Relevant bibliographies by topics / Adrenergic and thyroid signalling

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

Academic literature on the topic 'Adrenergic and thyroid signalling'

Author: Grafiati
Published: 28 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Adrenergic and thyroid signalling"

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Gachkar, Sogol, Sebastian Nock, Cathleen Geissler, Rebecca Oelkrug, Kornelia Johann, Julia Resch, Awahan Rahman, Anders Arner, Henriette Kirchner, and Jens Mittag. "Aortic effects of thyroid hormone in male mice." Journal of Molecular Endocrinology 62, no. 3 (April 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, we observed reduced vasoconstriction under low and high T3 concentrations, indicating an inversed U-shaped curve with maximal constrictive capacity at euthyroid conditions. We then tested for possible genomic actions of thyroid hormones on vasocontractility by treating mice for 4 days with 1 mg/L thyroxine in drinking water. The study revealed that in contrast to the non-genomic actions the aortas of these animals were hyperresponsive to the contractile stimulus, an effect not observed in endogenously hyperthyroid TRβ knockout mice. To identify targets of genomic thyroid hormone action, we analysed aortic gene expression by microarray, revealing several altered genes including the well-known thyroid hormone target gene hairless. Taken together, the findings demonstrate that thyroid hormones regulate aortic tone through genomic and non-genomic actions, although genomic actions seem to prevail in vivo. Moreover, we identified several novel thyroid hormone target genes that could provide a better understanding of the molecular changes occurring in the hyperthyroid aorta.
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Pantos, Constantinos, Iordanis Mourouzis, Christodoulos Xinaris, Alexandros D. Kokkinos, Konstantinos Markakis, Antonios Dimopoulos, Matthew Panagiotou, Theodosios Saranteas, Georgia Kostopanagiotou, and Dennis V. Cokkinos. "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, no. 4 (April 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 expression towards a fetal phenotype in the non-infarcted area. Cardiac hypertrophy was evident in AMI hearts after 13 weeks but not at 2 weeks. This response was associated with a differential pattern of TH changes at 2 and 13 weeks; T3 and T4 levels in plasma were not changed at 2 weeks but T3 was significantly lower and T4 remained unchanged at 13 weeks. A twofold increase in TRα1 expression was observed after 13 weeks in the non-infarcted area, P<0.05 versus sham operated, while TRα1 expression remained unchanged at 2 weeks. A 2.2-fold decrease in TRβ1 expression was found in the non-infarcted area at 13 weeks, P<0.05, while no change in TRβ1 expression was seen at 2 weeks. Parallel studies with neonatal cardiomyocytes showed that phenylephrine (PE) administration resulted in 4.5-fold increase in the expression of TRα1 and 1.6-fold decrease in TRβ1 expression versus untreated, P<0.05. In conclusion, cardiac dysfunction which occurs at late stages after AMI is associated with increased expression of TRα1 receptor and lower circulating tri-iodothyronine levels. Thus, apo-TRα1 receptor state may prevail contributing to cardiac fetal phenotype. Furthermore, down-regulation of TRβ1 also contributes to fetal phenotypic changes. α1-adrenergic signalling is, at least in part, involved in this response.
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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 (May 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 transition of compensated hypertrophy to heart failure. In this review different possible mechanisms responsible for decreased transcriptional regulation of the SERCA2 gene are examined, which appear to be the primary cause for decreased SERCA2 expression in heart failure. The experimental evidence suggests that several signalling pathways are involved in the downregulation of SERCA2 expression in the hypertrophic and failing cardiomyocyte. Therapeutic upregulation of SERCA2 expression using replication deficient adenoviral expression vectors, pharmacological interventions using thyroid hormone analogues, β-adrenergic receptor antagonists, and novel metabolically active compounds are currently under investigation for the treatment of uncompensated cardiac hypertrophy and heart failure.
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DAZA, Francisco J., Roberto PARRILLA, and 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, no. 1 (April 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 respiration and release of Ca2+ and H+, but not the glycogenolytic or gluconeogenic responses, in perfused liver. In isolated liver cells, T3 enhanced the α1-agonist-induced increase in cytosolic free Ca2+ and impeded the intracellular alkalinization. Since T3 also prevented the α1-adrenoreceptor-mediated activation of protein kinase C, its effects on pH seem to be the result of a lack of activation of the Na+/H+ exchanger. The failure of T3 to prevent the α1-adrenergic stimulation of gluconeogenesis despite the inhibition of protein kinase C activation indicates that the elevation of cytosolic free Ca2+ is a sufficient signal to elicit that response. T3 also impaired some of the angiotensin-II-mediated responses, but did not alter the effects of PMA on hepatic metabolism, indicating, therefore, that some postreceptor event is the target for T3 actions. The differential effect of T3 in enhancing the α1-adrenoreceptor-mediated increase in cytosolic free Ca2+ and preventing the activation of protein kinase C, provides a unique tool for further investigating the role of each branch of the signalling pathway in controlling the hepatic functions. Moreover, the low effective concentrations of T3 (⩽ 10 nM) in perturbing the α1-adrenoreceptor-mediated response suggests its physiological significance.
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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 (May 1, 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 cells. This led us to assume that PIA augments P2-purinergic arachidonic acid release by increasing [Ca2+]i which, in turn, activates Ca(2+)-sensitive phospholipase A2. The arachidonic acid-releasing response to PIA was, however, always considerably higher (3.1-fold increase) than the Ca2+ response (1.3-fold increase) to the adenosine derivative. In addition, arachidonic acid release induced by the [Ca2+]i increase caused by thapsigargin, an endoplasmic-reticulum Ca(2+)-ATPase inhibitor, or calcium ionophores was also potentiated by PIA without any effect on [Ca2+]i and phospholipase C activity. This action of PIA was also PTX-sensitive, but not affected by the forskolin- or cholera toxin-induced increase in the cellular cyclic AMP (cAMP), suggesting that a PTX-sensitive G-protein(s) and not cAMP mediates the PIA-induced potentiation of Ca(2+)-generated phospholipase A2 activation. Although acute phorbol ester activation of protein kinase C induced arachidonic acid release, P2-purinergic and alpha 1-adrenergic stimulation of arachidonic acid release was markedly increased by the protein kinase C down-regulation caused by the phorbol ester. This suggests a suppressive role for protein kinase C in the agonist-induced activation of arachidonic acid release. We conclude that PIA (and perhaps any of the G1-activating agonists) augments an agonist (maybe any of the Ca(2+)-mobilizing agents)-induced arachidonic acid release by activation of Ca(2+)-dependent phospholipase A2 in addition to enhancement of agonist-induced phospholipase C followed by an increase in [Ca2+]i.
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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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Kanagy, Nancy L. "α2-Adrenergic receptor signalling in hypertension." Clinical Science 109, no. 5 (October 24, 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 and vasculature. However, each differentially influences blood pressure and sympathetic transmission. Activation of α2A-ARs in cardiovascular control centres of the brain lowers blood pressure and decreases plasma noradrenaline (norepinephrine), activation of peripheral α2B-ARs causes sodium retention and vasoconstriction, whereas activation of peripheral α2C-ARs causes cold-induced vasoconstriction. In addition, non-selective agonists elicit endothelium-dependent vasodilation and presynaptic inhibition of noradrenaline release. The evidence that each of these receptor subtypes uniquely participates in cardiovascular control is discussed in this review.
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McMacken, Grace, and Hanns Lochmuller. "ADRENERGIC SIGNALLING AND CONGENITAL MYASTHENIC SYNDROMES." Journal of Neurology, Neurosurgery & Psychiatry 87, no. 12 (November 15, 2016): e1.77-e1. http://dx.doi.org/10.1136/jnnp-2016-315106.168.

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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 (March 2016): 238–39. http://dx.doi.org/10.1308/rcsann.2016.0097.

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McMacken, Grace, Sally Spendiff, Rachel Howarth, Dan Cox, Clarke Slater, Andreas Roos, Roger Whittaker, and Hanns Lochmuller. "PO167 Adrenergic signalling and congenital myasthenic syndromes." Journal of Neurology, Neurosurgery & Psychiatry 88, Suppl 1 (December 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 is the mechanistic target of rapamycin (mTOR). There are two different complexes of mTOR; mTORC1 and mTORC2, and they are essential in the control of cell growth, metabolism and energy homeostasis. Since mTOR is one of the major signalling nodes for anabolic actions of insulin it was thought that catecholamines might oppose this action by inhibiting the complexes. However, lately there are studies demonstrating that this may not be the case. mTOR is for instance part of the adrenergic signalling pathway resulting in hypertrophy of cardiac and skeletal muscle cells and inhibition of smooth muscle relaxation and helps to regulate browning in white adipose tissue and thermogenesis in brown adipose tissue (BAT). In this thesis I show that β-adrenergic signalling leading to glucose uptake occurs independently of insulin in skeletal muscle and BAT, and does not activate either Akt or mTORC1, but that the master regulator of this pathway is mTORC2. Further, my co-workers and I demonstrates that β-adrenergic stimulation in skeletal muscle and BAT utilizes different glucose transporters. In skeletal muscle, GLUT4 is translocated to the plasma membrane upon stimulation. However, in BAT, β-adrenergic stimulation results in glucose uptake through translocation of GLUT1. Importantly, in both skeletal muscle and BAT, the role of mTORC2 in β-adrenergic stimulated glucose uptake is to regulate GLUT-translocation.

At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 4: Manuscript.

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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 GLUT4 and the kinase mTOR, a molecule involved in several metabolic processes but not previously known to be activated by β-ARs.   The classical second messenger downstream of β-ARs, cAMP, was surprisingly found to be only partly involved in the β-adrenergic glucose uptake. We also found that a molecule called GRK2 is very important for this glucose uptake.   A novel effect of β-AR stimulation presented in this thesis is the inhibition of myosin II-dependent contractility in skeletal muscle cells. The intracellular pathway regulating this event was different from that regulating glucose uptake and involved both classical and novel molecules in the β-AR pathway.   Another stimulus that we found to activate insulin-independent glucose uptake in skeletal muscle cells was the natural compound Shikonin. Shikonin increased glucose uptake in skeletal muscle cells via a calcium- and GLUT4-dependent mechanism and improved glucose homeostasis in diabetic rats.   Taken together, we have identified new key molecules in the adrenergic signaling pathway as well as novel downstream effects. We conclude that glucose uptake in muscles can be activated by β-adrenergic stimulation or by Shikonin and that both treatments improves glucose homeostasis in diabetic animals. This knowledge can hopefully be used in the search for new drugs to combat type II diabetes.

At the time of doctoral defence the following papers were unpublished and had a status as follows. Paper 1: Manuscript; Paper 3: Manuscript

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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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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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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 is composed of a dimer of unique α 2 and β 5 subunits. Although thyrostimulin has not been detected in the circulation. However, both subunits have been shown to be expressed in different tissues including the skin. The aim of this study is to examine the expression of the TSHR and thyrostimulin in the skin. In addition, to investigate the expression of a variant form of the TSHR in human and mouse skin and, other mouse tissues. RT-PCR using primers specific for the full length receptor and the truncated variant revealed that although the variant was widely expressed in mouse tissues including skin, it was not found in human skin. The full length receptor and thyrostimulin were found to be co-expressed in eye, testis and skin. Immunohistochemistry of frozen skin and thyroid sections using commercially available antibodies against the extracellular (A9) and transmembrane domains (A7) of TSHR demonstrates that TSHR is not expressed in the epidermis but expressed in dermal fibroblasts and in myoepithelium around sweat glands. A new β5 antibody was characterised by western blotting and immunohistochemistry for future investigation of β5 expression in the skin. These data suggest a functional role for TSHR signalling possibly via thyrostimulin in the skin and that the variant form,although potentially present in some tissues, is unlikely to be important in human skin.
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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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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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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 the mechanisms governing their assembly and maintenance are not completely understood yet. Initially, we addressed this question by exploring AC2 interaction with beta2-adrenergic receptors (beta2ARs) and heterotrimeric G proteins as parts of a pre-assembled signalling complex. Using a combination of biophysical and biochemical techniques, we showed that AC2 interacts with them before it is trafficked to the cell surface in transfected HEK-293 cells. These interactions are constitutive and do not require stimulation by receptor agonists. Furthermore, the use of dominant-negative Rab/Sar monomeric GTPases and dominant-negative heterotrimeric G protein subunits proved that AC2/beta2AR and AC2/Gbetagamma interactions occurred in the ER as measured using both BRET and co-immunoprecipitation experiments, while interaction of the Galpha subunits with the above complexes occurred at a slightly later stage. Both Galpha and Gbetagamma played a role in stabilizing these complexes. Our data also demonstrated that stimulation of AC was still possible when the complex remained on the inside of the cell but was reduced when the GalphaS/AC2 interaction was blocked, suggesting that the addition of the GalphaS subunit was required to render the nascent complexes functional prior to trafficking to proper sites of action. Next, we tackled the issue of higher order assembly of effectors and G proteins, using two different AC isoforms and GalphaS as a model. We demonstrated that AC2 can form heterodimers with AC5 through direct molecular interaction in unstimulated HEK-293 cells. AC2/5 heterodimerization resulted in a reduced total level of AC2 expression, which affected cellular accumulation of cAMP upon forskolin stimulation. The AC2/5 complex was stable in presence of receptor or forskolin stimulation. We provided evidence that co-expression with GalphaS increased the affinity of AC2 for AC5 as monitored by BRET. In particular, the complex formed by AC2/5 lead to synergistic accumulation of cAMP in presence of GalphaS and forskolin, with respect to either of the parent AC isoforms themselves. Finally, we also showed that this complex can be detected in native tissues, as AC2 and AC5 could be co-immunoprecipiated from lysates of mouse heart. Taken together, we provided evidence for stable formation of signalling complexes involving receptor/G proteins/adenylyl cyclase or G proteins/heterodimeric adenylyl cyclases and that G proteins play a crucial role for their assembly and function.
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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. Thyroid storm must be considered in the differential diagnosis of patients with this presentation so that prompt treatment with beta-adrenergic blockers and antithyroid drugs can be given.
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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, 215–44. Cham: 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, M. G. Borrello, G. Butti, A. Greco, C. Mariani, M. Miozzo, C. Miranda, and G. Sozzi. "RET/ptc and TRK Oncogenes in Papillary Thyroid Carcinoma." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling, 87–98. Berlin, Heidelberg: 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, 257–60. Boston, MA: 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, 449–71. Dordrecht: 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, Kalju Paju, Jorma J. Ohisalo, Roland Vetter, and Urmo Braun. "Mechanisms of thyroid hormone control over sensitivity and maximal contractile responsiveness to β-adrenergic agonists in atria." In Bioenergetics of the Cell: Quantitative Aspects, 419–26. Boston, MA: 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, 317–27. 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, I. van der Pluijm, E. Kaptein, R. Brandt, H. van Toor, 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, P2–594—P2–594. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p12.p2-594.

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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, 2245–57. 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 (e.g. vitamin D, retinoic acid, thyroid hormone)—these act by crossing the plasma membrane to interact with intracellular receptors, with hormone action via nuclear receptors altering cellular gene expression directly.
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Gurnell, Mark, Jacky Burrin, and V. Krishna Chatterjee. "Principles of hormone action." In Oxford Textbook of Medicine, 1787–98. 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 substances (e.g. vitamin D, retinoic acid, thyroid hormone)—these act by crossing the plasma membrane to interact with intracellular receptors, with hormone action via nuclear receptors altering cellular gene expression directly....
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Taich, Alexander, and Adam S. Hassan. "Management of Eyelid Retraction." In Surgery of the Eyelid, Lacrimal System, and Orbit. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780195340211.003.0015.

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Eyelid retraction has numerous causes. Most notably eyelid retraction is caused by thyroid eye disease (TED), trauma, and postsurgical changes. The upper eyelid margin is typically measured at 3.5 to 4.5 mm above the center of the cornea. The lower eyelid margin is typically situated at the inferior border of the limbus. Eyelid retraction is a condition in which the upper eyelid margin is displaced superiorly or the lower eyelid margin is displaced inferiorly. Eyelid retraction may result in exposure keratopathy and disturbing ocular symptoms, including blurred vision, photophobia, foreign body sensation, burning, and reactive tearing. Eyelid retraction in TED is thought to be due to a combination of inflammation, fibrosis, and adrenergic stimulation of the eyelid retractors. Proptosis can also contribute to eyelid retraction. In the upper eyelid, factors responsible for eyelid retraction include (1) inflammation and fibrosis of the levator and Müller’s muscles, (2) adrenergic stimulation of Müller’s muscle, and (3) inflammation and fibrosis of the inferior rectus muscle, causing hypodeviation of the globe and compensatory overaction of the superior rectus–levator complex. In the lower eyelid, factors responsible for eyelid retraction include (1) inflammation and fibrosis of the inferior rectus muscle with consequent traction on its anterior extension, the capsulopalpebral fascia, which is the main lower lid retractor, and (2) adrenergic stimulation of the smooth muscle fibers within the lower lid retractor complex. A combination of eyelid retraction and proptosis in TED may result in ocular exposure with symptoms of ocular irritation, an undesirable cosmetic appearance, corneal erosion and infection, or (rarely) globe luxation. Mild exposure problems can be managed with topical lubricants. Guanethidine, a topical sympatholytic agent, is of limited usefulness in the management of eyelid retraction due to its variable efficacy and frequent ocular side effects, including irritation, hyperemia, photophobia, pain, edema, burning sensation, and punctate keratitis. It may be more tolerable if used in lower concentrations. Exposure problems in the inflammatory phase of the condition present a special challenge as surgical correction of eyelid retraction is best performed in the pos-tinflammatory, stable phase. Several reports have described using Botulinum toxin injections, 2.5 to 15 U, either subconjunctivally or percutaneously, just above the superior border of the tarsus.
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Conference papers on the topic "Adrenergic and thyroid signalling"

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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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