Relevant bibliographies by topics / P2X3

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Academic literature on the topic 'P2X3'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "P2X3"

1

Ruan, Huai-Zhen, Lori A. Birder, William C. de Groat, Changfeng Tai, James Roppolo, Charles A. Buffington, and Geoffrey Burnstock. "Localization of P2X and P2Y Receptors in Dorsal Root Ganglia of the Cat." Journal of Histochemistry & Cytochemistry 53, no. 10 (June 27, 2005): 1273–82. http://dx.doi.org/10.1369/jhc.4a6556.2005.

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The distribution of P2X and P2Y receptor subtypes in upper lumbosacral cat dorsal root ganglia (DRG) has been investigated using immunohistochemistry. Intensity of immunoreactivity for six P2X receptors (P2X5 receptors were immuno-negative) and the three P2Y receptors examined in cat DRG was in the order of P2Y2 = P2Y4>P2X3>P2X2 = P2X7>P2X6>P2X1 = P2X4>P2Y1. P2X3, P2Y2, and P2Y4 receptor polyclonal antibodies stained 33.8%, 35.3%, and 47.6% of DRG neurons, respectively. Most P2Y2, P2X1, P2X3, P2X4, and P2X6 receptor staining was detected in small- and medium-diameter neurons. However, P2Y4, P2X2, and P2X7 staining was present in large- and small-diameter neurons. Double-labeling immunohistochemistry showed that 90.8%, 32.1%, and 2.4% of P2X3 receptor-positive neurons coexpressed IB4, CGRP, and NF200, respectively; whereas 67.4%, 41.3%, and 39.1% of P2Y4 receptor-positive neurons coexpressed IB4, CGRP, and NF200, respectively. A total of 18.8%, 16.6%, and 63.5% of P2Y2 receptor-positive neurons also stained for IB4, CGRP, and NF200, respectively. Only 30% of DRG neurons in cat were P2X3-immunoreactive compared with 90% in rat and in mouse. A further difference was the low expression of P2Y1 receptors in cat DRG neurons compared with more than 80% of the neurons in rat. Many small-diameter neurons were NF200-positive in cat, again differing from rat and mouse.
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2

Coutinho-Silva, Robson, Lynn Stahl, Kwok-Kuen Cheung, Nathalia Enes de Campos, Carolina de Oliveira Souza, David M. Ojcius, and Geoffrey Burnstock. "P2X and P2Y purinergic receptors on human intestinal epithelial carcinoma cells: effects of extracellular nucleotides on apoptosis and cell proliferation." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 5 (May 2005): G1024—G1035. http://dx.doi.org/10.1152/ajpgi.00211.2004.

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Extracellular nucleotides interact with purinergic receptors, which regulate ion transport in a variety of epithelia. With the use of two different human epithelial carcinoma cell lines (HCT8 and Caco-2), we have shown by RT-PCR that the cells express mRNA for P2X1, P2X3, P2X4, P2X5, P2X6, P2X7, P2Y1, P2Y2, P2Y4, P2Y6, P2Y11, and P2Y12 receptors. Protein expression for P2Y1 and P2Y2 receptors was also demonstrated immunohistochemically, and P2X receptor subtype protein was present in the following decreasing order: P2X4 > P2X7 > P2X1 > P2X3 > P2X6 > P2X5 >> P2X2. The functional presence of P2X7, P2Y1, P2Y2, and P2Y4 receptors was shown based on the effect of extracellular nucleotides on apoptosis or cell proliferation, and measurement of nucleotide-dependent calcium fluxes using a fluorometric imaging plate reader in the presence of different selective agonists and antagonists. ATP, at high concentrations, induced apoptosis through ligation of P2X7 and P2Y1 receptors; conversely, ATP, at lower concentrations, and UTP stimulated proliferation, probably acting via P2Y2 receptors. We therefore propose that stimulation or dysfunction of purinergic receptors may contribute at least partially to modulation of epithelial carcinoma cell proliferation and apoptosis.
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Ruan, Huai Zhen, Lori A. Birder, Zhenghua Xiang, Bikramjit Chopra, Tony Buffington, Changfeng Tai, James R. Roppolo, William C. de Groat, and Geoffrey Burnstock. "Expression of P2X and P2Y receptors in the intramural parasympathetic ganglia of the cat urinary bladder." American Journal of Physiology-Renal Physiology 290, no. 5 (May 2006): F1143—F1152. http://dx.doi.org/10.1152/ajprenal.00333.2005.

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The distribution and function of P2X and P2Y receptor subtypes were investigated on intact or cultured intramural ganglia of the cat urinary bladder by immunocytochemistry and calcium-imaging techniques, respectively. Neurons were labeled by all seven P2X receptor subtype antibodies and antibodies for P2Y2, P2Y4, P2Y6, and P2Y12 receptor subtypes with a staining intensity of immunoreactivity in the following order: P2X3=P2Y2=P2Y4=P2Y6=P2Y12>P2X1=P2X2=P2X4>P2X5=P2X6=P2X7. P2Y1 receptor antibodies labeled glial cells, but not neurons. P2X3 and P2Y4 polyclonal antibodies labeled ∼95 and 40% of neurons, respectively. Double staining showed that 100, 48.8, and 97.4% of P2X3 receptor-positive neurons coexpressed choline acetyl transferase (ChAT), nitric oxide synthase (NOS), and neurofilament 200 (NF200), respectively, whereas 100, 59.2, and 97.6% of P2Y4 receptor-positive neurons coexpressed ChAT, NOS, and NF200, respectively. Application of ATP, α,β-methylene ATP, and uridine triphosphate elevated intracellular Ca2+ concentration in a subpopulation of dissociated cultured cat intramural ganglia neurons, demonstrating the presence of functional P2Y4 and P2X3 receptors. This study indicates that P2X and P2Y receptor subtypes are expressed by cholinergic parasympathetic neurons innervating the urinary bladder. The neurons were also stained for NF200, usually regarded as a marker for large sensory neurons. These novel histochemical properties of cholinergic neurons in the cat bladder suggest that the parasympathetic pathways to the cat bladder may be modulated by complex purinergic synaptic mechanisms.
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Chen, Lin, Changlong Leng, Qin Ru, Qi Xiong, Mei Zhou, and Yuxiang Wu. "Retrograde Labeling of Different Distribution Features of DRG P2X2 and P2X3 Receptors in a Neuropathic Pain Rat Model." BioMed Research International 2020 (July 23, 2020): 1–15. http://dx.doi.org/10.1155/2020/9861459.

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The distributions of P2X subtypes during peripheral neuropathic pain conditions and their differential roles are not fully understood. To explore these characteristics, the lumbosacral dorsal root ganglion (DRG) in the chronic constriction injury (CCI) sciatic nerve rat model was studied. Retrograde trace labeling combined with immunofluorescence technology was applied to analyze the distribution of neuropathic nociceptive P2X1-6 receptors. Our results suggest that Fluoro-Gold (FG) retrograde trace labeling is an efficient method for studying lumbosacral DRG neurons in the CCI rat model, especially when the DRG neurons are divided into small, medium, and large subgroups. We found that neuropathic nociceptive lumbosacral DRG neurons (i.e., FG-positive cells) were significantly increased in medium DRG neurons, while they declined in the large DRG neurons in the CCI group. P2X3 receptors were markedly upregulated in medium while P2X2 receptors were significantly decreased in small FG-positive DRG neurons. There were no significant changes in other P2X receptors (including P2X1, P2X4, P2X5, and P2X6). We anticipate that P2X receptors modulate nociceptive sensitivity primarily through P2X3 subtypes that are upregulated in medium neuropathic nociceptive DRG neurons and/or via the downregulation of P2X2 cells in neuropathic nociceptive small DRG neurons.
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Birder, L. A., H. Z. Ruan, B. Chopra, Z. Xiang, S. Barrick, C. A. Buffington, J. R. Roppolo, A. P. D. W. Ford, W. C. de Groat, and G. Burnstock. "Alterations in P2X and P2Y purinergic receptor expression in urinary bladder from normal cats and cats with interstitial cystitis." American Journal of Physiology-Renal Physiology 287, no. 5 (November 2004): F1084—F1091. http://dx.doi.org/10.1152/ajprenal.00118.2004.

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Purinergic mechanisms appear to be involved in motor as well as sensory functions in the urinary bladder. ATP released from efferent nerves excites bladder smooth muscle, whereas ATP released from urothelial cells can activate afferent nerves and urothelial cells. In the present study, we used immunohistochemical techniques to examine the distribution of purinoceptors in the urothelium, smooth muscle, and nerves of the normal cat urinary bladder as well as possible changes in the expression of these receptors in cats with a chronic painful bladder condition termed feline interstitial cystitis (FIC) in which ATP release from the urothelium is increased. In normal cats, a range of P2X (P2X1, P2X2, P2X3, P2X4, P2X5, P2X6, and P2X7) and P2Y (P2Y1, P2Y2, and P2Y4) receptor subtypes was expressed throughout the bladder urothelium. In FIC cats, there is a marked reduction in P2X1 and loss of P2Y2 receptor staining. Both P2X3 and P2Y4 are present in nerves in normal cat bladder, and no obvious differences in staining were detected in FIC. Smooth muscle in the normal bladder did not exhibit P2Y receptor staining but did exhibit P2X (P2X2, P2X1) staining. In the FIC bladder smooth muscle, there was a significant reduction in P2X1 expression. These findings raise the possibility that purinergic mechanisms in the urothelium and bladder smooth muscle are altered in FIC cats. Because the urothelial cells appear to have a sensory function in the bladder, it is possible that the plasticity in urothelial purinergic receptors is linked with the painful bladder symptoms in IC.
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Baines, Abigail, Katie Parkinson, Joan A. Sim, Laricia Bragg, Christopher R. L. Thompson, and R. Alan North. "Functional Properties of Five Dictyostelium discoideum P2X Receptors." Journal of Biological Chemistry 288, no. 29 (June 5, 2013): 20992–1000. http://dx.doi.org/10.1074/jbc.m112.445346.

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The Dictyostelium discoideum genome encodes five proteins that share weak sequence similarity with vertebrate P2X receptors. Unlike vertebrate P2X receptors, these proteins are not expressed on the surface of cells, but populate the tubules and bladders of the contractile vacuole. In this study, we expressed humanized cDNAs of P2XA, P2XB, P2XC, P2XD, and P2XE in human embryonic kidney cells and altered the ionic and proton environment in an attempt to reflect the situation in amoeba. Recording of whole-cell membrane currents showed that four receptors operated as ATP-gated channels (P2XA, P2XB, P2XD, and P2XE). At P2XA receptors, ATP was the only effective agonist of 17 structurally related putative ligands that were tested. Extracellular sodium, compared with potassium, strongly inhibited ATP responses in P2XB, P2XD, and P2XE receptors. Increasing the proton concentration (pH 6.2) accelerated desensitization at P2XA receptors and decreased currents at P2XD receptors, but increased the currents at P2XB and P2XE receptors. Dictyostelium lacking P2XA receptors showed impaired regulatory volume decrease in hypotonic solution. This phenotype was readily rescued by overexpression of P2XA and P2XD receptors, partially rescued by P2XB and P2XE receptors, and not rescued by P2XC receptors. The failure of the nonfunctional receptor P2XC to restore the regulatory volume decrease highlights the importance of ATP activation of P2X receptors for a normal response to hypo-osmotic shock, and the weak rescue by P2XB and P2XE receptors indicates that there is limited functional redundancy among Dictyostelium P2X receptors.
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Stoop, Ron, Annmarie Surprenant, and R. Alan North. "Different Sensitivities to pH of ATP-Induced Currents at Four Cloned P2X Receptors." Journal of Neurophysiology 78, no. 4 (October 1, 1997): 1837–40. http://dx.doi.org/10.1152/jn.1997.78.4.1837.

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Stoop, Ron, Annmarie Surprenant, and R. Alan North. Different sensitivities to pH of ATP-induced currents at four cloned P2X receptors. J. Neurophysiol. 78: 1837–1840, 1997. The effect of changing extracellular pH was studied on the currents induced by ATP or αβ-methylene-ATP in HEK293 cells transfected with different P2X receptor subunits. In cells expressing P2X1, P2X3, or P2X4 receptors, the effect of ATP was decreased by acidification. In cells expressing P2X2 receptors, acidification increased the ATP-induced current; this effect was also seen in cells expressing heteromeric P2X2 and P2X3 receptors. At P2X2 receptors, acidification caused a leftward shift in the ATP concentration-response curve, without change in maximum; the pKa for this effect was 7.3. At P2X4 receptors, acidification caused a rightward shift in the ATP concentration-response curve, without change in the maximum; the pKa for this effect was 6.8. The pH dependence of the action of ATP should be taken into account in studies of synaptic transmission, and it may provide a further tool to assign molecular identity to P2X receptors expressed by brain neurons.
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Lee, B. M., H. Jo, G. Park, Y. H. Kim, C. K. Park, S. J. Jung, G. Chung, and S. B. Oh. "Extracellular ATP Induces Calcium Signaling in Odontoblasts." Journal of Dental Research 96, no. 2 (October 2, 2016): 200–207. http://dx.doi.org/10.1177/0022034516671308.

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Odontoblasts form dentin at the outermost surface of tooth pulp. An increasing level of evidence in recent years, along with their locational advantage, implicates odontoblasts as a secondary role as sensory or immune cells. Extracellular adenosine triphosphate (ATP) is a well-characterized signaling molecule in the neuronal and immune systems, and its potential involvement in interodontoblast communications was recently demonstrated. In an effort to elaborate the ATP-mediated signaling pathway in odontoblasts, the current study performed single-cell reverse transcription polymerase chain reaction (RT-PCR) and immunofluorescent detection to investigate the expression of ATP receptors related to calcium signal in odontoblasts from incisal teeth of 8- to 10-wk-old rats, and demonstrated an in vitro response to ATP application via calcium imaging experiments. While whole tissue RT-PCR analysis detected P2Y2, P2Y4, and all 7 subtypes (P2X1 to P2X7) in tooth pulp, single-cell RT-PCR analysis of acutely isolated rat odontoblasts revealed P2Y2, P2Y4, P2X2, P2X4, P2X6, and P2X7 expression in only a subset (23% to 47%) of cells tested, with no evidence for P2X1, P2X3, and P2X5 expression. An increase of intracellular Ca2+ concentration in response to 100μM ATP, which was repeated after pretreatment of thapsigargin or under the Ca2+-free condition, suggested function of both ionotropic and metabotropic ATP receptors in odontoblasts. The enhancement of ATP-induced calcium response by ivermectin and inhibition by 5-(3-bromophenyl)-1,3-dihydro-2H-benzofuro[3,2-e]-1,4-diazepin-2-one (5-BDBD) confirmed a functional P2X4 subtype in odontoblasts. Positive calcium response to 2′,3′-O-(benzoyl-4-benzoyl)-ATP (BzATP) and negative response to α,β-methylene ATP suggested P2X2, P2X4, and P2X7 as functional subunits in rat odontoblasts. Single-cell RT-PCR analysis of the cells with confirmed calcium response and immunofluorescent detection further corroborated the expression of P2X4 and P2X7 in odontoblasts. Overall, this study demonstrated heterogeneous expression of calcium-related ATP receptor subtypes in subsets of individual odontoblasts, suggesting extracellular ATP as a potential signal mediator for odontoblastic functions.
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Nakamura, Ei'Ichiro, Yasuhito Uezono, Ken'Ichiro Narusawa, Izumi Shibuya, Yosuke Oishi, Masahiro Tanaka, Nobuyuki Yanagihara, Toshitaka Nakamura, and Futoshi Izumi. "ATP activates DNA synthesis by acting on P2X receptors in human osteoblast-like MG-63 cells." American Journal of Physiology-Cell Physiology 279, no. 2 (August 1, 2000): C510—C519. http://dx.doi.org/10.1152/ajpcell.2000.279.2.c510.

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In human osteoblast-like MG-63 cells, extracellular ATP increased [3H]thymidine incorporation and cell proliferation and synergistically enhanced platelet-derived growth factor- or insulin-like growth factor I-induced [3H]thymidine incorporation. ATP-induced [3H]thymidine incorporation was mimicked by the nonhydrolyzable ATP analogs adenosine 5′- O-(3-thiotriphosphate) and adenosine 5′-adenylylimidodiphosphate and was inhibited by the P2 purinoceptor antagonist suramin, suggesting involvement of P2 purinoceptors. The P2Y receptor agonist UTP and UDP and a P2Y receptor antagonist reactive blue 2 did not affect [3H]thymidine incorporation, whereas the P2X receptor antagonist pyridoxal phosphate-6-azophenyl-2′,4-disulfonic acid inhibited ATP-induced [3H]thymidine incorporation, suggesting that ATP-induced DNA synthesis was mediated by P2X receptors. RT-PCR analysis revealed that MG-63 cells expressed P2X4, P2X5, P2X6, and P2X7, but not P2X1, P2X2, and P2X3, receptors. In fura 2-loaded cells, not only ATP, but also UTP, increased intracellular Ca2+concentration, and inhibitors for several Ca2+-activated protein kinases had no effect on ATP-induced DNA synthesis, suggesting that an increase in intracellular Ca2+concentration is not indispensable for ATP-induced DNA synthesis. ATP increased mitogen-activated protein kinase activity in a Ca2+-independent manner and synergistically enhanced platelet-derived growth factor- or insulin-like growth factor I-induced kinase activity. Furthermore, the mitogen-activated protein kinase kinase inhibitor PD-98059 totally abolished ATP-induced DNA synthesis. We conclude that ATP increases DNA synthesis and enhances the proliferative effects of growth factors through P2X receptors by activating a mitogen-activated protein kinase pathway.
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Samways, Damien S. K., and Terrance M. Egan. "Acidic Amino Acids Impart Enhanced Ca2+ Permeability and Flux in Two Members of the ATP-gated P2X Receptor Family." Journal of General Physiology 129, no. 3 (February 26, 2007): 245–56. http://dx.doi.org/10.1085/jgp.200609677.

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P2X receptors are ATP-gated cation channels expressed in nerve, muscle, bone, glands, and the immune system. The seven family members display variable Ca2+ permeabilities that are amongst the highest of all ligand-gated channels (Egan and Khakh, 2004). We previously reported that polar residues regulate the Ca2+ permeability of the P2X2 receptor (Migita et al., 2001). Here, we test the hypothesis that the formal charge of acidic amino acids underlies the higher fractional Ca2+ currents (Pf%) of the rat and human P2X1 and P2X4 subtypes. We used patch-clamp photometry to measure the Pf% of HEK-293 cells transiently expressing a range of wild-type and genetically altered receptors. Lowering the pH of the extracellular solution reduced the higher Pf% of the P2X1 receptor but had no effect on the lower Pf% of the P2X2 receptor, suggesting that ionized side chains regulate the Ca2+ flux of some family members. Removing the fixed negative charges found at the extracellular ends of the transmembrane domains also reduced the higher Pf% of P2X1 and P2X4 receptors, and introducing these charges at homologous positions increased the lower Pf% of the P2X2 receptor. Taken together, the data suggest that COO− side chains provide an electrostatic force that interacts with Ca2+ in the mouth of the pore. Surprisingly, the glutamate residue that is partly responsible for the higher Pf% of the P2X1 and P2X4 receptors is conserved in the P2X3 receptor that has the lowest Pf% of all family members. We found that neutralizing an upstream His45 increased Pf% of the P2X3 channel, suggesting that this positive charge masks the facilitation of Ca2+ flux by the neighboring Glu46. The data support the hypothesis that formal charges near the extracellular ends of transmembrane domains contribute to the high Ca2+ permeability and flux of some P2X receptors.
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Dissertations / Theses on the topic "P2X3"

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Schiavuzzo, Jalile Garcia 1980. "Mecanismos envolvidos na ação hiperalgésica induzida pela ativação de receptores P2X3 e P2X2/3 no músculo gastrocnêmio de ratos." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/244518.

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Orientador: Maria Cláudia Gonçalves de Oliveira Fusaro
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Aplicadas
Made available in DSpace on 2018-08-24T04:40:35Z (GMT). No. of bitstreams: 1 Schiavuzzo_JalileGarcia_M.pdf: 1205741 bytes, checksum: b599c1bee7cda79ed3554fcb789eea9d (MD5) Previous issue date: 2013
Resumo: Existem evidências do envolvimento do ATP via ativação do receptor P2X3 na dor muscular. Portanto, o objetivo deste estudo foi verificar se a ativação do receptor P2X3 no músculo gastrocnêmio de ratos induz hiperalgesia mecânica, e em caso afirmativo, analisar os mecanismos inflamatórios pelo qual os receptores P2x3 induzem hiperalgesia mecânica. O Antagonista não seletivo para o receptor P2X3 ?,?meATP foi administrado no músculo gastrocnêmio de ratos, induzindo hiperalgesia, a qual foi significativamente reduzida pelo antagonista seletivo do receptor P2X3 e P2X2/3 - A-317491. A hiperalgesia mecânica induzida pelo ?,?meATP foi reduzida pelo inibidor de ciclooxigenase Indometacina, pelo antagonista seletivo do receptor de Bradicinina B1 e B2- Dalbk e Bradyzide, respectivamente, antagonista dos adrenoceptores ?1 e ?2 - Atenolol e ICI 118,551 respectivamente, e inibidor não específico de selectinas Fucoidan. O ?,?meATP também induziu o aumento da concentração local de citocinas pro inflamatórias TNF-?, IL-1?, IL-6 e CIN e migração de neutrófilos. Juntos estes achados sugerem que o ?,?meATP induz hiperalgesia mecânica no músculo gastrocnêmio via ativação de receptor periférico P2X3, o qual envolve bradicinina, prostaglandinas e aminas simpatomiméticas e migração de neutrófilos. Portanto, nós sugerimos que os receptores P2X3 sejam um importante alvo no controle da dor muscular
Abstract: There is evidence of the involvement of endogenous ATP via activation of P2X3 in muscle pain. Therefore, the aim of this study was to verify whether the activation of P2X3 receptors in the gastrocnêmio muscle of rats induces mechanical hyperalgesia and, if so, to analyze the inflammatory mechanisms by which P2X3 receptors induce mechanical hyperalgesia. Intramuscular administration of the non-selective P2X3 receptor agonist ?,?-meATP in the gastrocnemius muscle of rats induced mechanical hyperalgesia, which was significantly reduced by the selective P2X3 and P2X2/3 receptors antagonist A-317491. The ?,?-meATP-induced mechanical hyperalgesia was prevented by the indomethacin cyclooxygenase inhibitor, the selective bradykinin B1- or B2- receptor antagonist DALBK and bradyzide, respectively, the ?1- or ?2-adrenoceptor antagonist atenolol and ICI 118,551, respectively, and the nonspecific selectin inhibitor fucoidan. ?,?-meATP also induced increase in the local concentration of the pro-inflammatory cytokines TNF-?, IL-1?, IL-6 and CINC-1 and the neutrophil migration. Together, these findings suggest that ?,?-meATP induced mechanical VIII hyperalgesia in the gastrocnemius muscle of rats via activation of peripheral P2X3 receptors, which involves bradykinin, prostaglandins, sympathetic amines, pro-inflammatory cytokines and neutrophil migration. Therefore, we suggest that P2X3 receptors are important targets to control muscle inflammatory pain
Mestrado
Biodinâmica do Movimento Humano e Esporte
Mestra em Ciências da Nutrição e do Esporte e Metabolismo
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Chabot-Doré, Anne-Julie. "Metabotropic regulation of ATP-gated P2X3 receptors." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101708.

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Among the ATP-gated channels, the P2X3 subtype is exclusively expressed in nociceptors of dorsal root ganglia (DRG) and trigeminal ganglia, where it plays a major role in enhanced pain sensation observed in chronic pain states. We tested the hypothesis that P2X3 receptors are modulated by metabotropic receptors, such as 5-HT2A, mG1uR5 and trkA, leading to increased P2X3-mediated currents. Double fluorescence labeling confirmed that P2X3-expressing neurons are labeled by the lectin IB4 and we showed that 5-HT2A and mGluR5 receptors, but not trkA, are expressed in a fraction of IB4-positive neurons. Using confocal microscopy, we examined the subcellular distribution of P2X3 and we observed that 5-HT induced a translocation of P2X3 labeling in a significant number of neurons. In Xenopus oocytes, we recorded a short-lasting and kinase-dependent potentiation of P2X3 currents by activation of co-expressed 5-HT2A and mGluR5 receptors. The data presented here show that both 5-HT2A and mG1uR5 are potential modulators of P2X3 receptors in a subset of nociceptors in DRG.
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Wang, Haihong. "Amino acid residues constituting the agonist binding site of the human P2X3 receptor and subunit stoichiometry of heteromeric P2X2/3 and P2X2/6 receptors." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-112913.

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Homotrimeric P2X3 and heteromeric P2X2/3 receptors are present in sensory ganglia and participate in pain perception. In order to develop pharmacological antagonists for these receptors, it is important to clarify which amino acid (AA) residues constitute the agonist binding pouch as well as to learn the stoichiometry of the receptor subunits forming a heteromeric receptor. We expressed the homomeric human (h)P2X3 receptor or its mutants in HEK293 cells and measured the ATP-induced responses by the whole-cell patch-clamp method. For the binding-site mutants, all conserved and some non-conserved AAs in the four nucleotide binding segments (NBSs) of the P2X3 subunit were sequentially replaced by alanine. Especially the positively charged AAs Lys and Arg appeared to be of critical importance for the agonist effects. We concluded that groups of AAs organized in NBSs rather than individual amino acids appear to be responsible for agonist binding at the P2X3 receptor. These NBSs are located at the interface of the three subunits forming a functional receptor. We were also interested to find out, whether two heteromeric receptors (P2X2/3 and P2X2/6), where P2X2 combines with two different partners, have an obligatory subunit stoichiometry of 1:2 or whether the subunit stoichiometry may be variable. For this purpose we used non-functional P2X2, P2X3 and P2X6 subunit-mutants to investigate the composition of heteromeric P2X2/3 and P2X2/6 receptors. The subunit stoichiometry of P2X2/3 and P2X2/6 was found to be 1:2 and 2:1, respectively. Thus, recognitions sites between P2X2 and its partners rather than random association may govern the subunit compositions of the receptor trimers.
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Mo, Gary. "Molecular physiology of sensory P2X3 ATP receptor channels." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107793.

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Purinergic transmission mediated by extracellular release of ATP has been shown to be involved in numerous physiological processes, ranging from bladder function to taste and hearing. The diverse roles of ATP mediated signaling is largely due to widespread distribution of P2 ATP receptors. Since their initial cloning, various P2 receptors have been found to mediate a wide range of cellular processes in different tissues. One P2 receptor in particular, the P2X3 receptor, is almost exclusively expressed on nociceptive dorsal root ganglion (DRG) sensory neurons. Due to its specific distribution, the P2X3 receptor has been a prominent target in pain research, especially in studies of chronic pain conditions. Numerous studies have indicated involvement of P2X3 receptor in mediating increased pain behavior associated with chronic inflammation or neuropathic injury. However, the exact contribution of the P2X3 in chronic pain conditions is still unclear, especially in the case of neuropathic pain. There is inconsistency in reports of changes in P2X3 expression or activity during neuropathic pain. The underlying element of enhanced pain behavior after nerve injury is increased excitability of sensory neurons. The first study of described in this thesis investigates the contribution of the P2X3 receptor to changes in excitability of injured neurons. Activation of protein kinase C (PKC) has been shown to facilitate chronic pain behavior by modulating the activity of various ion channels. Thus, the contribution of PKC to hyperexcitability in injured neurons was also investigated in the first study.Nerve injury induces very dynamic changes in cellular physiology including activation of various intracellular signaling pathways. The activity of the P2X3 receptor may be affected by such cellular processes. Understanding the molecular physiology of the P2X3 receptor may provide additional insight into the specific contribution of the P2X3 receptor in pain physiology. A common component of many cellular signaling pathways is the cleavage of phosphatidylinositol 4,5-bisphosphate (PIP2) by phospholipase C (PLC), and changes in PIP2 levels modulate the activity of various ion channels, including the P2X2 receptor. The second study in this thesis investigates the modulation of P2X3 by changes in intracellular levels of PIP2. Recent studies have demonstrated possible co-expression of metabotropic P2Y receptors on P2X3 positive sensory neurons. ATP release on sensory neurons that express both P2Y and P2X3 receptors will likely trigger activation of both types of purinergic receptors. The third study in this thesis investigated the modulation of P2X3 receptor activity by metabotropic P2Y receptors. Our understanding of the P2X3 receptor predominantly comes from rodent studies. Because interspecies differences in the functional characteristics of certain P2X receptor subtypes have been reported, there is a pressing need to verify if our understanding of the rodent P2X3 receptor is translatable to species closer to man. To this end, the last study of this thesis compares the pharmacological properties of native P2X3 receptor on rat sensory neurons to native P2X3 receptors on monkey sensory neurons.
Il a été montré que la transmission purinergique médiée par la libération extracellulaire d'ATP est impliquée dans de nombreux processus physiologiques, allant du fonctionnement de la vessie aux sens du goût et de l'audition. Les rôles variés de la signalisation par l'ATP sont expliqués principalement par la distribution étendue des récepteurs P2 de l'ATP dans l'organisme. Depuis leur clonage initial dans les années '90, une variété de récepteurs P2 régissant divers mécanismes cellulaires a été découverte dans plusieurs tissus. Un récepteur canal P2 en particulier, P2X3, se trouve exprimé quasi-exclusivement dans les neurones nocicepteurs des ganglions spinaux (DRG). De par cette distribution spécifique, le récepteur P2X3 est une cible importante dans la recherche sur la douleur, principalement dans les études sur la douleur chronique. De nombreuses études indiquent le rôle du récepteur P2X3 dans l'augmentation des réponses à la douleur associée à une inflammation chronique ou une lésion neuropathique. Cependant, la contribution exacte de P2X3 dans la douleur chronique reste incertaine, surtout dans les cas de douleur neuropathqiue. Il existe des contradictions dans les articles sur les changements d'expression ou d'activité de P2X3 en conditions de douleur neuropathique. Un élément clé dans l'exacerbation des comportements douloureux après lésion neuropathique est l'augmentation d'excitabilité des neurones sensoriels. La première étude décrite dans cette thèse explore la contribution de P2X3 dans les changements d'excitabilité des neurones de DRG endommagé. Il a été rapporté que l'activation de la protéine kinase C (PKC) facilite les comportements douloureux en modulant l'activité de certains canaux ioniques. Ainsi, la contribution de PKC à l'hyperexcitabilité des neurones de DRG neuropathique a aussi été étudiée dans ce premier chapitre. Une insulte à un nerf périphérique induit des changements très dynamiques dans sa physiologie cellulaire, incluant l'activation de voies de signalisation intracellulaires. La fonction de P2X3 peut se trouver affectée par ces mécanismes neuronaux. Comprendre la physiologie moléculaire du récepteur P2X3 peut nous éclairer sur sa contribution spécifique dans la douleur. Une étape commune à de nombreuses voies de signalisation cellulaire est le clivage du phosphatidylinositol 4,5-bisphosphate (PIP2) par la phospholipase C (PLC). Les variations de niveaux de PIP2 modulent l'activité de plusieurs canaux ioniques, y compris le récepteur P2X2. Le deuxième chapitre dans cette thèse se concentre sur la modulation de P2X3 par les niveaux intracellulaires de PIP2. Des études récentes ont démontré la co-expression potentielle de récepteurs métabotropiques P2Y et ionotropiques P2X3 sur les neurones sensoriels. L'ATP pouvant activer les deux types de récepteurs, le troisième chapitre se penche sur la modulation de la fonction de P2X3 par les récepteurs P2Y couplés à la phospholipase C.Notre compréhension du récepteur P2X3 provient principalement des données obtenues dans des modèles précliniques de rongeurs. Sachant que des différences interspécifiques marquées dans les propriétés fonctionnelles de certains sous-types de récepteurs P2X ont été documentées, il est urgent et important de vérifier que nos connaissances sur le récepteur P2X3 de rongeur sont transférables aux primates ou à l'homme. À cette fin, dans la dernière étude de cette thèse, nous comparons les propriétés pharmacologiques du récepteur P2X3 natif à la surface des neurones sensoriels de rat avec celles du récepteur P2X3 exprimé dans les neurones sensoriels de singe.
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Günther, Janka [Verfasser]. "Generierung und Charakterisierung transgener BAC-P2X3-Mäuse / Janka Günther." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2014. http://d-nb.info/1051414172/34.

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Teixeira, Juliana Maia 1984. "Involvement of P2X3 and P2X7 purinergic receptors in inflammatory articular hyperalgesia in the knee joint of rats and the study of the peripheral mechanisms involved = Participação dos receptores purinérgicos P2X3 e P2X7 na hiperalgesia inflamatória articular em joelho de ratos e o estudo dos mecanismos periféricos envolvidos." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314054.

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Orientador: Cláudia Herrera Tambeli
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: A osteoartrite (OA) é uma doença degenerativa e progressiva, caracterizada pela degradação da cartilagem que reveste as extremidades ósseas e inflamação da membrana sinovial, causando incapacidade física, inchaço articular e dor. Embora o alívio da dor severa seja o principal objetivo no tratamento agudo, pouco se sabe sobre os mecanismos envolvidos no desenvolvimento da dor na OA. Estudos demonstram a participação do ATP (adenosina 5¿-trifosfato) em processos de hiperalgesia através da ativação dos receptores purinérgicos P2X3, P2X2/3 e P2X7. Portanto, os objetivos deste estudo foram: (1) investigar a participação dos receptores P2X3, P2X2/3 e P2X7 na hiperalgesia articular em modelo de artrite na articulação do joelho de ratos machos e fêmeas em estro e se há diferenças sexuais no efeito induzido pelos antagonistas de receptores P2X3, P2X2/3 e P2X7. (2) testar a hipótese de que a inflamação articular induzida pela carragenina aumenta a expressão do receptor P2X3 nos condrócitos da cartilagem articular da articulação do joelho de ratos. (3) verificar se o mecanismo pelo qual a ativação dos receptores P2X3, P2X2/3 e P2X7 contribui para a hiperalgesia articular depende da liberação prévia de citocinas pró-inflamatórias e da migração de neutrófilos. (4) investigar se a ativação dos receptores P2X3, P2X2/3 e P2X7 induz hiperalgesia na articulação do joelho de ratos dependente da liberação de mediadores inflamatórios. (5) testar a hipótese de que a ativação dos receptores P2X3, P2X2/3 e P2X7 contribui para a hiperalgesia articular induzida pelos mediadores inflamatórios: bradicinina, citocinas pró-inflamatórias, PGE2 e dopamina. Para os objetivos 1, 4 e 5, a hiperalgesia articular foi quantificada através do teste de Incapacitação Articular. Para o objetivo 2, foi utilizado o ensaio de imunofluorescência. Para os objetivos 3 e 4 foram utilizados os ensaios imuno-enzimáticos ELISA e MPO. Os resultados demonstram que a ativação dos receptores P2X3, P2X2/3 e P2X7 pelo ATP endógeno é essencial para o desenvolvimento da hiperalgesia articular induzida pela carragenina na articulação do joelho de ratos machos e fêmeas em estro, que são mais sensíveis do que os machos aos efeitos anti-hiperalgésicos e anti-inflamatórios induzidos pelo antagonista de receptor P2X7. Durante a inflamação articular induzida pela carragenina ocorre um aumento na expressão dos receptores P2X3 nos condrócitos da cartilagem articular. O papel dos receptores P2X3, P2X2/3 e P2X7 na hiperalgesia articular é mediado pela sensibilização indireta dos nociceptores aferentes primários, dependente da liberação prévia de citocinas pró-inflamatórias e da migração de neutrófilos. Além disso, a ativação dos receptores P2X3, P2X2/3 e P2X7 induz hiperalgesia articular dependente da liberação de bradicinina, aminas simpatomiméticas, prostaglandinas e citocinas pró-inflamatórias. Finalmente, a hiperalgesia articular induzida pelos mediadores inflamatórios bradicinina, PGE2 e dopamina depende da ativação de receptores P2X3 e P2X2/3, enquanto que a ativação de receptor P2X7 contribui para a hiperalgesia articular induzida pela bradicinina e dopamina. Concluindo, os resultados apresentados sugerem que os receptores P2X3, P2X2/3 e P2X7 são alvos farmacológicos interessantes para o tratamento das doenças inflamatórias articulares como a osteoartrite. Particularmente em relação ao receptor P2X7, antagonistas seletivos podem ser usados para reduzir a dor e inflamação no joelho, especialmente em mulheres
Abstract: Osteoarthritis (OA) is a degenerative and progressive disease, characterized by cartilage breakdown which covers the bone ends and by synovial membrane inflammation, causing disability, joint swelling and pain. The relief of severe pain is the main goal of the acute treatment, but little is known about the mechanisms involved in the development of pain in OA. It has been demonstrated the role of ATP (adenosine 5'-triphosphate) in processes of hyperalgesia through activation of purinergic receptors P2X3, P2X2/3 and P2X7. Therefore, the aims of this study were: (1) to investigate the role of P2X3, P2X2/3 and P2X7 receptors in articular hyperalgesia in the knee joint arthritis model in males and estrus females rats and, if so, whether there are sex differences in the effect induced by the selective P2X3, P2X2/3 and P2X7 receptors antagonists. (2) to test the hypothesis that the carrageenan-induced articular inflammation increases the expression of P2X3 receptor in chondrocytes of articular cartilage of the knee joint. (3) to verify whether the mechanism by which the P2X3, P2X2/3 and P2X7 receptors activation contributes to articular hyperalgesia depends on previous pro-inflammatory cytokines release and neutrophil migration. (4) to investigate whether the P2X3, P2X2/3 and P2X7 receptors activation induces articular hyperalgesia in the rat¿s knee joint which depends on release of inflammatory mediators. (5) to verify whether the activation of P2X3, P2X2/3 and P2X7 receptors contributes to the articular hyperalgesia induced by the inflammatory mediators bradykinin, pro-inflammatory cytokines, PGE2 and dopamine. For the aims 1, 4 and 5, the articular hyperalgesia was quantified by the rat knee joint Incapacitation Test. The immuno?uorescence method was used for the aim 2. For aims 3 and 4, the ELISA and MPO immunoenzymatic assays were used. The results demonstrate that P2X3, P2X2/3 and P2X7 receptors activation by endogenous ATP is essential for the development of carrageenan-induced articular hyperalgesia in the knee joint of male and estrus female rats, which are more sensitive than males to anti-hyperalgesic and anti-inflammatory effects induced by the P2X7 receptor antagonist. During carrageenan-induced joint inflammation occurs an increased of P2X3 receptors expression in chondrocytes of the articular cartilage. The essential role played by P2X3, P2X2/3 and P2X7 receptors in the development of articular hyperalgesia is mediated by an indirect sensitization of the primary afferent nociceptors dependent on the previous pro-inflammatory cytokines release and neutrophil migration. Moreover, the P2X3, P2X2/3 and P2X7 receptors activation induces articular hyperalgesia which depends on bradykinin, sympathomimetic amines, prostaglandins and pro-inflammatory cytokines release. Finally, the articular hyperalgesia induced by inflammatory mediators bradykinin, PGE2 and dopamine depends on the P2X3 and P2X2/3 receptors activation, while the P2X7 receptor activation contributes to the bradykinin- and dopamine-induced articular hyperalgesia. In conclusion, our results suggest that P2X3, P2X2/3 and P2X7 receptors are interesting pharmacological targets for the treatment of inflammatory joint diseases such as osteoarthritis. In particular, selective P2X7 receptor antagonists can be used to reduce inflammation and pain in the knee joint, especially in women
Doutorado
Fisiologia
Doutora em Biologia Funcional e Molecular
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Rashed, Mahmoud [Verfasser]. "Syntheses and structure-activity relationships of novel P2X3 receptor antagonists / Mahmoud Rashed." Bonn : Universitäts- und Landesbibliothek Bonn, 2018. http://d-nb.info/1160594392/34.

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Prado, Filipe César do. "Papel do receptor P2X3 e da ativação da proteína kinase C épsilon dos neurônios nociceptivos periféricos na dor inflamatória." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314727.

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Orientador: Carlos Amílcar Parada
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Enquanto a hiperalgesia inflamatória depende da liberação de prostaglandinas e/ou de aminas simpatomiméticas que sensibilizam os neurônios aferentes primários, nosso grupo demonstrou recentemente que o bloqueio do receptor P2X3 no tecido periférico previne a hiperalgesia induzida pela carragenina.. No entanto, o mecanismo pelo qual a ativação dos receptores P2X3 neuronais contribui para a hiperalgesia inflamatória não está completamente estabelecido. O presente estudo verifica se a ativação do receptor P2X3 dos neurônios aferentes primários contribui para a hiperalgesia mecânica induzida pela prostaglandina E2 ou pela dopamine no tecido periférico. A co-administração de A317491 (60 µg / paw), um antagonista seletivo do receptor P2X3, ou o prétratamento com dexametasona (1 mg / mL / kg), preveniu a hiperalgesia mecânica medida 3 horas depois da administraçao de carragenina (300 µg / paw) na pata posterior de ratos. A administração de ??meATP (50 µg /paw) induziu hiperalgesia mecânica 1 hora, mas não 3 horas, depois da sua administração, que foi prevenida pela dexametasona ou pelo A317491. Doses sublimiares de PGE2 (4 ng / paw) ou dopamina (0.4 µg / paw) que não induzem hiperalgesia por si só, induziram hiperalgesia, 3 horas depois, quando administradas logo depois de ??meATP ou carragenina em ratos tratados com dexametasona. Esses estados de hiperalgesia ("priming") revelados pelas doses sublimiares de PGE2 ou dopamine foram prevenidos pelo A317491 ou pelo tratamento com administração intraganglionar (DRG-L5) de ODN antisense, mas não pelo ODN mismatch, contra o receptor P2X3 (40 µg /5µL once a day for 4 days). ODN antisense, mas não o ODN mismatch, reduziu a expressão dos receptores P2X3 no nervo safeno e no DRG-L5. Para verificar se a PKC? media esse estado de hiperalgesia, inibidor de translocação de PKC? (1 µg/paw) foi administrado no tecido periférico 45 minutos antes do ??meATP ou PGE2 (100 ng/paw). O inibidor de PKC? preveniu o estado de hiperalgesia induzido pelo ??meATP ("priming"), mas não a hiperalgesia mecânica induzida pela PGE2 (100 ng/paw). Dessa maneira, os resultados desse estudo sugerem que a hiperalgesia inflamatória depended a ativação dos receptores P2X3 neuronais e da subsequente translocação da PKC? , que aumenta a susceptibilidade dos neurônios aferentes primários (priming) à ação de outros mediadores inflamatórios como a PGE2 e as aminas simpatomiméticas
Abstract: While inflammatory hyperalgesia depends on the release of prostaglandins and/or sympathetic amines that ultimately sensitize the primary afferent neurons, we have recently demonstrated that blockade of P2X3 receptor in the peripheral tissue completely prevents carrageenan-induced hyperalgesia. However, the mechanism by which the activation of neuronal P2X3 receptor contributes to the inflammatory hyperalgesia is not completely clear. The present study verifies whether the activation of P2X3 receptor on primary afferent neurons contributes to the mechanical hiperalgesia induced by prostaglandin E2 or dopamine in the peripheral tissue. Co-administration of A317491(60 µg / paw), a selective P2X3,2/3 receptor antagonist, or pre-treatment with dexamethasone (1 mg / mL / Kg), prevented the mechanical hyperalgesia measured 3 hours after the administration of carrageenan (300 µg / paw) in the rat's hind paw. The administration of ??meATP (50 µg /paw) induced mechanical hiperalgesia 1 hour, but not 3 hours, after its administration, which also was prevented by dexamethasone or A317491. Sub-threshold doses of PGE2 (4 ng / paw) or dopamine (0.4 µg / paw) that do not induce hyperalgesia by themselves, induced maximal hyperalgesia, 3 hours after, when administrated Just following ??meATP or carrageenan in rats treated with dexamethasone. These hyperalgesic states ("priming") revealed by sub-threshold doses of PGE2 or dopamine were prevented by A317491 or treatment with ganglionar administrations (DRG-L5) of ODN antisense, but not ODN mismatch, against P2X3 receptor (40 µg /5µL once a day for 4 days). ODN antisense, but not ODN mismatch reduced the expression of P2X3 receptors in the saphenous nerve and in DRG-L5. To verify whether PKC? mediates this hyperalgesic state, PKC? translocation inhibitor (1 µg/paw) was administrated in peripheral tissue 45 min. before ??meATP or PGE2 (100 ng/paw). PKC? inhibitor inhibited the hyperalgesic state induced by ??meATP ("priming"), but not the mechanical hyperalgesia induced by PGE2 (100 ng/paw). Briefly, the findings of this study suggest that the inflammatory hyperalgesia depends on neuronal activation of P2X3 receptor and the subsequent PKC? translocation, which increases the susceptibility of primary afferent neurons (priming) to others inflammatory mediators such as PGE2 and symphatetic amines
Mestrado
Fisiologia
Mestre em Biologia Funcional e Molecular
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Chen, Zhicheng. "Molecular cloning and characterisation of a sensory neuron-specific ATP-gated channel (P2X3)." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285158.

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Helms, Nick. "Wechselwirkungen von Agonisten und kompetitiven Antagonisten mit der Ligandenbindungsstelle des schnell desensitisierenden P2X3-Rezeptors." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-197364.

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Purinerge P2X3-Rezeptoren spielen eine bedeutende Rolle in der Vermittlung chronischer Schmerzen, welche ein führendes Problem des Gesundheitswesens mit vielen sozioökonomischen Konsequenzen darstellen. Die Tatsache, dass P2X3-Rezeptoren fast ausschließlich von nozizeptiven Neuronen exprimiert werden, macht sie trotz ihres besonderen Desensitisierungsverhaltens zu vielversprechenden Angriffspunkten zukünftiger Schmerztherapien, beispielsweise mithilfe kompetitiver Antagonisten an diesen Rezeptoren. Zur Analyse der Wechselwirkungen zwischen Agonist und kompetitivem Antagonist wird meist der Schild-Plot benutzt. Jedoch ist dieser im Falle der sehr schnell desensitisierenden P2X3-Rezeptoren ungeeignet, da die Vorbedingung eines stabilen Gleichgewichts zwischen Agonist und Antagonist aufgrund der Desensitisierung nicht erfüllt ist. Ziel der vorliegenden Arbeit war es, eine neue Methode zur Analyse der Interaktion kompetitiver Antagonisten mit ihrer Bindungsstelle am Beispiel des P2X3-Rezeptors zu entwickeln und so für die Antagonistenbindung bedeutende Aminosäuren der Bindungsstelle zu identifizieren. Mittels der Patch-Clamp-Technik wurden die Effekte der Antagonisten A-317491, TNP-ATP und PPADS auf die vom P2X1,3-Rezeptor-selektiven Agonisten α,β-MeATP induzierten Ströme am P2X3-Wildtyp-Rezeptor und an fünf Rezeptormutanten mit veränderter Ligandenbindungsstelle untersucht. Alle Rezeptoren wurden in HEK293-Zellen exprimiert. Anhand der gemessenen Daten wurde ein Hidden Markov Model (HMM) erstellt, welches die sequentiellen Übergänge des Rezeptors von geschlossen zu offen und desensitisiert in An- und Abwesenheit des Antagonisten miteinander kombiniert. Die am P2X3-Rezeptor induzierten Ströme konnten mithilfe dieses Modells korrekt gefittet und die für die Antagonistenbindung wichtigen Aminosäuren innerhalb der Bindungsstelle bestimmt werden. Als Resultat dieser Arbeit konnte außerdem gezeigt werden, dass das HMM eine geeignete Methode zur Analyse der Wirkung kompetitiver Antagonisten an schnell desensitisierenden Rezeptoren darstellt. Die untersuchten Antagonisten A-317491 und TNP-ATP haben einen kompetitiven Wirkmechanismus, während PPADS eine pseudoirreversible Blockade verursacht.
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Books on the topic "P2X3"

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Nicke, Annette, ed. The P2X7 Receptor. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2384-8.

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Villars, P., and K. Cenzual, eds. Structure Types. Part 2: Space Groups (218) P-43n - (195) P23. Berlin/Heidelberg: Springer-Verlag, 2005. http://dx.doi.org/10.1007/b11233.

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United States. Bureau of the Census, ed. Current Population Reports, Poverty Among Families: etc., Special Studies, 1998, P23-203, Issued September 2000. [S.l: s.n., 2000.

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CV, Panca Bhakti, ed. Himpunan peraturan perundang-undangan keselamatan dan kesehatan kerja: Dilengkapi dengan Pedoman Operasional Panitia Pembina Keselamatan dan Kesehatan Kerja (P2K3). Jakarta: Panca Bhakti, 2008.

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Fairbairn, Ian Paul. Investigations of a novel mechanism of anti-tuberculous immunity mediated by purinergic (P2X[inferior seven]) receptors. Birmingham: University of Birmingham, 2001.

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Yeung, Davy. Molecular and functional analysis of the purinergic P2X receptors in normal and dystrophic skeletal muscle: A thesis. Portsmouth: University of Portsmouth, School of Pharmacy and Biomedical Sciences, 2004.

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Nicke, Annette. P2X7 Receptor: Methods and Protocols. Springer, 2022.

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Kopanski, Tomasz J. PZL P23 Karas. Mushroom Model Publications,Poland, 2004.

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Zalewski, Sharon. How Should Drugs Be Legally Prescribed (P213). Greenhaven Press, 1988.

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Lau, Chung-Ming, Chi-Sum Wong, Kenneth K. S. Law, and David K. Tse. Asian Management Matters. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2000. http://dx.doi.org/10.1142/p203.

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Book chapters on the topic "P2X3"

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Kennedy, Charles. "P2X3 Receptors and Sensory Transduction." In Sensing with Ion Channels, 247–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72739-2_12.

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Fabbretti, Elsa. "ATP-Gated P2X3 Receptors Are Specialised Sensors of the Extracellular Environment." In Advances in Experimental Medicine and Biology, 7–16. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_56.

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Sluyter, Ronald. "The P2X7 Receptor." In Advances in Experimental Medicine and Biology, 17–53. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_59.

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Evans, Richard J., Annmarie Surprenant, and R. Alan North. "P2X Receptors." In The P2 Nucleotide Receptors, 43–61. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1800-5_2.

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Chessell, I. P., A. D. Michel, and P. P. A. Humphrey. "P2X Receptors." In Purinergic and Pyrimidinergic Signalling I, 47–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-662-09604-8_3.

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Kawate, Toshimitsu. "P2X Receptor Activation." In Advances in Experimental Medicine and Biology, 55–69. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_55.

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Shen, Jian-Bing, Bruce T. Liang, and Florentina Soto. "Nucleotide Receptor P2x." In Encyclopedia of Signaling Molecules, 3616–29. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_50.

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Rehn, Alexandra Beatrice, and Johannes Buchner. "p23 and Aha1." In Subcellular Biochemistry, 113–31. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-11731-7_6.

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Horstkorte, Rüdiger, Bettina Büttner, Kaya Bork, Navdeep Sahota, Sarah Sabir, Laura O’Regan, Joelle Blot, et al. "Nucleotide Receptor P2x." In Encyclopedia of Signaling Molecules, 1275–87. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_50.

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Rassendren, François, and Lauriane Ulmann. "P2X Receptors and Pain." In Pathologies of Calcium Channels, 615–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_30.

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Conference papers on the topic "P2X3"

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Wortley, Michael, Eric Dubuis, Sarah Maher, Sara Bonvini, Mark Birrell, and Maria Belvisi. "TRPM3, P2X2 and P2X3 expression patterns in single airway sensory nerves." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa4411.

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Smith, Jaclyn, and Rachel Giles. "Novel P2X3 antagonist can SOOTHE chronic cough." In ATS 2022 International Conference, edited by Richard Dekhuijzen. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/7e412546.

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Friedrich, Christian, Klaus Francke, Surinder S. Birring, J. W. K. Van Den Berg, Paul Marsden, Lorcan Mcgarvey, Alice Turner, et al. "Safety and efficacy of P2X3 antagonist BAY 1902607 in refractory chronic cough." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4566.

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Martinez, F. J., A. Afzal, M. M. Kitt, A. Ford, J. J. Li, Y. P. Li, and J. Smith. "The Treatment of Chronic Cough in Idiopathic Pulmonary Fibrosis Patients with Gefapixant, a P2x3 Receptor Antagonist." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2638.

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Birrell, Mark, Sara J. Bonvini, Katie E. Baker, Bilel Dekkak, Anthony Ford, Montse Miralpeix, Gema Tarrason, Jaclyn A. Smith, and Maria G. Belvisi. "Central role for the TRPV4-ATP-P2X3 axis in sensory nerve activation and the late asthmatic response." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa5069.

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Garceau, D., N. Chauret, and L. Harvey. "BLU-5937 a Highly Selective P2X3 Homotrimeric Receptor Antagonist with Improved Taste Safety Profile in Healthy Subjects." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7396.

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Morice, A. H., J. Smith, L. McGarvey, S. Birring, S. M. Parker, A. Turner, I. Gashaw, et al. "Safety and Efficacy of BAY 1817080, a P2X3 Receptor Antagonist, in Patients with Refractory Chronic Cough (RCC)." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7648.

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Ishihara, Hiroyuki, Hideaki Hida, Mitsuaki Machida, Yoshiyuki Tsuda, and Sayaka Miyazaki. "Design of phase 2b randomised controlled trial of S-600918, P2X3 receptor antagonist for refractory chronic cough." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2271.

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Smith, Jaclyn, Lorcan P. Mcgarvey, Alyn H. Morice, Surinder S. Birring, Michael M. Kitt, Mandel R. Sher, Andrew M. Tershakovec, Wen-Chi Wu, Zhi Jin Xu, and David R. Muccino. "The effect of baseline factors on treatment response with MK-7264, a P2X3 antagonist, in refractory chronic cough." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa811.

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McGarvey, Lorcan, Jaclyn Smith, Surinder Birring, Alyn Morice, Mandel Sher, Wen-Chi Wu, and David Muccino. "Characterization of chronic cough patients participating in a phase 2b clinical trial of gefapixant, a P2X3 receptor antagonist." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa612.

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Reports on the topic "P2X3"

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Kimbler, Donald. Therapeutic Targeting of P2X7 after TBI. Fort Belvoir, VA: Defense Technical Information Center, November 2012. http://dx.doi.org/10.21236/ada616284.

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Dawson, William O., and Moshe Bar-Joseph. Creating an Ally from an Adversary: Genetic Manipulation of Citrus Tristeza. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7586540.bard.

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Abstract:
Citrus is one of the major agricultural crops common to Israel and the United States, important in terms of nutrition, foreign exchange, and employment. The economy of both citrus industries have been chronically plagued by diseases caused by Citrus tristeza virus (CTV). The short term solution until virus-resistant plants can be used is the use of mild strain cross-protection. We are custom designing "ideal" protecting viruses to immunize trees against severe isolates of CTV by purposely inoculating existing endangered trees and new plantings to be propagated as infected (protected) citrus budwood. We crossed the substantial technological hurdles necessary to accomplish this task which included developing an infectious cDNA clone which allows in vitro manipulation of the virus and methods to then infect citrus plants. We created a series of hybrids between decline-inducing and mild CTV strains, tested them in protoplasts, and are amplifying them to inoculate citrus trees for evaluation and mapping of disease determinants. We also extended this developed technology to begin engineering transient expression vectors based on CTV as tools for genetic improvement of tree crops, in this case citrus. Because of the long periods between genetic transformation and the ultimate assay of mature tree characteristics, there is a great need for an effective system that allows the expression or suppression of target genes in fruiting plants. Virus-based vectors will greatly expedite progress in citrus genetic improvement. We characterized several components of the virus that provides necessary information for designing virus-based vectors. We characterized the requirements of the 3 ’-nontranslated replication promoter and two 3 ’-ORF subgenomic (sg) mRNA controller elements. We discovered a novel type of 5’-terminal sgRNAs and characterized the cis-acting control element that also functions as a strong promoter of a 3 ’-sgRNA. We showed that the p23 gene controls negative-stranded RNA synthesis and expression of 3 ’ genes. We identified which genes are required for infection of plants, which are host range determinants, and which are not needed for plant infection. We continued the characterization of native dRNA populations and showed the presence of five different classes including class III dRNAs that consists of infectious and self-replicating molecules and class V dRNAs that contain all of the 3 ’ ORFs, along with class IV dRNAs that retain non-contiguous internal sequences. We have constructed and tested in protoplasts a series of expression vectors that will be described in this proposal.
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