Relevant bibliographies by topics / Adrenergic and thyroid signalling

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  2. Dissertations / Theses
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Academic literature on the topic 'Adrenergic and thyroid signalling'

Author: Grafiati
Published: 28 June 2021
Last updated: 29 July 2025

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Journal articles on the topic "Adrenergic and thyroid signalling"

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Gachkar, Sogol, Sebastian Nock, Cathleen Geissler, et al. "Aortic effects of thyroid hormone in male mice." Journal of Molecular Endocrinology 62, no. 3 (2019): 91–99. http://dx.doi.org/10.1530/jme-18-0217.

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It is well established that thyroid hormones are required for cardiovascular functions; however, the molecular mechanisms remain incompletely understood, especially the individual contributions of genomic and non-genomic signalling pathways. In this study, we dissected how thyroid hormones modulate aortic contractility. To test the immediate effects of thyroid hormones on vasocontractility, we used a wire myograph to record the contractile response of dissected mouse aortas to the adrenergic agonist phenylephrine in the presence of different doses of T3 (3,3′,5-triiodothyronine). Interestingly
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Zarain-Herzberg, Angel. "Regulation of the sarcoplasmic reticulum Ca2+-ATPase expression in the hypertrophic and failing heartThis paper is part of a series in the Journal's “Made in Canada” section. The paper has undergone peer review." Canadian Journal of Physiology and Pharmacology 84, no. 5 (2006): 509–21. http://dx.doi.org/10.1139/y06-023.

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The sarcoplasmic reticulum (SR) plays a central role in the contraction and relaxation coupling in the myocardium. The SR Ca2+-ATPase (SERCA2) transports Ca2+ inside the SR lumen during relaxation of the cardiac myocyte. It is well known that diminished contractility of the hypertrophic cardiac myocyte is the main factor of ventricular dysfunction in the failing heart. A key feature of the failing heart is a decreased content and activity of SERCA2, which is the cause of some of the physiological defects observed in the hypertrophic cardiomyocyte performance that are important during transitio
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Pantos, Constantinos, Iordanis Mourouzis, Christodoulos Xinaris та ін. "Time-dependent changes in the expression of thyroid hormone receptor α1 in the myocardium after acute myocardial infarction: possible implications in cardiac remodelling". European Journal of Endocrinology 156, № 4 (2007): 415–24. http://dx.doi.org/10.1530/eje-06-0707.

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The present study investigated whether changes in thyroid hormone (TH) signalling can occur after acute myocardial infarction (AMI) with possible physiological consequences on myocardial performance. TH may regulate several genes encoding important structural and regulatory proteins particularly through the TRα1 receptor which is predominant in the myocardium. AMI was induced in rats by ligating the left coronary artery while sham-operated animals served as controls. This resulted in impaired cardiac function in AMI animals after 2 and 13 weeks accompanied by a shift in myosin isoforms express
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DAZA, Francisco J., Roberto PARRILLA та Angeles MARTÍN-REQUERO. "3,5,3′-Tri-iodo-l-thyronine acutely regulates a protein kinase C-sensitive, Ca2+-independent, branch of the hepatic α1-adrenoreceptor signalling pathway". Biochemical Journal 331, № 1 (1998): 89–97. http://dx.doi.org/10.1042/bj3310089.

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This work aimed to investigate the acute effect of the thyroid hormone 3,5,3´-tri-iodo-l-thyronine (T3) in regulating the hepatic metabolism either directly or by controlling the responsiveness to Ca2+-mobilizing agonists. We did not detect any acute metabolic effect of T3 either in perfused liver or in isolated liver cells. However, T3 exerted a powerful inhibitory effect on the α1-adrenoreceptor-mediated responses. The promptness of this T3 effect rules out that it was the result of rate changes in gene(s) transcription. T3 inhibited the α1-adrenoreceptor-mediated sustained stimulation of re
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Shimegi, S., F. Okajima, and Y. Kondo. "Permissive stimulation of Ca(2+)-induced phospholipase A2 by an adenosine receptor agonist in a pertussis toxin-sensitive manner in FRTL-5 thyroid cells: a new ‘cross-talk’ mechanism in Ca2+ signalling." Biochemical Journal 299, no. 3 (1994): 845–51. http://dx.doi.org/10.1042/bj2990845.

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We have described the pertussis toxin (PTX)-sensitive potentiation of P2-purinergic agonist-induced phospholipase C activation, Ca2+ mobilization and arachidonic acid release by an adenosine receptor agonist, N6-(L-2-phenylisopropyl)adenosine (PIA), which alone cannot influence any of these cellular activities [Okajima, Sato, Nazarea, Sho and Kondo (1989) J. Biol. Chem. 264, 13029-13037]. In the present study we have found that arachidonic acid release was associated with lysophosphatidylcholine production, and conclude that arachidonic acid is produced by phospholipase A2 in FRTL-5 thyroid ce
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Sohn, Rebecca, Gundula Rösch, Marius Junker, Andrea Meurer, Frank Zaucke, and Zsuzsa Jenei-Lanzl. "Adrenergic signalling in osteoarthritis." Cellular Signalling 82 (June 2021): 109948. http://dx.doi.org/10.1016/j.cellsig.2021.109948.

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McMacken, Grace, and Hanns Lochmuller. "ADRENERGIC SIGNALLING AND CONGENITAL MYASTHENIC SYNDROMES." Journal of Neurology, Neurosurgery & Psychiatry 87, no. 12 (2016): e1.77-e1. http://dx.doi.org/10.1136/jnnp-2016-315106.168.

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Kanagy, Nancy L. "α2-Adrenergic receptor signalling in hypertension". Clinical Science 109, № 5 (2005): 431–37. http://dx.doi.org/10.1042/cs20050101.

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Cardiovascular regulation by the sympathetic nervous system is mediated by activation of one or more of the nine known subtypes of the adrenergic receptor family; α1A-, α1B-, α1D-, α2A-, α2B-, α2C-, β1-, β2- and β3-ARs (adrenoceptors). The role of the α2-AR family has long been known to include presynaptic inhibition of neurotransmitter release, diminished sympathetic efferent traffic, vasodilation and vasoconstriction. This complex response is mediated by one of three subtypes which all uniquely affect blood pressure and blood flow. All three subtypes are present in the brain, kidney, heart a
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Suddle, A., and S. Klimach. "Lactate and adrenergic signalling in trauma." Annals of The Royal College of Surgeons of England 98, no. 03 (2016): 238–39. http://dx.doi.org/10.1308/rcsann.2016.0097.

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McMacken, Grace, Sally Spendiff, Rachel Howarth, et al. "PO167 Adrenergic signalling and congenital myasthenic syndromes." Journal of Neurology, Neurosurgery & Psychiatry 88, Suppl 1 (2017): A56.3—A56. http://dx.doi.org/10.1136/jnnp-2017-abn.194.

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Dissertations / Theses on the topic "Adrenergic and thyroid signalling"

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Olsen, Jessica M. "β-Adrenergic Signalling Through mTOR". Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-142169.

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Adrenergic signalling is part of the sympathetic nervous system and is activated upon stimulation by the catecholamines epinephrine and norepinephrine. This regulates heart rate, energy mobilization, digestion and helps to divert blood flow to important organs. Insulin is released to regulate metabolism of carbohydrates, fats and proteins, mainly by taking up glucose from the blood. The insulin and the catecholamine hormone systems are normally working as opposing metabolic regulators and are therefore thought to antagonize each other. One of the major regulators involved in insulin signalling
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Öberg, Anette I. "β-adrenergic signalling and novel effects in skeletal muscle". Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-87205.

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Skeletal muscles have, due to their large mass, a big impact on the whole body metabolism. There are many signals that can regulate the functions of skeletal muscles and one such signal is activation of α- and β-adrenoceptors (α- and β-ARs) by epinephrine and norepinephrine. This activation leads to several effects which are examined in this thesis.   Stimulation of β-AR on muscle cells induces glucose uptake, an event that both provides the muscle with energy and lowers the blood glucose levels. We discovered two key components in the β-ARs signal to glucose uptake: the transporter protein GL
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Glass, Rainer. "Purinergic signalling in endocrine organs : testis, thyroid, thymus." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250178.

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El, Mansori Ibtessam Mustafa. "Thyrotropin receptor signalling links skin and thyroid disease." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/46110/.

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Thyroid dysfunction is frequently associated with skin and hair diseases; however, the underlying pathogenic mechanisms are poorly understood. Pathological activation of the thyroid stimulating hormone receptor (TSHR) is the key feature of both hyper- and hypo-thyrodism. Expression of the (TSHR) has been reported in several extra-thyroidal locations including adipose tissue, bone and skin fibroblasts. TSHR expression may explain the association between the thyroid and skin disease. The TSHR can also be activated by a newly discovered glycoprotein hormone, known as thyrostimulin. This hormone i
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Balthasar, Sonja. "Sphingolipid signalling in normal and malignant thyroid cells /." Turku : Painosalama Oy, 2007. http://catalogue.bnf.fr/ark:/12148/cb41077764x.

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Schramm, Moritz Walter Joachim. "Adrenergic signalling in the central nervous system modulates the reconsolidation of alcohol memories." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648515.

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Barnard, Joanna Catherine. "The effect of thyroid hormones on fibroblast growth factor signalling in bone." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419226.

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Mitchell, Fiona Elizabeth. "Thyroid hormone signalling and action : the role of iodothyronine transporters and metabolites." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510634.

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Baragli, Alessandra. "Assembly and function of multimeric adenylyl cyclase signalling complexes." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111888.

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G protein coupled receptors, G proteins and their downstream effectors adenylyl cyclase (ACs) were thought to transiently interact at the plasma membrane by random collisions following agonist stimulation. However a growing number of studies have suggested that a major revision of this paradigm was necessary to account for signal transduction specificity and efficiency. The revised model suggests that signalling proteins are pre-assembled as stable macromolecular complexes together with modulators of their activity prior to receptor activation. How and where these signalling complexes form and
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McCormick, Wanda Denise. "Characterisation of calcium-sensing receptor signalling and feedback regulation in endogenous expression systems." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493946.

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Books on the topic "Adrenergic and thyroid signalling"

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Nucera, Carmelo, ed. Targeting thyroid cancer microenvironment and epigenetic signalling: new frontiers in cancer endocrinology basic and clinical research. Frontiers Media SA, 2014. http://dx.doi.org/10.3389/978-2-88919-240-3.

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Nucera, Carmelo, ed. Targeting Thyroid Cancer Microenvironment and Epigenetic Signalling: New Frontiers in Cancer Endocrinology Basic and Clinical Research, 2nd Edition. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-198-5.

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New Scoping Document on in vitro and ex vivo Assays for the Identification of Modulators of Thyroid Hormone Signalling. OECD, 2017. http://dx.doi.org/10.1787/9789264274716-en.

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Nasman, Johnny. Alpha-2 Adrenergic Receptors and Signal Transduction: Effector Output in Relation to G-Protein Coupling and Signalling Cross-Talk (Comprehensive Summaries ... from the Faculty of Medicine, 1105). Uppsala Universitet, 2002.

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Horn, Nicole D. Thyrotoxicosis. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0033.

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Thyrotoxicosis is a severe form of hyperthyroidism that can lead to a life-threatening episode of thyroid storm. The onset of hyperthyroidism can be gradual and unrecognized. Triggers such as infection and surgery can result in large releases of thyroid hormone, causing a hypermetabolic condition called thyroid storm that produces tachycardia, dysrhythmias, and hypotension. Because of the elevated heart rate and increased myocardial contractility, patients with hyperthyroidism have a decreased cardiac reserve and are at increased risk for adverse cardiac events during the perioperative period.
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Newell-Price, John, Alia Munir, and Miguel Debono. Normal function of the endocrine system. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0182.

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Endocrinology is the study of hormones (and their glands of origin), their receptors, the intracellular signalling pathways they invoke, and their associated diseases. The clinical specialty of endocrinology focuses specifically on the endocrine organs, that is, the organs whose primary function is hormone secretion, including the hypothalamus, the pituitary, the thyroid, the parathyroid, the adrenal glands, the pancreas, and the reproductive organs.
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Book chapters on the topic "Adrenergic and thyroid signalling"

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Hammond, J., and J. L. Balligand. "Signalling Microdomains: The Beta-3 Adrenergic Receptor/NOS Signalosome." In Microdomains in the Cardiovascular System. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54579-0_11.

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Pierotti, M. A., E. Arighi, I. Bongarzone, et al. "RET/ptc and TRK Oncogenes in Papillary Thyroid Carcinoma." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78247-3_7.

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Insel, Paul A., Rennolds S. Ostrom, Martin C. Michel, and Rainer Büscher. "α1-Adrenergic Receptors of MDCK-D1 Cells Utilize Multiple Signalling Components." In Catecholamine Research. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3538-3_60.

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Ryall, James G., and Gordon S. Lynch. "Role of β-Adrenergic Signalling in Skeletal Muscle Wasting: Implications for Sarcopenia." In Sarcopenia – Age-Related Muscle Wasting and Weakness. Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_19.

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Seppet, Enn K., Allen Kaasik, Ave Minajeva, et al. "Mechanisms of thyroid hormone control over sensitivity and maximal contractile responsiveness to β-adrenergic agonists in atria." In Bioenergetics of the Cell: Quantitative Aspects. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5653-4_29.

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Krasel, C., and M. J. Lohse. "Signalling in the β-adrenergic receptor system." In Pharmacochemistry Library. Elsevier, 1997. http://dx.doi.org/10.1016/s0165-7208(97)80075-x.

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Visser, W. E., G. A. Garinis, C. Bombardieri, et al. "Thyroid Hormone Signalling Is Suppressed in Progeroid and Normal Aging." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p12.p2-594.

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Akaike, Takaaki, and Katsuhisa Inoue. "Nitrosothiol detection by HPLC coupled with flow reactors ofHg2+ and Griess reagent." In Experimental protocols for reactive oxygen and nitrogen species. Oxford University PressOxford, 2000. http://dx.doi.org/10.1093/oso/9780198506683.003.0005.

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Abstract NO-related intermediates, including NO1-like species, can participate in nitrosating additions to nucleophilic centres of biological molecules. Sulfhydrylcontaining molecules such as glutathione are particularly susceptible to nitrosation and form nitrosothiol adducts (nitrosothiols; RS-NOs). It seems that these adducts in biological systems play an important role in NO-mediated signalling cascades such as the downregulation of 7V-methyl-D-aspartate receptor, and the regulation of transcriptional factors (1); they might also be involved in non-adrenergic and non-cholinergic neuronal r
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Fowkes, Rob, V. Krishna Chatterjee, and Mark Gurnell. "Principles of hormone action." In Oxford Textbook of Medicine, edited by Mark Gurnell. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0243.

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Hormones, produced by glands or cells, are messengers which act locally or at a distance to coordinate the function of cells and organs. Types of hormone include: peptides (e.g. hypothalamic releasing factors) and proteins (e.g. insulin, growth hormone)—these generally interact with membrane receptors located on the cell surface, causing activation of downstream signalling pathways leading to alteration in gene transcription or modulation of biochemical pathways to effect a physiological response; steroids (e.g. cortisol, progesterone, testosterone, oestradiol) and other lipophilic substances
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Gurnell, Mark, Jacky Burrin, and V. Krishna Chatterjee. "Principles of hormone action." In Oxford Textbook of Medicine. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.1301_update_001.

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Hormones, produced by glands or cells, are messengers which act locally or at a distance to coordinate the function of cells and organs. Types of hormone include (1) peptides (e.g hypothalamic releasing factors) and proteins (e.g. insulin, growth hormone)—these generally interact with membrane receptors located on the cell surface, causing activation of downstream signalling pathways leading to alteration in gene transcription or modulation of biochemical pathways to effect a physiological response; (2) steroids (e.g. cortisol, progesterone, testosterone, oestradiol) and other lipophilic subst
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Conference papers on the topic "Adrenergic and thyroid signalling"

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Archała, Aneta, та Anita Płazińska. "β2-adrenergic receptor polymorphism in intracellular signalling pathways". У 1st International Electronic Conference on Biomedicine. MDPI, 2021. http://dx.doi.org/10.3390/ecb2021-10265.

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Changoer, Prashant, Zeinab Mamdouh, Christian Grätz, et al. "Targeting Signalling Modules in Thyroid Cancer." In RExPO24. REPO4EU, 2024. http://dx.doi.org/10.58647/rexpo.24000069.v1.

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Kang, HY, CK Chou, and RT Liu. "PO-343 The microRNA-146b-IRAK1 signalling axis in tumour recurrence of papillary thyroid 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-eacr25.855.

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Baloglu, Emel, Thomas Reingruber, Peter Bartsch, and Heimo Mairbaurl. "In-vivo Hypoxia And Terbutaline-treatment Impairs Beta-2-adrenergic Signalling Ain ATII Cells But Blunts Hypoxic Inhibition Of Alveolar Reabsorption." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6363.

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