Relevant bibliographies by topics / Neuropeptides – Mechanism of action

Academic literature on the topic 'Neuropeptides – Mechanism of action'

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Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Neuropeptides – Mechanism of action"

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Lestanova, Z., Z. Bacova, and Jan Bakos. "Mechanisms involved in the regulation of neuropeptide-mediated neurite outgrowth: a minireview." Endocrine Regulations 50, no. 2 (April 1, 2016): 72–82. http://dx.doi.org/10.1515/enr-2016-0011.

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AbstractThe present knowledge, regarding the neuronal growth and neurite extension, includes neuropeptide action in the central nervous system. Research reports have brought much information about the multiple intracellular signaling pathways of neuropeptides. However, regardless of the differences in the local responses elicited by neuropeptides, there exist certain functional similarities in the effects of neuropeptides, mediated by their receptors. In the present review, data of the relevant studies, focused on G protein-coupled receptors activated by neuropeptides, are summarized. Particularly, receptors that activate phosphatidylinositol-calcium system and protein kinase C pathways, resulting in the reorganization of the neuronal cytoskeleton and changes in the neuronal morphology, are discussed. Based on our data received, we are showing that oxytocin increases the gene expression of GTPase cell division cycle protein 42 (Cdc42), implicated in many aspects of the neuronal growth and morphology. We are also paying a special attention to neurite extension and retraction in the context of neuropeptide regulation.
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Chandrasekharan, Bindu, Behtash Ghazi Nezami, and Shanthi Srinivasan. "Emerging neuropeptide targets in inflammation: NPY and VIP." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 11 (June 1, 2013): G949—G957. http://dx.doi.org/10.1152/ajpgi.00493.2012.

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The enteric nervous system (ENS), referred to as the “second brain,” comprises a vast number of neurons that form an elegant network throughout the gastrointestinal tract. Neuropeptides produced by the ENS play a crucial role in the regulation of inflammatory processes via cross talk with the enteric immune system. In addition, neuropeptides have paracrine effects on epithelial secretion, thus regulating epithelial barrier functions and thereby susceptibility to inflammation. Ultimately the inflammatory response damages the enteric neurons themselves, resulting in deregulations in circuitry and gut motility. In this review, we have emphasized the concept of neurogenic inflammation and the interaction between the enteric immune system and enteric nervous system, focusing on neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP). The alterations in the expression of NPY and VIP in inflammation and their significant roles in immunomodulation are discussed. We highlight the mechanism of action of these neuropeptides on immune cells, focusing on the key receptors as well as the intracellular signaling pathways that are activated to regulate the release of cytokines. In addition, we also examine the direct and indirect mechanisms of neuropeptide regulation of epithelial tight junctions and permeability, which are a crucial determinant of susceptibility to inflammation. Finally, we also discuss the potential of emerging neuropeptide-based therapies that utilize peptide agonists, antagonists, siRNA, oligonucleotides, and lentiviral vectors.
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Gołyszny, Miłosz, and Ewa Obuchowicz. "Are neuropeptides relevant for the mechanism of action of SSRIs?" Neuropeptides 75 (June 2019): 1–17. http://dx.doi.org/10.1016/j.npep.2019.02.002.

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Borg, Christian B., Nina Braun, Stephanie A. Heusser, Yasmin Bay, Daniel Weis, Iacopo Galleano, Camilla Lund, et al. "Mechanism and site of action of big dynorphin on ASIC1a." Proceedings of the National Academy of Sciences 117, no. 13 (March 12, 2020): 7447–54. http://dx.doi.org/10.1073/pnas.1919323117.

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Acid-sensing ion channels (ASICs) are proton-gated cation channels that contribute to neurotransmission, as well as initiation of pain and neuronal death following ischemic stroke. As such, there is a great interest in understanding the in vivo regulation of ASICs, especially by endogenous neuropeptides that potently modulate ASICs. The most potent endogenous ASIC modulator known to date is the opioid neuropeptide big dynorphin (BigDyn). BigDyn is up-regulated in chronic pain and increases ASIC-mediated neuronal death during acidosis. Understanding the mechanism and site of action of BigDyn on ASICs could thus enable the rational design of compounds potentially useful in the treatment of pain and ischemic stroke. To this end, we employ a combination of electrophysiology, voltage-clamp fluorometry, synthetic BigDyn analogs, and noncanonical amino acid-mediated photocrosslinking. We demonstrate that BigDyn binding results in an ASIC1a closed resting conformation that is distinct from open and desensitized states induced by protons. Using alanine-substituted BigDyn analogs, we find that the BigDyn modulation of ASIC1a is primarily mediated through electrostatic interactions of basic amino acids in the BigDyn N terminus. Furthermore, neutralizing acidic amino acids in the ASIC1a extracellular domain reduces BigDyn effects, suggesting a binding site at the acidic pocket. This is confirmed by photocrosslinking using the noncanonical amino acid azidophenylalanine. Overall, our data define the mechanism of how BigDyn modulates ASIC1a, identify the acidic pocket as the binding site for BigDyn, and thus highlight this cavity as an important site for the development of ASIC-targeting therapeutics.
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Bakkali-Kassemi, Lamiae, Seloua El Ouezzani, Rabia Magoul, Ikram Merroun, Maria Lopez-Jurado, and Mohammed Errami. "Effects of cannabinoids on neuropeptide Y and β-endorphin expression in the rat hypothalamic arcuate nucleus." British Journal of Nutrition 105, no. 4 (December 7, 2010): 654–60. http://dx.doi.org/10.1017/s0007114510004095.

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The control of appetite and satiety is extremely complex and involves a balance between neurotransmitters and neuropeptides to stimulate and/or inhibit feeding behaviour. The effect of cannabinoids on food intake is well established, but little is known about the mechanism of action underlying their activity. In the present report, the effect of pharmacological manipulation of the cannabinoid receptor on the expression of hypothalamic neuropeptides is investigated. We used an immunohistochemical approach to examine the effect of intracerebroventricular administration of the cannabinoid receptor agonist WIN55,212-2 and the inverse agonist AM251 on neuropeptide Y (NPY) and the β-endorphin (β-end) neuronal hypothalamic systems. Double immunohistochemistry (c-fos/β-end) was used to assess the number of β-end neurons activated by the cannabinoid agonist. The present results showed that 1 μg WIN 55,212-2 increases β-end immunoreactivity within the arcuate nucleus while no significant changes were noted in the NPY-immunoreactive nerve fibres network in comparison to the control group. Injection of 1 μg AM251 decreases both NPY and β-end immunoreactivity within the arcuate nucleus. The number of β-end neurons exhibiting c-fos increased significantly in WIN 55,212-2 compared with the control group. These results suggest that cannabinoids affect the expression of hypothalamic neuropeptides, notably the NPY and β-end systems, which may have implications in the orexigenic action of cannabinoids.
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Bodea, Alina, and Amorin Remus Popa. "Orectic And Anorectic Peptides And Their Implication In Obesity And The Metabolic Syndrome." Romanian Journal of Diabetes Nutrition and Metabolic Diseases 22, no. 2 (June 1, 2015): 187–91. http://dx.doi.org/10.1515/rjdnmd-2015-0023.

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AbstractBackground and aims: Cardiovascular diseases, diabetes mellitus, the metabolic syndrome and obesity are now globally widespread clinical conditions, addressing different ages, lately extending to young and children. The causes are multiple, involving an interaction between individual genetic risk factors and environmental factors. Many studies showed the importance of the hypothalamic neuropeptides and other neuropeptides in the regulation of the balance between food intake and energy consumption. We reviewed 25 recent research studies describing the physiological and physiopathological mechanisms of the orectic and anorectic peptides and their interaction to adjust the balance between food intake and energy expenditure.Conclusions: The hypothalamus, through its nuclei (arcuate and paraventricular) controls the balance between food intake and energy expenditure. The proopiomelanocortin (POMC) / Cocaine and amphetamine-related transcript (CART) neurons represent the anorectic centre. The neurons that release neuropeptide Y (NPY) and agouti-related protein (AgRP) by stimulation form the orectic centre. The neuropeptide Y (NPY) is the main hypothalamic orectic neuropeptide. Its action, besides stimulating the orectic effect, is to modulate the release of other hypothalamic orectic and anorectic neuropeptides. In addition, the energy balance is regulated by adipokines released by the adipose cells, hormones and neurotransmitters, blood glucose level and other metabolites.
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Petrera, Agnese, Beat Amstutz, Magda Gioia, Janine Hähnlein, Antonio Baici, Petra Selchow, Davide M. Ferraris, et al. "Functional characterization of the Mycobacterium tuberculosis zinc metallopeptidase Zmp1 and identification of potential substrates." Biological Chemistry 393, no. 7 (July 1, 2012): 631–40. http://dx.doi.org/10.1515/hsz-2012-0106.

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Abstract Zinc metallopeptidases of bacterial pathogens are widely distributed virulence factors and represent promising pharmacological targets. In this work, we have characterized Zmp1, a zinc metallopeptidase identified as a virulence factor of Mycobacterium tuberculosis and belonging to the neprilysin (NEP; M13) family, whose X-ray structure has been recently solved. Interestingly, this enzyme shows an optimum activity toward a fluorogenic substrate at moderately acidic pH values (i.e., 6.3), which corresponds to those reported for the Mtb phagosome where this enzyme should exert its pathological activity. Substrate specificity of Zmp1 was investigated by screening a peptide library. Several sequences derived from biologically relevant proteins were identified as possible substrates, including the neuropeptides bradykinin, neurotensin, and neuropeptide FF. Further, subsequences of other small bioactive peptides were found among most frequently cleaved sites, e.g., apelin-13 and substance P. We determined the specific cleavage site within neuropeptides by mass spectrometry, observing that hydrophobic amino acids, mainly phenylalanine and isoleucine, are overrepresented at position P1′. In addition, the enzymatic mechanism of Zmp1 toward these neuropeptides has been characterized, displaying some differences with respect to the synthetic fluorogenic substrate and indicating that the enzyme adapts its enzymatic action to different substrates.
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Werner, Felix-Martin, and Rafael Coveñas. "Neural Networks in Generalized Epilepsy and Novel Antiepileptic Drugs." Current Pharmaceutical Design 25, no. 4 (June 3, 2019): 396–400. http://dx.doi.org/10.2174/1381612825666190319121505.

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Background:In previous works, alterations of neurotransmitters and neuropeptides in the brain areas involved in generalized epilepsy have been reported.Objective:We reviewed the alterations of these neurotransmitters and neuropeptides in the following brain areas involved in generalized epilepsy: hippocampus, hypothalamus, thalamus and cerebral cortex. In these brain areas, the neural networks are also actualized. The mechanisms of action of newer antiepileptic drugs in the treatment of generalized epilepsy are also discussed.Results:Up-dating the neurotransmitter and neuropeptide alterations, we found that hippocampal GABAergic neurons presynaptically inhibit epileptogenic neurons via GABAB receptors. Epilepsy modulating neuropeptides (galanin, neuropeptide Y, dynorphin) are also involved. GABA deficiency, serotonin hyperactivity, dopamine hyperactivity and glutamate excitotoxicity can enhance ictogenesis: neurons containing these neurotransmitters form the main neural circuit. An increased excitability occurs when the alteration of these neurotransmitters is permanent.Conclusion:In preclinical studies, the GABAB receptor agonist GS 39,783 exerted a good antiepileptic effect. Perampanel, an AMPA receptor antagonist, showed good clinical effects in the treatment of partial-onset seizures and primary generalized tonic-clonic seizures. In this treatment, perampanel can be combined with other antiepileptic drugs. Brivaracetam, which shows a high affinity for the synaptic vesicle 2A, exerted a good efficacy in the treatment of adult focal seizures and secondarily generalized tonic-clonic seizures.
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Dalvi, Prasad S., Anaies Nazarians-Armavil, Matthew J. Purser, and Denise D. Belsham. "Glucagon-Like Peptide-1 Receptor Agonist, Exendin-4, Regulates Feeding-Associated Neuropeptides in Hypothalamic Neurons in Vivo and in Vitro." Endocrinology 153, no. 5 (February 14, 2012): 2208–22. http://dx.doi.org/10.1210/en.2011-1795.

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Exendin-4, a long-acting glucagon-like peptide-1 receptor (GLP-1R) agonist, is a potential regulator of feeding behavior through its ability to inhibit gastric emptying, reduce food intake, and induce satiety. GLP-1R activation by exendin-4 induces anorexia; however, the specific populations of neuropeptidergic neurons activated by exendin-4 within the hypothalamus, the central regulator of energy homeostasis, remain unclear. This study determines whether exendin-4 regulates hypothalamic neuropeptide expression and explores the signaling mechanisms involved. The distribution and quantity of exendin-4-induced c-Fos immunoreactivity were evaluated to determine activation of α-melanocyte-stimulating hormone/proopiomelanocortin, neuropeptide Y, neurotensin (NT), and ghrelin neurons in hypothalamic nuclei during exendin-4-induced anorexia in mice. Additionally, exendin-4 action on NT and ghrelin transcript regulation was examined in immortalized hypothalamic neurons. With anorexia induced by intracerebroventricular exendin-4, α-melanocyte-stimulating hormone/proopiomelanocortin and neuropeptide Y neurons were activated in the arcuate nucleus, with simultaneous activation of NT-expressing neurons in the paraventricular nucleus, and ghrelin-expressing neurons in the arcuate nucleus, paraventricular nucleus, and periventricular hypothalamus, suggesting that neurons in one or more of these areas mediate the anorexic action of exendin-4. In the hypothalamic neuronal cell models, exendin-4 increased cAMP, cAMP response element-binding protein/activating transcription factor-1 and c-Fos activation, and via a protein kinase A-dependent mechanism regulated NT and ghrelin mRNA expression, indicating that these neuropeptides may serve as downstream mediators of exendin-4 action. These findings provide a previously unrecognized link between central GLP-1R activation by exendin-4 and the regulation of hypothalamic NT and ghrelin. Further understanding of this central GLP-1R activation may lead to safe and effective therapeutics for the treatment of metabolic disorders.
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Zingale, Gabriele Antonio, Francesco Bellia, Ikhlas Mohamed Mohamud Ahmed, Przemyslaw Mielczarek, Jerzy Silberring, and Giuseppe Grasso. "IDE Degrades Nociceptin/Orphanin FQ through an Insulin Regulated Mechanism." International Journal of Molecular Sciences 20, no. 18 (September 10, 2019): 4447. http://dx.doi.org/10.3390/ijms20184447.

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Insulin-degrading enzyme (IDE) was applied to catalyze hydrolysis of Nociceptin/Orphanin 1-16 (OFQ/N) to show the involvement of the enzyme in degradation of neuropeptides engaged in pain transmission. Moreover, IDE degradative action towards insulin (Ins) was inhibited by the OFQ/N fragments, suggesting a possible regulatory mechanism in the central nervous system. It has been found that OFQ/N and Ins affect each other degradation by IDE, although in a different manner. Indeed, while the digestion of OFQ/N is significantly affected by the presence of Ins, the kinetic profile of the Ins hydrolysis is not affected by the presence of OFQ/N. However, the main hydrolytic fragments of OFQ/N produced by IDE exert inhibitory activity towards the IDE-mediated Ins degradation. Here, we present the results indicating that, besides Ins, IDE cleaves neuropeptides and their released fragments act as inhibitors of IDE activity toward Ins. Having in mind that IDE is present in the brain, which also contains Ins receptors, it cannot be excluded that this enzyme indirectly participates in neural communication of pain signals and that neuropeptides involved in pain transmission may contribute to the regulation of IDE activity. Finally, preliminary results on the metabolism of OFQ/N, carried out in the rat spinal cord homogenate in the presence of various inhibitors specific for different classes of proteases, show that OFQ/N proteolysis in rat spinal cord could be due, besides IDE, also to a cysteine protease not yet identified.
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Dissertations / Theses on the topic "Neuropeptides – Mechanism of action"

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Gruber, Susanne H. M. "Novel mechanism of action of antipsychotic drugs : effects on neuropeptides in rat brain /." Stockholm : [Karolinska institutets bibliotek], 2002. http://diss.kib.ki.se/2002/91-7349-229-9.

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Cheng, Shao Koon Graduate School of Biomedical Engineering Faculty of Engineering UNSW. "The role of brain tissue mechanical properties and cerebrospinal fluid flow in the biomechanics of the normal and hydrocephalic brain." Awarded by:University of New South Wales. Graduate School of Biomedical Engineering, 2006. http://handle.unsw.edu.au/1959.4/27292.

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The intracranial system consists of three main basic components - the brain, the blood and the cerebrospinal fluid. The physiological processes of each of these individual components are complex and they are closely related to each other. Understanding them is important to explain the mechanisms behind neurostructural disorders such as hydrocephalus. This research project consists of three interrelated studies, which examine the mechanical properties of the brain at the macroscopic level, the mechanics of the brain during hydrocephalus and the study of fluid hydrodynamics in both the normal and hydrocephalic ventricles. The first of these characterizes the porous properties of the brain tissues. Results from this study show that the elastic modulus of the white matter is approximately 350Pa. The permeability of the tissue is similar to what has been previously reported in the literature and is of the order of 10-12m4/Ns. Information presented here is useful for the computational modeling of hydrocephalus using finite element analysis. The second study consists of a three dimensional finite element brain model. The mechanical properties of the brain found from the previous studies were used in the construction of this model. Results from this study have implications for mechanics behind the neurological dysfunction as observed in the hydrocephalic patient. Stress fields in the tissues predicted by the model presented in this study closely match the distribution of histological damage, focused in the white matter. The last study models the cerebrospinal fluid hydrodynamics in both the normal and abnormal ventricular system. The models created in this study were used to understand the pressure in the ventricular compartments. In this study, the hydrodynamic changes that occur in the cerebral ventricular system due to restrictions of the fluid flow at different locations of the cerebral aqueduct were determined. Information presented in this study may be important in the design of more effective shunts. The pressure that is associated with the fluid flow in the ventricles is only of the order of a few Pascals. This suggests that large transmantle pressure gradient may not be present in hydrocephalus.
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Buxton, David. "The impact of striatal neuropeptides and topography on action sequence selection." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22081/.

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Many common behaviours are a sequence of several actions. As action sequences are learned their activation often becomes habitual, allowing smooth, rapid, and semi-automatic execution; learning and performing action sequences is central to normal motor function. The striatum is the primary input nucleus for the basal ganglia and receives glutamatergic cortical afferents. These afferents innervate localised populations of medium spiny neurons (MSNs) and may encode 'action requests'. Striatal interactions ensure that only non-conflicting, high salience requests are selected, but the mechanisms enabling clean, rapid switching between sequential actions are poorly understood. Substance P (SP) and enkephalin are neuropeptides co-released with GABA by MSNs preferentially expressing D1 or D2 dopamine receptors respectively. SP facilitates subsequent glutamatergic inputs to target MSNs while enkephalin has an inhibitory effect. We construct models of these glutamatergic effects and integrate them into a basal ganglia model to demonstrate that diffuse neuropeptide connectivity enhances action selection. For action sequences with an ordinal structure, patterning SP connectivity to reflect this ordering enhances the selection of correctly–ordered actions and suppresses disordered selection. We also show that selectively pruning SP connections allows context–sensitive inhibition of specific undesirable requests that otherwise interfere with action group selection. We then construct a striatal microcircuit model with physical topography and show that inputs to this model generate oscillations in MSN spiking. Input salience and active neuronal density have differentiable impacts on oscillation amplitude and frequency, but the presence of oscillations has little effect on the mean MSN firing rate or action selection. Our model suggests that neuropeptide interactions enhance the contrast between selected and rejected action requests, and that patterned SP connectivity enhances the selection of ordered sequences. Our model further suggests that striatal topography does not directly impact action selection, but that evoked oscillations may represent an additional form of population coding that could bind together semantically related MSN groups.
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Lo, William Wing-Yan. "A study of receptor-mediated phosphoinositide signalling mechanism using the human pituitary cell line flow 9000 as a model system." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328913.

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Tatarski, Miloš. "Molecular mechanism of dBigH1 action." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/663021.

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INTRODUCTION: For decades it was known that many species contain embryo specific linker histone H1 variants that replace the somatic H1 during early embryogenesis. This is especially important because the early embryo shows typically zero to very little activity of transcription, and the first cleavages of the embryo depend exclusively on maternally deposited factors that are important for transcription and chromatin assembly. The first species shown to contain an embryo specific histone H1 was the sea urchin. Other species like the mouse, Xenopus or the zebrafish followed. Even in humans there are embryo specific H1 variants. Drosophila seemed to be an exception to this, until in 2013 the first linker histone H1 variant was discovered that was called dBigH1. Like other embryo H1 variants, dBigH1 is expressed in the early embryo and disappears when cellularization starts and it gets replaced by the somatic H1. Likewise, to its counterparts in other species, dBigH1 is responsible for the inhibition of transcription during the early stage of fly development. OBJECTIVES: In this thesis, we addressed the questions about the mechanism of inhibition of dBigH1 as well as the factors that are responsible for its deposition into chromatin. RESULTS: To answer the first question, we used an in vitro system for chromatin reconstitution based on an extract from early Drosophila embryos (DREX) that contains dBigH1 and all other factors needed for proper chromatin assembly. We then used the reconstituted chromatin in transcription experiments using HeLa nuclear extract that contains all factors needed for transcription. We saw that transcription for chromatin reconstituted in DREX could be reduced when the extract was previously depleted from dBigH1 using specific antibodies against it. By adding back recombinant dBigH1 to the depleted extract we were able to restore the initial lever of transcription. This showed us that dBigH1 was the repressive factor, as it was already confirmed in vivo. We then used a truncated construct of dBigH1 where we depleted the N-terminal domain of the protein. This was of particular interest as the N-terminal region of dBigH1 is the one that differs most form the somatic H1. It is much longer and more importantly very enriched with acidic residues, something that is very unique amongst all embryo specific H1 variants. We saw that when using the truncated construct, transcription was inhibited to a much lesser extent than with the full length dBigH1, proposing that the N-terminal domain is indeed responsible for the inhibition of transcription. To answer the second question about the factors needed for dBigH1 deposition, we used Drosophila testis to study dBigH1 in vivo. dBigH1 shows a very similar expression pattern in testis as the chromatin remodeler ACF1. This is why we decided to investigate a possible interaction between those two proteins. Additionally, we knew that ACF1 uses NAP1 as a histone chaperone for H1 in some species, so we also asked if NAP1 could play a role in dBigH1 deposition as well. Indeed, we saw that when using flies deficient for ACF1 we see much less dBigH1 in the testis tip where the germal stem cells (GSC) reside, suggesting that ACF1 plays an important role in dBigH1 deposition. In accordance, we see more dBigH1 in the GSCs when using flies overexpressing ACF1. At the same time, we can see that when depleting NAP1 from DREX, we see more dBigH1.
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Attarzadeh, Yazdi Ghassem. "Molecular mechanism of glucocorticoid action." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/26161.

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The aim of this thesis project was to investigate the mechanisms by which glucocorticoid hormones regulate the activity of BK channels in human embryonic kidney 293 (HEK293) cells as the model system for glucocorticoids-action. It was shown that glucocorticoids act via endogenously expressed type II receptors in a concentration- and time-dependent manner in these cells. Dexamethasone (100 nM) had no significant effect on Dexras1 mRNA but significantly increased serum- and glucocorticoid-induced protein kinase 1 (SGK-1) mRNA. Biochemical analysis showed that SGK-1 protein is increased by dexamethasone in a Triton X-100 insoluble fraction. Further work was directed toward analysing the possible association of SGK-1 and protein phosphatases with two BK channel α-subunit variants: ZERO-BK and STREX-BK, the latter contains the 59 amino-acid splice insert encoded by the stress hormone induced exon (STREX). HEK293 cells stably expressing the respective channel subunits were analysed. Immunoprecipitations with antisera directed against the BK α-subunits showed that protein phosphatase 2A (PP2A) but not SGK-1 is constitutively associated with the STREX as well as the ZERO variant BK channel. Furthermore, the cytoplasmic C-terminal segment of the STREX-BK channel was necessary for cell-surface expression of the channel and the association of the channel with PP2A. Dexamethasone, failed to change the apparent amount of immunoreactive PP2A co-immunoprecipitating with the channel. In conclusion: SGK-1 but not Dexras1 is a protein rapidly induced by dexamethasone in HEK293 cells. PP2A but not SGK-1 is in complex with both ZERO and STREX-BK channels, and dexamethasone does not alter this association. The cytoplasmic tail of the BK channels is essential for PP2A interaction.
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Conti, Lucio. "The molecular mechanism of TFL1 action." Thesis, University of East Anglia, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423575.

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During Arabidopsis development the shoot apical meristem (SAM) generates lateral primordia which display stage-specific traits. In long days, wild-type Arabidopsis generates leaves in an initial vegetative phase (V). Upon integration of environmental and endogenous signals, the SAM enters the reproductive phase. First it makes an 11 phase, which consists of 2-3 leaves (cauline) subtending secondary shoots (coflorescences). Next it enters the 12 phase and produces flowers on its flanks. The TFL 1 gene is a key component of the phase change machinery as mutations in TFL 1 affect the timing of phase switching. Also ffl1 mutants enter a novel phase whereby the SAM, after 12, is converted into a terminal flower, a phase normally absent in wild type. The molecular mechanism of how TFL 1 protein acts is unclear. In animal systems, TFL 1-like proteins have been shown to be components of signal transduction pathways. To understand the mechanism underlying TFL 1 function I aimed to identify proteins interacting with TFL 1 by introducing into Arabidopsis a functional TAP tag version of TFL 1 under the control of the 35S promoter. I set up conditions which allowed me to isolate and visualize by total protein staining TAPtag TFL 1. However, no obvious proteins appeared to co-purify with TFL 1. To understand how TFL 1 is modified, and to follow TFL 1 protein expression throughout development and in cell fractions, I developed polyclonal antibodies against TFL 1. These antibodies recognized TFL 1 in vivo and were used to characterize TFL 1 biochemically. TFL 1 detection by immunoblots in conjunction with mass-spectrometry analysis showed that TFL 1 was not subjected to obvious modifications unlike animal homologues. Moreover, from cellular fractionation experiments TFL 1 was located in the cytosol. To reveal essential downstream functions required for TFL 1 signaling, I characterized a suppressor mutant, called sof1, of plants ectopically expressing TFL 1. I mapped sof1 within a confined region on the bottom of chromosome 3. Physiological analysis of sof1 led to a model of SOT1 action in controlling phase change. TFL 1 mRNA is found in a unique expression domain which comprises a group of cells in the centre of the SAM and yet TFL 1 affects the identity of lateral primordia. By using affinity purified anti-TFL 1 antibodies I showed that TFL 1 protein moves and is distributed throughout the SAM. This might account for the effect of TFL 1 on controlling overall shoot identity and raises important questions on the role of the TFL 1 protein outside its mRNA expression domain.
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Beastall, J. C. "The mechanism of action of azone." Thesis, University of Nottingham, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380112.

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Williams, Daffydd Griffin. "Mechanism of action of penetration enhancers." Thesis, Cardiff University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320625.

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Phisit, Prapunwattana Yongyuth Yuthavong. "Mechanism of antimalarial action of tetracycline /." abstract, 1986. http://mulinet3.li.mahidol.ac.th/thesis/2529/29E-Phisit-P.pdf.

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Books on the topic "Neuropeptides – Mechanism of action"

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Hiroshi, Takagi, ed. Regulatory roles of neuropeptides: Proceedings of the Sixth Workshop on Neurotransmitters and Diseases, Kobe, June 17, 1989. Amsterdam, The Netherlands: Excerpta Medica, 1989.

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Govil, J. N., Amani S. Awaad, and Geetanjali Kaushik. Mechanism and action of phytoconstituents. Houston, TX: Studium Press, 2011.

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Golan, Adam E. Cellulase: Types and action, mechanism, and uses. New York, N.Y: Nova Science Publishers, 2011.

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Lewis, John. Mechanism of action of overbased additives in hydrocarbon media. Norwich: University of East Anglia, 1991.

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Deans, Bryan. Studies on the mechanism of action on antitumour imidazotetrazinones. Birmingham: Aston University. Department ofPharmaceutical and Biological Sciences, 1994.

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Hickman, John Angus. Studies of the mechanism of action of antitumour compounds. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1989.

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Bogusz, Edwina J. The mechanism of the depressant action of dextrin on pyrite. [s.l: s.n.]., 1995.

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Kenyon, Janette. Investigation into the mechanism of action of coronatine - a phytotoxin. Norwich: University of East Anglia, 1990.

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Tsang, Chris. Mechanism of [alpha]-latrotoxin action at the frog neuromuscular junction. Ottawa: National Library of Canada, 2000.

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Ruddock, Mark Wiliam. The mechanism of action of the selective tumour radiosensitizer nicotinamide. [s.l: The Author], 1998.

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Book chapters on the topic "Neuropeptides – Mechanism of action"

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Tilders, F. J. H., J. W. A. M. van Oers, A. White, F. Menzaghi, and A. Burlet. "Antibodies to Neuropeptides: Biological Effects and Mechanisms of Action." In Advances in Experimental Medicine and Biology, 135–46. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5799-5_8.

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Denko, C. W. "Mechanism of action of neuropeptides: a group of naturally occurring (endogenous) anti-inflammatory analgesic compounds." In Side-Effects of Anti-Inflammatory Drugs, 449–50. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_50.

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Bohus, B. "Behavioural effects of neuropeptides: central and peripheral mechanisms of action of vasopressin." In The Peptidergic Neuron, 267–77. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-9010-6_29.

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Safe, Stephen H., Thomas Gasiewicz, and James P. Whitlock. "Mechanism of Action." In Environmental Toxin Series, 61–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-70556-4_3.

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Soultanas, Panos, and Edward Bolt. "Helicase Mechanism of Action." In Molecular Life Sciences, 516–26. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_291.

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White, Morris F. "Mechanism of Insulin Action." In Textbook of Diabetes, 114–32. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924853.ch8.

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Mostafa, Manal, Amal-Asran, Hassan Almoammar, and Kamel A. Abd-Elsalam. "Nanoantimicrobials Mechanism of Action." In Nanotechnology in the Life Sciences, 281–322. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91161-8_11.

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Soultanas, Panos, and Edward Bolt. "Helicase Mechanism of Action." In Molecular Life Sciences, 1–12. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6436-5_291-1.

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Rasmussen, Howard, and Irving L. Schwartz. "Mechanism of Hormone Action." In Endocrinology, 335–68. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4614-7436-4_12.

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Kliewer, Steven. "PPARγ Mechanism of Action Studies." In Medical Science Symposia Series, 49–53. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1171-7_8.

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Conference papers on the topic "Neuropeptides – Mechanism of action"

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Williams, T. J., M. Rampart, S. Nourshargh, P. G. Hellewell, S. D. Brain, and P. J. Jose. "INTERACTION OF POLYMORPHONUCLEAR LEUKOCYTES AND ENDOTHELIAL CELLS : FUNCTIONAL CONSEQUENCES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643985.

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The mechanisms involved in the accumulation of polymorphonuclear leukocytes (PMNs) in an inflammatory reaction are complex. A key phase in this process is the attachment of the PMN to the microvascular (venular in most tissues) endothelial cell, initiated by the extravascular generation of a chemical mediator. Experiments in vitro suggest that mediators, such as C5a, may act in vivo by stimulating the increased expression of the CD18 complex on the surface of the PMN within the venule lumen (1), whereas IL-1 may act by causing the expression of an adhesive molecule on the endothelial cell (2). In vitro the former process is rapid whereas the latter is slow in onset. We have measured the local accumulation of intravenously-injected Ulln-PMNs in response to intradermally-injected mediators in the rabbit, in order to investigate possible mechanisms in vivo. PMN accumulation was found to be rapid in onset in response to C5a, the rate of accumulation falling progressively to low levels by 4 hours. In contrast PMN accumulation in response to IL-1 was slow in onset, reaching a peak rate at 3-4 hours. Intradermal injection of the vasodilator prostaglandins PGI2; PGE2 and the neuropeptides VIP and CGRP caused a marked potentiation of the rate of leukocyte accumulation. PMN accumulation induced by C5a was associated with increased microvascular permeability, as indicated by the leakage of intravenously-injected 125I-albumin with a time-course in parallel with the rate of PMN accumulation enhanced by intradermally-injected vasodilators. Depletion of circulating PMNs abolishes these responses to C5a (3). In contrast, leukocyte accumulation induced by IL-1 was associated with little plasma protein leakage, even in the presence of intradermal vasodilators. This observation indicates that PMN emigration itself does not lead to increased microvascular permeability. C5a, but not IL-1, may stimulate emigrating PMNs to secrete an endogenous factor that increases permeability by an action on endothelial cells (3). This factor does not appear to be the phospholipid PAF (4). In contrast to the enhancing effects of local PGI2, intravenously-infused PGI2 inhibited PMN accumulation induced by C5a and IL-1, and plasma protein leakage induced by C5a (5). This effect is probably mediated by elevation of cyclic AMP in intravascular PMNs. We have shown that C5a stimulation of PMNs in contact with endothelial cells in vitro induces endothelial cell PGI2 secretion (6). Thus, PGI2 may be part of a negative feedback system in vivo to control interactions between PMNs and endothelial cells.These observations provide some clues to the intricacies of mechanisms of leukocyte accumulation in vivo.
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Sláma, Karel. "A myth about the "potent cardiostimulating" action of insect neuropeptides has been unfounded." In XIIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2011. http://dx.doi.org/10.1135/css201113130.

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Cai, Yiheng, Xinran Kong, and Xueyan Wang. "Temporal Action Detection with Long Action Seam Mechanism." In the 2nd International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3278198.3278224.

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Wang, Wenhao, Xiaobo Lu, Pengguo Zhang, Huibin Xie, and Wenbin Zeng. "Driver Action Recognition Based on Attention Mechanism." In 2019 6th International Conference on Systems and Informatics (ICSAI). IEEE, 2019. http://dx.doi.org/10.1109/icsai48974.2019.9010589.

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Xiaoping, Liu, and Qi Liangqun. "Research on Enterprise's Dynamic Capabilities Action Mechanism." In 2011 International Conference on Information Management, Innovation Management and Industrial Engineering (ICIII). IEEE, 2011. http://dx.doi.org/10.1109/iciii.2011.415.

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Chai Lihong, Jiang Ling, Shi Yanfei, and Wang Hongyuan. "Toxicity effects and action mechanism of fluoride." In 2011 International Symposium on Water Resource and Environmental Protection (ISWREP). IEEE, 2011. http://dx.doi.org/10.1109/iswrep.2011.5893495.

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Shih, Hsiao-Yi, and Arnost Reiser. "Mechanism of inhibitor action in novolak film." In SPIE's 1995 Symposium on Microlithography, edited by Robert D. Allen. SPIE, 1995. http://dx.doi.org/10.1117/12.210351.

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Masoudi, Ramin, Stephen Birkett, and John McPhee. "Dynamic Model of a Vertical Piano Action Mechanism." In ASME 2009 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/detc2009-87680.

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The dynamic behavior of a vertical piano action mechanism is studied using a simulation model and compared qualitatively to observations obtained by high-speed imaging of a real action. The simulated response of all components is obtained for two different prescribed input force profiles applied at the key front. These inputs represent in simplified form the general shape of a typical force input by a pianist measured at the key surface for a strong (forte) strike, or two key strikes in rapid succession. The graph-theoretic multibody model constructed represents the components and their interactions. Explicit contact edges provide forces generated between two bodies as a function of their kinematic states, using a special contact model to represent the compression of felt lined interfaces that can separate during the key stroke. Masses and geometrical parameters of the action were measured by importing scanned images from a real action into CAD software. The highly nonlinear system of five ordinary differential equations of motion was derived symbolically and solved by a numerical stiff solver in Maple. The effects of two components not present in the horizontal grand piano action, the bridle strap and hammer butt spring, were examined using simulations. The butt spring is seen to serve an important function in assisting the return of the hammer to its rest position on key release. The model will be useful in future studies to compare vertical actions to horizontal grand piano actions, as these are known to exhibit quite different playing characteristics.
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Mel'chenko, Sergey V., Sergei E. Kunts, Katherine D. Mel'chenko, Eleonora V. Saprykina, Vladimir M. Shipulin, and Eugeni P. Gordov. "Mechanism of UV laser action on arterial wall." In BiOS '97, Part of Photonics West, edited by Steven L. Jacques. SPIE, 1997. http://dx.doi.org/10.1117/12.275476.

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Alhaj, Fatima, Duha Qutishat, Heba Al Harahsheh, Nadim Obeid, and Bassam Hammo. "Detecting DDI Using Ontology: Drug Mechanism of Action." In 2019 IEEE Jordan International Joint Conference on Electrical Engineering and Information Technology (JEEIT). IEEE, 2019. http://dx.doi.org/10.1109/jeeit.2019.8717527.

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Reports on the topic "Neuropeptides – Mechanism of action"

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Roberts, Jr, and Charles T. A Novel Mechanism of Androgen Receptor Action. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada489364.

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Roberts, Jr, and Charles T. A Novel Mechanism of Androgen Receptor Action. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada503252.

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Bates, Paula J. Mechanism of Action of Novel Antiproliferative Oligonucleotides. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada406133.

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Roberts, Jr, and Charles T. A Novel Mechanism of Androgen Receptor Action. Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ada466168.

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Kamasani, Uma R., and George Prendergast. Mechanism of RhoB/FTI Action in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada446332.

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Rane, Neena S., and George C. Prendergast. Mechanism of RhoB/FTI Action in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada412302.

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Rogers, Terry B. Mechanism of Action of the Presynaptic Neurotoxin, Tetanus Toxin. Fort Belvoir, VA: Defense Technical Information Center, July 1991. http://dx.doi.org/10.21236/ada246780.

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Rogers, Terry B. Mechanism of Action of the Presynaptic Neurotoxins Tetanus Toxin. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada246495.

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Kaiser, Ivan I. Rattlesnake Neurotoxin Structure, Mechanism of Action, Immunology and Molecular Biology. Fort Belvoir, VA: Defense Technical Information Center, September 1990. http://dx.doi.org/10.21236/ada228003.

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Leoni, Lorenzo M. Mechanism of Action of Substituted Indanones in Multidrug Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada424665.

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