthesis pathway and auxin signalling that support a role in pollen thermotolerance. Results from this study have identified metabolic pathways and candidate genes of potential use in improving HS tolerance in pollen. Additionally, we developed new FACS-based methodology that can quantify the stress response for individual pollen in a high-throughput fashion. This technology is being adapted for biological screening of crop plant’s pollen to identify novel thermotolerance traits. Implications, both scientific and agricultural. This study has provided a reference data on the pollen HSR from a model plant, and supports a model that the HSR in pollen has many differences compared to vegetative cells. This provides an important foundation for understanding and improving the pollen HSR, and therefor contributes to the long-term goal of improving productivity in crop plants subjected to temperature stress conditions. A specific hypothesis that has emerged from this study is that pollen thermotolerance can be improved by increasing flavonol accumulation before or during a stress response. Efforts to test this hypothesis have been initiated, and if successful have the potential for application with major seed crops such as maize and rice.
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4

Sionov, Edward, Nancy Keller, and Shiri Barad-Kotler. Mechanisms governing the global regulation of mycotoxin production and pathogenicity by Penicillium expansum in postharvest fruits. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604292.bard.

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The original objectives of the study, as defined in the approved proposal, are: To characterize the relationship of CreA and LaeA in regulation of P T production To understand how PacC modulates P. expansumpathogenicity on apples To examine if other secondary metabolites are involved in virulence or P. expansumfitness To identify the signaling pathways leading to PAT synthesis Penicilliumexpansum, the causal agent of blue mould rot, is a critical health concern because of the production of the mycotoxinpatulin (PAT) in colonized apple fruit tissue. Although PAT is produced by many Penicilliumspecies, the factors activating its biosynthesis were not clear. This research focused on host and fungal mechanisms of activation of LaeA (the global regulator of secondary metabolism), PacC (the global pH modulator) and CreA (the global carbon catabolite regulator) on PAT synthesis with intention to establish P. expansumas the model system for understanding mycotoxin synthesis in fruits. The overall goal of this proposal is to identify critical host and pathogen factors that mechanistically modulate P. expansumgenes and pathways to control activation of PAT production and virulence in host. Several fungal factors have been correlated with disease development in apples, including the production of PAT, acidification of apple tissue by the fungus, sugar content and the global regulator of secondary metabolism and development, LaeA. An increase in sucrose molarity in the culture medium from 15 to 175 mM negatively regulated laeAexpression and PAT accumulation, but, conversely, increased creAexpression, leading to the hypothesis that CreA could be involved in P. expansumPAT biosynthesis and virulence, possibly through the negative regulation of LaeA. We found evidence for CreAtranscriptional regulation of laeA, but this was not correlated with PAT production either in vitro or in vivo, thus suggesting that CreA regulation of PAT is independent of LaeA. Our finding that sucrose, a key ingredient of apple fruit, regulates PAT synthesis, probably through suppression of laeAexpression, suggests a potential interaction between CreA and LaeA, which may offer control therapies for future study. We have also identified that in addition to PAT gene cluster, CreA regulates other secondary metabolite clusters, including citrinin, andrastin, roquefortine and communesins, during pathogenesis or during normal fungal growth. Following creation of P. expansumpacCknockout strain, we investigated the involvement of the global pH regulator PacC in fungal pathogenicity. We demonstrated that disruption of the pH signaling transcription factor PacC significantly decreased the virulence of P. expansumon deciduous fruits. This phenotype is associated with an impairment in fungal growth, decreased accumulation of gluconic acid and reduced synthesis of pectolytic enzymes. We showed that glucose oxidase- encoding gene, which is essential for gluconic acid production and acidification during fruit colonization, was significantly down regulated in the ΔPepacCmutant, suggesting that gox is PacC- responsive gene. We have provided evidence that deletion of goxgene in P. expansumled to a reduction in virulence toward apple fruits, further indicating that GOX is a virulence factor of P. expansum, and its expression is regulated by PacC. It is also clear from the present data that PacC in P. expansumis a key factor for the biosynthesis of secondary metabolites, such as PAT. On the basis of RNA-sequencing (RNA-seq) analysis and physiological experimentation, the P. expansumΔlaeA, ΔcreAand ΔpacCmutants were unable to successfully colonize apples for a multitude of potential mechanisms including, on the pathogen side, a decreased ability to produce proteolytic enzymes and to acidify the environment and impaired carbon/nitrogen metabolism and, on the host side, an increase in the oxidative defence pathways. Our study defines these global regulatory factors and their downstream signalling pathways as promising targets for the development of strategies to fight against this post-harvest pathogen.
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