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Books on the topic 'Signalling pathway'

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Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

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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2

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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3

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

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4

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

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5

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

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6

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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7

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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8

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

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9

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

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10

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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11

Lo Schiavo, Fiorella, Robert L. Last, Giorgio Morelli, and Natasha V. Raikhel, eds. Cellular Integration of Signalling Pathways in Plant Development. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72117-5.

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12

Sheldon, Katherine. Cell signalling pathways: Productive sources of pharmaceutical targets. Westborough, MA: D & MD Publications, 2004.

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13

Taha, Celia. Signalling pathways regulating glucose transporter expression in muscle cells. Ottawa: National Library of Canada, 1996.

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14

Patel, Nayan Govindbhai. Signalling pathways important in human adipose tissue growth and function. Birmingham: University of Birmingham, 2003.

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15

Yang, Shen-Hsui. Insulin signalling pathways involved in selective control of hepatic gene expression. Manchester: University of Manchester, 1995.

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16

Kekkonen, Viktoria. Characterization of bacterial RNA and DNA signalling pathways that induce cellular dysfunction. Sudbury, Ont: Laurentian University, 2006.

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17

Yule, Jennifer M. Phosphatidylcholine and sphingomyelin signalling pathways in the control of proliferation and differentiation. Birmingham: University of Birmingham, 1996.

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18

Sittaro, Dino. c-Kit signalling pathways and survival signals in a factor-dependent leukemia. Ottawa: National Library of Canada, 2000.

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19

Woods, Stacy Ann. Signalling pathways regulating expression of vascular endothelial growth factor in human malignant astrocytomas. Ottawa: National Library of Canada, 2001.

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20

Derek, Chadwick, Goode Jamie, and Novartis Foundation, eds. Signalling pathways in acute oxygen sensing.: [editors Derek J. Chadwick and Jamie Goode]. Chichester: John Wiley, 2006.

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21

Perkins, Jonathan Edwards. A study of EGF-induced intracellular signalling pathways and effects in first trimester trophoblast. Birmingham: University of Birmingham, 2003.

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22

Radford, David John. Investigation of neutrophil signalling pathways activated by autoantibodies (ANCA) from patients with systemic vasculitis. Birmingham: University of Birmingham, 1998.

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23

Conroy, Louise Anne. The development of t-lymphocytes within the murine foetal thymus: The role of intracellular signalling pathways. Birmingham: University of Birmingham, 1992.

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24

Brant, Dawn Patricia. The signalling pathways involved in thrombin-induced morphological change and DNA synthesis in human neuroepithelial cells. Birmingham: University of Birmingham, 1997.

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25

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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26

Leroith, Derek. Jnk Signalling Pathway. Eurekah.com, Inc., 2006.

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27

Lam, Eric W.-F. Phosphoinositide 3-Kinase Signalling Pathway. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2006. http://dx.doi.org/10.1142/p428.

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28

Cheng, Zhiyong. Nutritional Signalling Pathway Activities in Obesity and Diabetes. Royal Society of Chemistry, The, 2020.

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29

Cheng, Zhiyong. Nutritional Signalling Pathway Activities in Obesity and Diabetes. Royal Society of Chemistry, The, 2020.

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30

Jakstat Signalling Methods And Protocols. Humana Press, 2012.

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31

Kockeritz, Lisa Karen. Roles of Wnt signalling pathway components in embryonic development and disease. 2005.

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32

Phosphoinositide 3-kinase Signalling Pathway: The Key to Cell Proliferation And Death. Imperial College Press, 2006.

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33

Kavsak, Peter. Smurfs are E3 ubiquitin protein ligases that inhibit the transforming growth factor beta signalling pathway. 2001.

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34

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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35

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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36

Hodgkiss, Andrew. Introduction to cancer biology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0001.

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A brief introduction to cancer biology, aimed at psychiatrists, is offered. Selective DNA transcription, the cell cycle, receptor tyrosine kinases, and cell signalling pathways are introduced, using the EGFR/RAS/MAPK pathway as an exemplar. The molecular pathology of oncogenesis is summarized, including discussion of oncogenes, tumour suppressor genes, and examples of driver mutations. The exploitation of such mutations in stratified medicine, using molecularly targeted agents, is mentioned. Finally, Hanahan and Weinberg’s six hallmarks of cancer are listed, adding angiogenesis and metastasis to the picture of oncogenesis.

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37

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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38

Pickens, Charles O. Cell Apoptotic Signalling Pathways. Nova Science Pub Inc, 2006.

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39

Watters, Dianne, and Martin Lavin. Signalling Pathways in Apoptosis. Taylor & Francis Group, 1999.

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40

Lavin, Martin, and Diane Watters. Signalling Pathways in Apoptosis. Taylor & Francis Group, 1999.

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41

Lavin, Martin, and Diane Watters. Signalling Pathways in Apoptosis. Taylor & Francis Group, 1999.

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42

Sanz-Ezquerro, Juan J., Andrea E. Münsterberg, and Sigmar Stricker, eds. Signalling Pathways in Embryonic Development. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-346-7.

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43

Lacal, Carlos. Signalling Pathways in Abiotic Stress. Arcler Education Inc, 2017.

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44

Kühn, Wolfgang, and Gerd Walz. The molecular basis of ciliopathies and cyst formation. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0303.

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Abnormalities of the cilium, termed ‘ciliopathies’, are the prime suspect in the pathogenesis of renal cyst formation because the gene products of cystic disease-causing genes localize to them, or near them. However, we only partially understand how cilia maintain the geometry of kidney tubules, and how abnormal cilia lead to renal cysts, and the diverse range of diseases attributed to them. Some non-cystic diseases share pathology of the same structures. Although still incompletely understood, cilia appear to orient cells in response to extracellular cues to maintain the overall geometry of a tissue, thereby intersecting with the planar cell polarity (PCP) pathway and the actin cytoskeleton. The PCP pathway controls two morphogenetic programmes, oriented cell division (OCD) and convergent extension (CE) through cell intercalation that both seem to play a critical role in cyst formation. The two-hit theory of cystogenesis, by which loss of the second normal allele causes tubular epithelial cells to form kidney cysts, has been largely borne out. Additional hits and influences may better explain the rate of cyst formation and inter-individual differences in disease progression. Ciliary defects appear to converge on overlapping signalling modules, including mammalian target of rapamycin and cAMP pathways, which can be targeted to treat human cystic kidney disease irrespective of the underlying gene mutation.

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45

Novartis, Foundation. Signalling Pathways in Acute Oxygen Sensing. Wiley & Sons, Incorporated, John, 2006.

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46

Goode, Jamie A., Derek J. Chadwick, and Novartis Foundation Staff. Signalling Pathways in Acute Oxygen Sensing. Wiley & Sons, Limited, John, 2007.

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47

Goode, Jamie A., and Derek J. Chadwick. Signalling Pathways in Acute Oxygen Sensing. Wiley & Sons, Incorporated, John, 2009.

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48

Luzo, Angela Cristina Malheiros, Kamal Dua, Raimar Löbenberg, Shakti Shukla, and Saurabh Satija. Targeting Cellular Signalling Pathways in Lung Diseases. Springer Singapore Pte. Limited, 2021.

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49

Taymans, Jean-Marc, ed. Molecular Signalling and Pathways Editor’s Picks 2021. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-112-3.

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50

Targeting Cellular Signalling Pathways in Lung Diseases. Springer, 2022.

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