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Books on the topic 'SIGNALLING MECHANISM'

Author: Grafiati

Published: 11 September 2023

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1

1927-, Segawa Tomio, ed. Physiology and pharmacology of transmembrane signalling: Proceedings of the Uehara Memorial Foundation Symposium on the Mechanism of Transmembrane Signalling, Tokyo, Japan May 12-14, 1988. Amsterdam: Excerpta Medica, 1989.

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2

1945-, Cohen P., and Houslay Miles D, eds. Molecular mechanisms of transmembrane signalling. Amsterdam: Elsevier, 1985.

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3

Frank, Entschladen, and Zänker Kurt S, eds. Cell migration: Signalling and mechanisms. Basel: Karger, 2010.

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4

M, Harnett Margaret, and Rigley Kevin P, eds. Lymphocyte signalling: Mechanisms, subversion, and manipulation. Chichester: J. Wiley, 1997.

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5

Wirtz, Karel W. A., ed. Molecular Mechanisms of Signalling and Membrane Transport. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60799-8.

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6

Brumell, John H. Phosphorylation-dependent signalling mechanisms in human neutrophils. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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7

Packer, Lester, and Karel W. A. Wirtz, eds. Signalling Mechanisms — from Transcription Factors to Oxidative Stress. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79675-3.

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8

Davies, Clare Charlotte. Mechanisms of CD40 signalling and apoptosis in carcinoma cells. Birmingham: University of Birmingham, 2003.

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9

O'Connor, Rodney Philip. A relationship between the amplitude and spectral characteristics of the geomagnetic field and the occurrence of sudden infant death in Canada: A possible cellular mechanism supported by a mathematical modeland experimental evidence for involvement of calcium signalling and nitric oxide. Sudbury, Ont: Laurentian University, Department of Biology, 2001.

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10

H, Michell R., Drummond Alan H, and Downes C. Peter, eds. Inositol lipids in cell signalling. London: Academic Press, 1989.

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11

Singh, Pratibha, Rajiv Kumar Singh, Madhulika Singh, and Sheo Mohan Prasad. Physiology of Salt Stress in Plants: Perception, Signalling, Omics and Tolerance Mechanism. Wiley & Sons, Incorporated, John, 2021.

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12

Singh, Pratibha, Rajiv Kumar Singh, Madhulika Singh, and Sheo Mohan Prasad. Physiology of Salt Stress in Plants: Perception, Signalling, Omics and Tolerance Mechanism. Wiley & Sons, Incorporated, John, 2021.

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13

Singh, Pratibha, Rajiv Kumar Singh, Madhulika Singh, and Sheo Mohan Prasad. Physiology of Salt Stress in Plants: Perception, Signalling, Omics and Tolerance Mechanism. Wiley & Sons, Incorporated, John, 2021.

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14

Physiology of Salt Stress in Plants: Perception, Signalling, Omics and Tolerance Mechanism. Wiley & Sons, Incorporated, John, 2021.

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15

Watanabe, Tetsuya. Biophysical Basis of Physiology and Calcium Signalling Mechanism in Cardiac and Smooth Muscle. Elsevier Science & Technology, 2018.

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16

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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17

Entschladen, F., and K. S. Z�nker, eds. Cell Migration: Signalling and Mechanisms. S. Karger AG, 2009. http://dx.doi.org/10.1159/isbn.978-3-8055-9322-9.

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18

Thiery, J. P. Molecular Mechanisms of Transcellular Signalling. Edited by J. P. Thiery. I O S PRESS, 1999.

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19

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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20

(Editor), Margaret M. Harnett, and Kevin P. Rigley (Editor), eds. Lymphocyte Signalling: Mechanisms, Subversion and Manipulation. John Wiley & Sons, 1997.

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21

Molecular mechanisms of signalling and membrane transport. Berlin: Springer, 1997.

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22

Wirtz, Karel W. A. Molecular Mechanisms of Signalling and Membrane Transport. Springer London, Limited, 2013.

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23

Witzel, Franziska, Titus Stahl, and Julia Christ. Mechanisms Conferring Robustness to Erk1/2 Signalling. Logos Verlag Berlin, 2015.

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24

Wirtz, Karel W. A. Molecular Mechanisms of Signalling and Membrane Transport ). Springer, 2011.

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25

Wirtz, Karel W. A. Molecular Mechanisms of Signalling and Membrane Transport. Springer, 2011.

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26

Signalling mechanisms-- from transcription factors to oxidative stress. [Berlin: Springer-Verlag, 1995.

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27

Packer, Lester, and Karel W. A. Wirtz. Signalling Mechanisms -- from Transcription Factors to Oxidative Stress. Springer London, Limited, 2013.

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28

Packer, Lester, and Karel W. A. Wirtz. Signalling Mechanisms - From Transcription Factors to Oxidative Stress. Springer London, Limited, 2012.

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29

Hormones and Cell Signalling. Guilford Pr, 1990.

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30

Singh, Vijay Pratap, Sheo Mohan Prasad, and Samiksha Singh. Mechanisms Behind Phytohormonal Signalling and Crop Abiotic Stress Tolerance. Nova Science Publishers, Incorporated, 2017.

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31

Cytoskeleton: Signalling and Cell Regulation: A Practical Approach. Oxford University Press, USA, 2000.

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32

L, Carraway K., and Carraway C. A. C, eds. Cytoskeleton: Signalling and cell regulation : a practical approach. New York: Oxford University Press, 2000.

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33

Adinolfi, Elena, Lin-Hua Jiang, and Sébastien Roger, eds. Ion Channel Signalling in Cancer: From Molecular Mechanisms to Therapeutics. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-124-6.

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34

Mehra, Arun. Mechanisms of signalling and antagonism in the TGF[Beta] superfamily. 2002.

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35

(Editor), Kermit L. Carraway, and Carolie A. Carothers Carraway (Editor), eds. Cytoskeleton: Signalling and Cell Regulation: A Practical Approach (Practical Approach Series). Oxford University Press, USA, 2000.

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36

Hua, Hong. Mechanisms of high glucose-induced altered endothelin-1 signalling in glomerular mesangial cells. 2003.

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37

Coecke, Bob, and Aleks Kissinger. Categorical Quantum Mechanics I: Causal Quantum Processes. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198748991.003.0012.

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We derive the category-theoretic backbone of quantum theory from a process ontology. More specifically, we treat quantum theory as a theory of systems, processes, and their interactions. We first present a general theory of diagrams, and in particular, of string diagrams, and discuss why diagrams are a very natural starting point for developing scientific theories. Then we define process theories, and define a very general notion of quantum type. We show how our process ontology enables us to assert causality, that is, compatibility of quantum theory and relativity theory, prove the no-signalling theorem, provide a new elegant derivation of the no-broadcasting theorem, unitarity of evolution, and Stinespring dilation, all for any `quantum' type in a general class of process theories.

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38

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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39

Endlich, Karlhans, and Rodger Loutzenhiser. Regulation of vasomotor tone in the afferent and efferent arterioles. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0208.

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Pre-glomerular vessels are regulated by membrane potential alterations affecting the activity of L-type voltage-activated Ca2+ channels; whereas voltage-independent mechanisms regulate the efferent arteriole, notably influenced by angiotensin II and therefore by angiotensin converting enzyme inhibitors, and by non-steroidal anti-inflammatory drugs.These properties underlie the physiologic control of glomerular capillary pressure, for example, by prostaglandin E2, during conditions of reduced renal perfusion and the stabilization of glomerular capillary pressure when the kidney is exposed to pressure fluctuations. A wealth of hormones affects the tone of renal vessels. The chapter focuses on basic regulatory and signalling mechanisms, emphasizing the unique aspects of the renal vasculature and the underlying features that facilitate the independent regulation of pre-glomerular and post-glomerular tone.

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40

The effect of thrombin on the shape of and the microfilament distribution in porcine aortic endothelial cells: Possible cellular signalling mechanisms. Ottawa: National Library of Canada, 1992.

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41

Wordsworth, B. P. Skeletal dysplasias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0150.

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Bone is metabolically active throughout life and metabolic disturbances may have wide-ranging consequences that are not restricted to altering its mechanics. The study of some genetic bone diseases has already provided remarkable insights into the normal regulation of bone metabolism. Skeletal dysplasias are developmental disorders of the chondro-osseous tissues commonly resulting in short stature, which is often disproportionate. The underlying mutations are often in the structural genes encoding components of the matrix but may also involve growth factors or cell signalling. In contrast, the dysostoses tend to affect single bones or groups of bones, reflecting the transient nature of the many different signalling factors to which they are responsive during development. Abnormalities of bone density (high or low) may be due to primary deficiency of bone matrix synthesis (e.g. osteogenesis imperfecta and hypophosphatasia) but may also reflect an imbalance between bone formation and resorption. This may be caused by abnormalities of bone formation (e.g. hyperostosis/sclerosteosis and osteoporosis pseudoglioma syndrome) or bone resorption (e.g. classic osteopetrosis and fibrous dysplasia).

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42

Puthucheary, Zudin, Hugh Montgomery, Nicholas Hart, and Stephen Harridge. Skeletal Muscle Mass Regulation in Critical Illness. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0035.

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Muscle is a dynamic, plastic, and malleable tissue that is highly sensitive to mechanical and metabolic signals. Muscle mass is regulated by protein homeostasis, with protein being continually turned over, reflecting a balance between synthesis and breakdown. This chapter discusses the effect of critical illness on skeletal muscle mass, protein homeostasis, and the intracellular signalling driving anabolism and catabolism. The focus will be on the unique challenges to which the skeletal muscle are exposed, such as inflammation, sepsis, sedation, and inadequate nutrition, which, in combination with the disuse signals of immobilization and bed rest, engender dramatic changes in muscle structure and function. The mechanisms regulating muscle loss during critical illness are being unravelled, but many questions remain unanswered. Detailed understanding of these mechanisms will help drive strategies to minimize or prevent intensive care-acquired muscle weakness and the long-term consequences experienced by ICU survivors.

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43

Carmeliet, Peter, Guy Eelen, and Joanna Kalucka. Arteriogenesis versus angiogenesis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0008.

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Higher organisms have a cardiovascular circulatory system with blood vessels to supply vital nutrients and oxygen to distant tissues. It is therefore not surprising that vascular disorders are leading causes of mortality. Understanding how new blood vessels form, creates opportunities to cure these life-threatening diseases. After birth, growth of blood vessels mainly occurs via two distinct mechanisms depending on the initial trigger: angiogenesis (referred here as capillary sprouting) is induced primarily by hypoxia, whereas arteriogenesis (referred here as the rapid enlargement of pre-existing collateral arteries, induced by vascular occlusion) is mainly driven by fluid shear stress. Arteriogenesis allows conductance of much larger volumes of blood per unit of time than does the increase in capillary density during angiogenesis. Notwithstanding these major differences, angiogenesis and arteriogenesis share a number of underlying mechanisms, e.g. the involvement of growth factor signalling. This chapter highlights the cellular and molecular events driving the two processes and discusses the therapeutic potential of targeting angiogenesis in cancer and arteriogenesis in cardiovascular diseases.

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44

McNamara, John M., and Olof Leimar. Game Theory in Biology. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198815778.001.0001.

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Game theory in biology seeks to predict social behaviour and other traits that influence how individuals interact. It does this by tentatively assuming that current traits are stable endpoints of evolution by natural selection. The theory is used to model aggressive behaviour, cooperation, negotiation, and signalling, as well as phenotypic attributes like an individual’s sex and mating type. This book covers the basic concepts and the traditional examples of biological game theory. It expands the frontiers of the field, emphasizing the importance of the co-evolution of traits and the implications of variation for reputation, markets, negotiation, and other social phenomena. It also highlights that it can be important to embed game interactions in the environment and an individual’s life. A major new direction developed in the book is that game theory can be extended by incorporating behavioural mechanisms, including mechanisms of reinforcement learning. By doing this the theory can successfully describe important phenomena like social dominance in group-living animals that previously have been difficult to model. By focusing on behavioural mechanisms, game theory can also make closer contact with empirical observation and with current research in fields like animal psychology and neuroscience.

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45

Gordon-Williams, Richard M., and Anthony H. Dickenson. Pathophysiology of pain in cancer and other terminal illnesses. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0092.

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Cancer pain involves a myriad of peripheral changes in the function of tissue and nerves, at the site of the tumour growth, as well as a number of consequent changes in the processing of pain messages at the spinal cord level with implications for the pain experience at higher centres. This chapter reviews the changes in peripheral pain signalling, notes the likely prevalence of both inflammatory and neuropathic components, and describes the altered events at spinal levels that can come some way towards explaining ongoing pain, hyperalgesia, and allodynias that patients with cancer and other terminal illnesses such as HIV/AIDs experience. Finally, changes induced by cancer at the level of the brain are discussed. The mechanisms of action of therapies, both existing and potential novel approaches, are included at peripheral and central levels.

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46

Olzer, Rachel, Rebecca L. Ehrlich, Justa L. Heinen-Kay, Jessie Tanner, and Marlene Zuk. Reproductive behavior. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198797500.003.0013.

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Sex and reproduction lie at the heart of studies of insect behavior. We begin by providing a brief overview of insect anatomy and physiology, followed by an introduction to the overarching themes of parental investment, sexual selection, and mating systems. We then take a sequential approach to illustrate the diversity of phenomena and concepts behind insect reproductive behavior from pre-copulatory mate signalling through copulatory sperm transfer, mating positions, and sexual conflict, to post-copulatory sperm competition, and cryptic female choice. We provide an overview of the evolutionary mechanisms driving reproductive behavior. These events are linked by the economic defendability of mates or resources, and how these are allocated in each sex. Under the framework of economic defendability, the reader can better understand how sexual antagonistic behaviors arise as the result of competing optimal fitness strategies between males and females.

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47

Valdes, Ana M. Genetics. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0009.

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Epidemiological studies have demonstrated that osteoarthritis (OA) is a complex trait with numerous environmental and genetic risk factors. A great deal of effort has been spent elucidating these risk factors and progress has been made. It is clear however that the causes behind OA development and progression continue to remain largely elusive. Identification of those genes that, in conjunction with environmental factors, predispose to OA severity will lead to a better understanding of the mechanisms underlying disease development and thus promote improved health strategies for prevention. An understanding of the molecular signalling pathways involved in the initiation and progression of the disease will improve clinical diagnosis and help identify improved, tailored treatment regimens. This chapter focuses on these issues, exploring the heritability of OA, known genetic risk factors, and specific traits and outcomes studied in the genetics of OA.

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48

Rosengart, Matthew R. Disorders of calcium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0253.

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Calcium is vitally important for normal cellular signalling and function. However, its toxicity necessitates that intracellular calcium concentration [Ca2+] be tightly regulated and compartmentalized. Evolutionary pressures have yielded several regulatory mechanisms to maintain intracellular and extracellular ionized calcium concentrations compatible with life. During periods of critical illness these process are commonly overwhelmed, and disorders of calcium homeostasis are highly prevalent among intensive care unit (ICU) patients. Indeed, hypocalcaemia occurs in up to 88% of critically-ill ICU patients suffering from trauma, sepsis, and burns. Contemporary evidence suggests that although hypocalcaemia may be associated with ICU mortality, it is not in the causal pathway. A systematic review concluded there are no data to support the routine parenteral administration of calcium in the management of asymptomatic critical illness-related hypocalcaemia. Asymptomatic hypocalcaemia of critical illness does not necessitate replacement. However, acute, symptomatic hypocalcaemia necessitates parenteral supplementation to prevent tetany, seizures, and cardiac arrhythmias

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49

Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.

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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.

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50

Wackerhage, Henning, Jonathon Smith, and Darren Wisniewski. Molecular exercise physiology. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0031.

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Molecular exercise physiology is the study of exercise physiology using molecular biology methods. The development of differentiated cell types is regulated by transcription factors like the muscle-making MyoD that specifies cell type, while others regulate the development of muscle, tendons, and bones. Maternal nutrition and exercise commonly affect embryonic development through epigenetic mechanisms. Adaptation to exercise involves sensor proteins detecting exercise-related signals, the processing of signals by signalling proteins and networks, and the regulation of the actual adaptations by effector proteins. Many sport- and exercise-related traits depend on both common and rare DNA sequence variations, including the muscle mass-increasing myostatin (GDF8) loss-of-function and the haematocrit-increasing EPOR gain-of-function mutations. Additionally, common DNA sequence variations contribute to the inherited variability of development, body height, strength, and endurance. Finally, in addition to ethical concerns, current genetic performance tests only explain a fraction of the variation of sport and exercise-related traits.

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