Relevant bibliographies by topics / TRPM8

Academic literature on the topic 'TRPM8'

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Published: 4 June 2021
Last updated: 14 March 2023

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Journal articles on the topic "TRPM8"

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Yang, Xiao-Ru, Mo-Jun Lin, Lionel S. McIntosh, and James S. K. Sham. "Functional expression of transient receptor potential melastatin- and vanilloid-related channels in pulmonary arterial and aortic smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 6 (June 2006): L1267—L1276. http://dx.doi.org/10.1152/ajplung.00515.2005.

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Transient receptor potential melastatin- (TRPM) and vanilloid-related (TRPV) channels are nonselective cation channels pertinent to diverse physiological functions. Multiple TRPM and TRPV channel subtypes have been identified and cloned in different tissues. However, their information in vascular tissue is scant. In this study, we sought to identify TRPM and TRPV channel subtypes expressed in rat deendothelialized intralobar pulmonary arteries (PAs) and aorta. With RT-PCR, mRNA of TRPM2, TRPM3, TRPM4, TRPM7, and TRPM8 of TRPM family and TRPV1, TRPV2, TRPV3, and TRPV4 of TRPV family were detected in both PAs and aorta. Quantitative real-time RT-PCR showed that TRPM8 and TRPV4 were the most abundantly expressed TRPM and TRPV subtypes, respectively. Moreover, Western blot analysis verified expression of TRPM2, TRPM8, TRPV1, and TRPV4 proteins in both types of vascular tissue. To examine the functional activities of these channels, we monitored intracellular Ca2+ transients ([Ca2+]i) in pulmonary arterial smooth muscle cells (PASMCs) and aortic smooth muscle cells (ASMCs). The TRPM8 agonist menthol (300 μM) and the TRPV4 agonist 4α-phorbol 12,13-didecanoate (1 μM) evoked significant increases in [Ca2+]i in PASMCs and ASMCs. These Ca2+ responses were abolished in the absence of extracellular Ca2+ or the presence of 300 μM Ni2+ but were unaffected by 1 μM nifedipine, suggesting Ca2+ influx via nonselective cation channels. Hence, for the first time, our results indicate that multiple functional TRPM and TRPV channels are coexpressed in rat intralobar PAs and aorta. These novel Ca2+ entry pathways may play important roles in the regulation of pulmonary and systemic circulation.
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Marshall-Gradisnik, Sonya M., Peter Smith, Ekua W. Brenu, Bernd Nilius, Sandra B. Ramos, and Donald R. Staines. "Examination of Single Nucleotide Polymorphisms (SNPs) in Transient Receptor Potential (TRP) Ion Channels in Chronic Fatigue Syndrome Patients." Immunology and Immunogenetics Insights 7 (January 2015): III.S25147. http://dx.doi.org/10.4137/iii.s25147.

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Background The transient receptor potential (TRP) superfamily in humans comprises 27 cation channels with permeability to monovalent and divalent cations. These channels are widely expressed within humans on cells and tissues and have significant sensory and regulatory roles on most physiological functions. Chronic fatigue syndrome (CFS) is an unexplained disorder with multiple physiological impairments. OBJECTIVES The purpose of this study was to determine the role of TRPs in CFS. Methods The study comprised 115 CFS patients (age = 48.68 ± 1.06 years) and 90 nonfatigued controls (age = 46.48 ± 1.22 years). CFS patients were defined according to the 1994 Center for Disease Prevention and Control criteria for CFS. A total of 240 single nucleotide polymorphisms (SNPs) for 21 mammalian TRP ion channel genes ( TRPA1, TRPC1, TRPC2, TRPC3, TRPC4, TRPC6, TRPC7, TRPM1, TRPM2, TRPM3, TRPM4, TRPM5, TRPM6, TRPM7, TRPM8, TRPV1, TRPV2, TRPV3, TRPV4, TRPV5, and TRPV6) were examined via the Agena Biosciences iPLEX Gold assay. Statistical analysis was performed using the PLINK analysis software. Results Thirteen SNPs were significantly associated with CFS patients compared with the controls. Nine of these SNPs were associated with TRPM3 (rs12682832; P < 0.003, rs11142508; P < 0.004, rs1160742; P < 0.08, rs4454352; P < 0.013, rs1328153; P < 0.013, rs3763619; P < 0.014, rs7865858; P ≤ 0.021, rs1504401; P ≤ 0041, rs10115622; P ≤ 0.050), while the remainder were associated with TRPA1 (rs2383844; P ≤ 0.040, rs4738202; P ≤ 0.018) and TRPC4 (rs6650469; P ≤ 0.016, rs655207; P ≤ 0.018). Conclusion The data from this pilot study suggest an association between TRP ion channels, predominantly TRPM3 and CFS. This and other TRPs identified may contribute to the etiology and pathomechanism of CFS.
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Nilius, B., F. Mahieu, Y. Karashima, and T. Voets. "Regulation of TRP channels: a voltage–lipid connection." Biochemical Society Transactions 35, no. 1 (January 22, 2007): 105–8. http://dx.doi.org/10.1042/bst0350105.

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TRP (transient receptor potential) channels respond to a plethora of stimuli in a fine-tuned manner. We show here that both membrane potential and the level of PI (phosphatidylinositol) phosphates are efficient regulators of TRP channel gating. Recent work has shown that this regulation applies to several members of the TRPV (TRP vanilloid) subfamily (TRPV1 and TRPV5) and the TRPM (TRP melastatin) subfamily (TRPM4/TRPM5/TRPM7/TRPM8), whereas regulation of members of the TRPC subfamily is still disputed. The mechanism whereby PIP2 (PI 4,5-bisphosphate) acts on TRPM4, a Ca2+- and voltage-activated channel, is shown in detail in this paper: (i) PIP2 may bind directly to the channel, (ii) PIP2 induces sensitization to activation by Ca2+, and (iii) PIP2 shifts the voltage dependence towards negative and physiologically more meaningful potentials. A PIP2-binding pocket seems to comprise a part of the TRP domain and especially pleckstrin homology domains in the C-terminus.
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Lötsch, Jörn, Dario Kringel, Gerd Geisslinger, Bruno G. Oertel, Eduard Resch, and Sebastian Malkusch. "Machine-Learned Association of Next-Generation Sequencing-Derived Variants in Thermosensitive Ion Channels Genes with Human Thermal Pain Sensitivity Phenotypes." International Journal of Molecular Sciences 21, no. 12 (June 19, 2020): 4367. http://dx.doi.org/10.3390/ijms21124367.

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Genetic association studies have shown their usefulness in assessing the role of ion channels in human thermal pain perception. We used machine learning to construct a complex phenotype from pain thresholds to thermal stimuli and associate it with the genetic information derived from the next-generation sequencing (NGS) of 15 ion channel genes which are involved in thermal perception, including ASIC1, ASIC2, ASIC3, ASIC4, TRPA1, TRPC1, TRPM2, TRPM3, TRPM4, TRPM5, TRPM8, TRPV1, TRPV2, TRPV3, and TRPV4. Phenotypic information was complete in 82 subjects and NGS genotypes were available in 67 subjects. A network of artificial neurons, implemented as emergent self-organizing maps, discovered two clusters characterized by high or low pain thresholds for heat and cold pain. A total of 1071 variants were discovered in the 15 ion channel genes. After feature selection, 80 genetic variants were retained for an association analysis based on machine learning. The measured performance of machine learning-mediated phenotype assignment based on this genetic information resulted in an area under the receiver operating characteristic curve of 77.2%, justifying a phenotype classification based on the genetic information. A further item categorization finally resulted in 38 genetic variants that contributed most to the phenotype assignment. Most of them (10) belonged to the TRPV3 gene, followed by TRPM3 (6). Therefore, the analysis successfully identified the particular importance of TRPV3 and TRPM3 for an average pain phenotype defined by the sensitivity to moderate thermal stimuli.
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Saito, Shigeru, and Ryuzo Shingai. "Evolution of thermoTRP ion channel homologs in vertebrates." Physiological Genomics 27, no. 3 (December 2006): 219–30. http://dx.doi.org/10.1152/physiolgenomics.00322.2005.

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In mammalian thermosensation, nine temperature-sensitive ion channels that are activated by distinct temperature thresholds have been identified as thermosensors. These ion channels belong to the transient receptor potential (TRP) superfamily and are referred to as “thermoTRPs” (TRPV1, TRPV2, TRPV3, TRPV4, TRPM2, TRPM4, TRPM5, TRPM8, and TRPA1). To elucidate the evolutionary processes of thermoTRPs, we conducted comprehensive searches for mammalian thermoTRP gene homologs in the draft genome sequences of chicken ( Gallus gallus), western clawed frog ( Xenopus tropicalis), zebrafish ( Danio rerio), and pufferfish ( Fugu rubripes). Newly identified homologs were compared with known thermoTRPs, and phylogenetic analyses were conducted. Our comparative analyses revealed that most of the mammalian thermo-TRP members already existed in the common ancestor of fishes and tetrapods. Tetrapods shared almost the same repertoire, except that the western clawed frog expanded TRPV4s (six copies) and TRPM8s (two copies), which were diversified considerably. Comparisons of nonsynonymous and synonymous substitution rates among TRPV4s suggested that one copy of the TRPV4 channel in the western clawed frog retained its original function, while the other copies diversified and obtained slightly different properties. In fish lineages, several members of thermo-TRPs have duplicated in the whole genome duplication occurred in the ancestral ray-finned fish; however, some of the copies have subsequently been lost. Furthermore, fishes do not possess the three members of thermoTRPs existed in mammals, e.g., thermoTRPs activated by noxious heat, warm, and cool temperatures. Our results suggest that thermosensation mechanisms have changed through vertebrate evolution with respect to thermosensor repertoires.
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Kühn, Frank J. P., Gabriel Knop, and Andreas Lückhoff. "The Transmembrane Segment S6 Determines Cation versus Anion Selectivity of TRPM2 and TRPM8." Journal of Biological Chemistry 282, no. 38 (June 29, 2007): 27598–609. http://dx.doi.org/10.1074/jbc.m702247200.

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TRPM2 and TRPM8, closely related members of the transient receptor potential (TRP) family, are cation channels activated by quite different mechanisms. Their transmembrane segments S5 and S6 are highly conserved. To identify common structures in S5 and S6 that govern interaction with the pore, we created a chimera in which the S5-pore-S6 region of TRPM8 was inserted into TRPM2, along with a lysine at each transition site. Currents through this chimera were induced by ADP-ribose (ADPR) in cooperation with Ca2+. In contrast to wild-type TRPM2 channels, currents through the chimera were carried by Cl-, as demonstrated in ion substitution experiments using the cation N-methyl-d-glucamine (NMDG) and the anion glutamate. Extracellular NMDG had no effects. The substitution of either intracellular or extracellular Cl- with glutamate shifted the reversal potential, decreased the current amplitude and induced a voltage-dependent block relieved by depolarization. The lysine in S6 was responsible for the anion selectivity; insertion of a lysine into corresponding sites within S6 of either TRPM2 or TRPM8 created anion channels that were activated by ADPR (TRPM2 I1045K) or by cold temperatures (TRPM8 V976K). The positive charge of the lysine was decisive for the glutamate block because the mutant TRPM2 I1045H displayed cation currents that were blocked at acidic but not alkaline intracellular pH values. We conclude that the distal part of S6 is crucial for the discrimination of charge. Because of the high homology of S6 in the whole TRP family, this new role of S6 may apply to further TRP channels.
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Yin, Ying, Mengyu Wu, Lejla Zubcevic, William F. Borschel, Gabriel C. Lander, and Seok-Yong Lee. "Structure of the cold- and menthol-sensing ion channel TRPM8." Science 359, no. 6372 (December 7, 2017): 237–41. http://dx.doi.org/10.1126/science.aan4325.

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Transient receptor potential melastatin (TRPM) cation channels are polymodal sensors that are involved in a variety of physiological processes. Within the TRPM family, member 8 (TRPM8) is the primary cold and menthol sensor in humans. We determined the cryo–electron microscopy structure of the full-length TRPM8 from the collared flycatcher at an overall resolution of ~4.1 ångstroms. Our TRPM8 structure reveals a three-layered architecture. The amino-terminal domain with a fold distinct among known TRP structures, together with the carboxyl-terminal region, forms a large two-layered cytosolic ring that extensively interacts with the transmembrane channel layer. The structure suggests that the menthol-binding site is located within the voltage-sensor–like domain and thus provides a structural glimpse of the design principle of the molecular transducer for cold and menthol sensation.
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Yee, Nelson S., Ada S. Chan, Julian D. Yee, and Rosemary K. Yee. "TRPM7 and TRPM8 Ion Channels in Pancreatic Adenocarcinoma: Potential Roles as Cancer Biomarkers and Targets." Scientifica 2012 (2012): 1–8. http://dx.doi.org/10.6064/2012/415158.

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Transient receptor potential (TRP) ion channels are essential for normal functions and health by acting as molecular sensors and transducing various stimuli into cellular and physiological responses. Growing evidence has revealed that TRP ion channels play important roles in a wide range of human diseases, including malignancies. In light of recent discoveries, it has been found that TRP melastatin-subfamily members, TRPM7 and TRPM8, are required for normal and cancerous development of exocrine pancreas. We are currently investigating the mechanisms which mediate the functional roles of TRPM7 and TRPM8 and attempting to develop these ion channels as clinical biomarkers and therapeutic targets for achieving the goal of personalized therapy in pancreatic cancer.
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Thiel, Gerald, and Oliver G. Rössler. "Expression of the C-Terminal Domain of Phospholipase Cβ3 Inhibits Signaling via Gαq-Coupled Receptors and Transient Receptor Potential Channels." International Journal of Molecular Sciences 23, no. 17 (August 24, 2022): 9590. http://dx.doi.org/10.3390/ijms23179590.

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Transient receptor potential (TRP) channels are cation channels that play a regulatory role in pain and thermosensation, insulin secretion, and neurotransmission. It has been proposed that activation of TRP channels requires phosphatidylinositol 4,5-bisphosphate, the major substrate for phospholipase C (PLC). We investigated whether inhibition of PLCβ has an impact on TRP channel signaling. A genetic approach was used to avoid off-target effects observed when using a pharmacological PLCβ inhibitor. In this study, we show that expression of PLCβct and PLCβ3ct, truncated forms of PLCβ1 or PLCβ3 that contain the C-terminal membrane binding domains, almost completely blocked the signal transduction of a Gαq-coupled designer receptor, including the phosphorylation of ERK1/2. In contrast, expression of the helix-turn-helix motif (Hα1-Hα2) of the proximal C-terminal domain of PLCβ3 did not affect Gαq-coupled receptor signaling. PLCβ3ct expression impaired signaling of the TRP channels TRPM3 and TRPM8, stimulated with either prognenolone sulfate or icilin. Thus, the C-terminal domain of PLCβ3 interacts with plasma membrane targets, most likely phosphatidylinositol 4,5-bisphosphate, and in this way blocks the biological activation of TRPM3 and TRPM8, which require interaction with this phospholipid. PLCβ thus regulates TRPM3 and TRPM8 channels by masking phosphatidylinositol 4,5-bisphosphate with its C-terminal domain.
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Yamamura, Hisao, Shinya Ugawa, Takashi Ueda, Akimichi Morita, and Shoichi Shimada. "TRPM8 activation suppresses cellular viability in human melanoma." American Journal of Physiology-Cell Physiology 295, no. 2 (August 2008): C296—C301. http://dx.doi.org/10.1152/ajpcell.00499.2007.

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The transient receptor potential melastatin subfamily (TRPM), which is a mammalian homologue of cell death-regulated genes in Caenorhabditis elegans and Drosophila, has potential roles in the process of the cell cycle and regulation of Ca2+ signaling. Among this subfamily, TRPM8 (also known as Trp-p8) is a Ca2+-permeable channel that was originally identified as a prostate-specific gene upregulated in tumors. Here we showed that the TRPM8 channel was expressed in human melanoma G-361 cells, and activation of the channel produced sustainable Ca2+ influx. The application of menthol, an agonist for TRPM8 channel, elevated cytosolic Ca2+ concentration in a concentration-dependent manner with an EC50 value of 286 μM in melanoma cells. Menthol-induced responses were significantly abolished by the removal of external Ca2+. Moreover, inward currents at a holding potential of −60 mV in melanoma cells were markedly potentiated by the addition of 300 μM menthol. The most striking finding was that the viability of melanoma cells was dose-dependently depressed in the presence of menthol. These results reveal that a functional TRPM8 protein is expressed in human melanoma cells to involve the mechanism underlying tumor progression via the Ca2+ handling pathway, providing us with a novel target of drug development for malignant melanoma.
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Dissertations / Theses on the topic "TRPM8"

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Quallo, Talisia Esme. "Roles of TRPM8 and TRPM3 in sensory transduction." Thesis, King's College London (University of London), 2015. https://kclpure.kcl.ac.uk/portal/en/theses/roles-of-trpm8-and-trpm3-in-sensory-transduction(3f273e84-d8cf-4efb-bbd3-ff455adabe17).html.

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Primary afferent neurons are equipped with sensory transduction channels which allow the conversion of physical and chemical stimuli into electrical signals. TRP channels are a heterogeneous superfamily of largely non-selective cation channels, which have been implicated in a myriad of sensory transduction mechanisms from the detection of temperature to the sensation of touch. Many TRP channels are key targets for the study of pain physiology due to their polymodal activation and expression in small diameter, unmyelinated sensory fibres. The aim of my project was to examine the roles of TRP channels in sensory transduction mechanisms. Three results chapters focusing on three different TRP channels are presented. A novel role for the established cold thermosensor, TRPM8, as a cellular osmosensor was determined. The studies presented establish that TRPM8 is activated by increases in extracellular osmolality and is partially activated at normal physiological osmolalities. Cool temperatures increase the sensitivity of TRPM8 to osmotic stimuli and activation of phospholipase enzymes modulates activation of TRPM8 by hyperosmotic solutions. TRPM8 is expressed within sensory neurons where it functions as the chief detector of increased osmolality in addition to a molecular sensor of cold sensations. The role of TRPM3 as a candidate heat transduction channel is examined. The findings presented demonstrate that recombinantly expressed TRPM3 channels are heat-sensitive and mice lacking functional TRPM3 channels lose a population of heat-activated neurons and have impaired behavioural responses to noxious heat. Moreover, modulation of TRPM3 by intracellular pathways downstream of G-protein coupled receptor activation has been determined. Activation of TRPM3 in sensory neurons is shown to be robustly inhibited by morphine in a predominantly mu-opioid receptor and Gi dependent mechanism. Additionally the role of TRPM3 in several pain states is examined. Finally, this thesis reports on the characterisation of a medium-throughput CGRP release assay for examining activation of TRPA1 natively expressed on the central terminals of dorsal root ganglion neurons. Activation of TRPA1 expressed on spinal cord synaptosomes by a selection of agonists evokes a concentration-dependent release of CGRP which is inhibited by TRPA1 antagonists. The VGCC subtypes important for TRPA1 and depolarisation-induced CGRP release are examined.
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Klumpp, Dominik [Verfasser], and Stephan [Akademischer Betreuer] Huber. "TRPM2- und TRPM8-vermittelte Radioresistenz in malignen Tumoren / Dominik Klumpp ; Betreuer: Stephan Huber." Tübingen : Universitätsbibliothek Tübingen, 2016. http://d-nb.info/1164169416/34.

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Tajino, Koji. "Cutaneous TRPM8 channels are thermostats against cooling." 京都大学 (Kyoto University), 2011. http://hdl.handle.net/2433/142123.

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Proudfoot, Clare W. J. "Analgesia mediated by the TRPM8 cold receptor in neuropathic pain." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/29953.

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To identify novel analgesic strategies for chronic pain, we investigated the phenomenon of analgesia produced by cutaneous cooling. The recent identification of specific cold sensory receptors has allowed, for the first time, investigation of the molecular mechanism underlying cooling-induced analgesia. We have shown that the cold-and-menthol receptor. TRPM8, is critically involved in cooling-induced analgesia. Activation of TRPM8 in a subpopulation of sensory afferents (by either cutaneous or intrathecal application of pharmacological agents or by modest cooling) elicits analgesia in neuropathic and other chronic pain models in rats, and inhibits the characteristic sensitisation of dorsal horn neurons that occurs ipsilateral to nerve injury. This analgesia is abolished following antisense knockdown of the TRPM8 receptor. In contrast, activation of the related putative cold-receptor TRPA1 produces hyperalgesia in naïve and neuropathic rats. TRPM8 expression was observed in small diameter sensory neurons in dorsal root ganglia and on afferent terminals in the spinal cord, with increases in specific subsets of sensory neurons following nerve injury. We further found that the central mechanism of TRPM8-mediated analgesia is mediated through inhibitory Group I/III metabotropic glutamate receptors, and is opioid-independent. These results identify TRPM8 as an essential molecular mediator of cooling-induced analgesia. We propose a novel analgesic axis in which activation of TRPM8-expressing afferents by innocuous cooling or chemical ligands leads to activation of inhibitory Group II/III metabotropic glutamate receptors in the spinal cord, which then exert inhibition over nociceptive inputs. These findings suggest that both TRPM8 and the inhibitory metabotropic glutamate receptors are promising targets for the development of novel analgesics for the treatment of neuropathic pain states.
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Kaiser, Simone. "Identification and characterization of the ion channel TRPM8 in prostate cancer." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972610359.

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Mak, Stephanie Wai Yin. "Modulation of temperature sensitive ion channels TRPV1 and TRPM8 by Bradykinin." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611520.

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Farhad, Jahanfar. "Identifying antagonist drugs for TRPM8 ion channel as candidates for repurposing." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1162721.

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Even though it is confirmed that ion channels are at the centre of many diseases, approved drugs are only available for small percentage of these proteins, and yet many pathologically important ion channels like transient receptor potential (TRP) cation channels remain without approved drugs. One reason could be the time-consuming and expensive process in drug discovery. Which has high possibility of failure in any step even after approval and marketing. Therefore, repurposing approved drugs might be considered as a solution and may offer an accelerated procedure in finding new treatments for patients. For the present research we selected TRPM8 ion channel as a neglected target despite growing number of studies regarding its association with numerous diseases. In this project we have first identified potent antagonists for TRPM8 ion channel among approved drugs, by using mainly the automated patch clamp device IonFlux 16. Such device allowed us to screen blocking potency of drugs against TRPM8 ion channel in time efficient way. Our approach consisted of using ligand-based virtual screening method, to optimize our screening by identifying candidates for further screening. We also studied possible interactions of identified drugs with antagonist binding site on TRPM8 channel by molecular docking. Furthermore, we have evaluated the effects of identified antagonists against different types of pancreatic ductal adenocarcinoma (PDAC) cells. We were able to identify four drugs with IC50 lower than 50 µM including propranolol, propafenone, carvedilol and nebivolol. Among them nebivolol with IC50 = 0.97± 0.15 µM and carvedilol with IC50 = 9.1 ± 0.6 µM were the most potent blockers. Studying the interactions of identified drugs with known binding site of TRPM8 by molecular docking, revealed high possibility of direct binding of nebivolol to binding site of TRPM8. Nebivolol was the most cytotoxic drug against PDACs, but it was also toxic against non-cancerous HEK-293 cells. While carvedilol had cytotoxic against PDACs, interestingly it wasn’t cytotoxic against HEK-293 cells. Result of these study will provide promising candidates for drug repurposing and will propose promising lead compound in drug discovery for new antagonists of TRPM8 ion channel. Also, our method of approach for identifying candidate drugs as agonist or antagonist could be applied for other ion channels.
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Dias, MarÃlia Leite. "Atividade antinociceptiva da riparina IV: participaÃÃo dos receptores TRPV1, TRPM8, receptores glutamatÃrgicos e do Ãxido nÃtrico." Universidade Federal do CearÃ, 2012. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=8632.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
A Riparina IV, uma alcamida sintetizada de Aniba riparia, foi testada em modelos animais padronizados de dor, bem como os possÃveis mecanismos de aÃÃo envolvidos. Foram utilizados camundongos Swiss (20-30g), e a Riparina IV foi administrada de forma aguda em todos os testes, nas doses de 25 e 50 mg/kg, por via oral. Foram utilizados os testes de contorÃÃes abdominais induzidas por Ãcido acÃtico; placa quente; teste da formalina; hipernocicepÃÃo mecÃnica induzida pela carragenina; teste da nocicepÃÃo induzida por capsaicina, cinamaldeÃdo, mentol; teste da nocicepÃÃo induzida por glutamato, bem como em modelos comportamentais que permitam excluir a possibilidade de uma atividade relaxante muscular ou induzir resultados falso-positivos nos modelos anteriores, tais como testes do campo aberto e rota Rod. Os resultados demonstraram que a Riparina IV possui uma atividade antinociceptiva no modelo de nocicepÃÃo visceral induzida por Ãcido acÃtico. A Riparina IV nÃo demonstrou atividade no modelo de nocicepÃÃo tÃrmica da placa quente. O prÃ-tratamento com a Riparina IV reduziu significativamente a nocicepÃÃo inflamatÃria induzida pela segunda fase da formalina, porÃm nÃo alterou a nocicepÃÃo neurogÃnica induzida pela primeira fase do teste da formalina. Os animais prÃ-tratados com a Riparina IV tambÃm exibiram uma reduÃÃo significativa na hipernocicepÃÃo mecÃnica induzida pela carragenina. Em relaÃÃo à participaÃÃo dos receptores de potencial transitÃrio (TRP), a Riparina IV demonstrou atividade nos modelos de nocicepÃÃo induzida pela administraÃÃo de capsaicina e mentol, porÃm nÃo apresentou atividade na nocicepÃÃo induzida por cinamaldeÃdo. TambÃm reduziu a nocicepÃÃo induzida pela administraÃÃo intraplantar de glutamato. Para o estudo dos mecanismos de aÃÃo da Riparina IV foi utilizada somente a dose de 50 mg/kg da substÃncia. Na avaliaÃÃo da participaÃÃo dos canais de potÃssio ATP-dependentes, o prÃ-tratamento com glibenclamida nÃo foi capaz de reverter a aÃÃo antinociceptiva da Riparina IV, descartando-se o seu envolvimento; da mesma forma, o prÃ-tratamento com ioimbina, um antagonista α2-adrenÃrgico, e pCPA, um depletor das reservas de serotonina, tambÃm nÃo foram capazes de reverter tal aÃÃo, nÃo havendo envolvimento com o mecanismo de aÃÃo da Riparina IV. O prÃ-tratamento com L-arginina, um precursor do Ãxido nÃtrico, reverteu a aÃÃo antinociceptiva da Riparina IV, sugerindo, em parte, a participaÃÃo da via do Ãxido nÃtrico no seu mecanismo de aÃÃo. Os resultados mostraram que essa substÃncia nÃo alterou a atividade locomotora no teste do campo aberto, nem diminuiu o nÃmero de quedas no teste do rota Rod, descartando a possibilidade de haver sedaÃÃo ou incoordenaÃÃo motora por parte da Riparina IV. Em sÃntese, os resultados demonstraram que a Riparina IV possui uma atividade em modelos animais de nocicepÃÃo, possivelmente envolvendo os receptores TRPV1, TRPM8, glutamatÃrgicos e a via do Ãxido nÃtrico.
Riparin IV, an alkamide synthesized from Aniba riparia, was tested in standard animal models of pain, as well as the possible mechanisms of action involved. It was used Swiss mice (20-30g), and Riparin IV was administred acutely in all tests, at the doses of 25 and 50 mg/kg, by gavage. It was used the tests of abdominal writhing induced by acetic acid, hot plate test, formalin test, mechanical hypernociception induced by carrageenan, nociception test induced by capsaicin, cinnamaldehyde and menthol, nociception test induced by glutamate, as well as models of behavior that ruled out the possibility of a muscle relaxing activity or induce false-positive results in previous models, such as the open field test and the rota Rod test. The results showed that Riparin IV has an antinociceptive activity at the model of visceral nociception induced by acetic acid. Riparin IV did not show any activity at the hot plate thermal nociception model. Pretreatment with Riparin IV reduced significantly the inflammatory nociception induced at the second phase of formalin test, but did not alter the neurogenic nociception induced at the first phase of formalin test. The animals pretreated with Riparin IV also exhibited a significant reduction at the mechanical hypernociception induced by carrageenan. Related to the participation of the Transient Potential Receptors (TRP), Riparin IV showed an activity at the models of nociception induced by capsaicin and menthol, but did not show any activity at the nociception induced by cinnamaldehyde. Also reduced the nociception induced by administration of glutamate at the rind paw. To study the mechanisms of action of Riparin IV, it was used only the dose of 50 mg/kg of the substance. At the evaluation of participation of the ATP-dependent potassium channels, pretreatment with glibenclamide was not able to reverse the antinociceptive action of Riparin IV, discharging its involvment; at the same way, pretreatment with yohimbine, an a2-adrenergic antagonist, and pCPA, a depletor of the serotonin reservations, were not able of reverse such action, not having any involvement with the mechanism of action of Riparin IV. Pretreatment with L-arginine, a precursor of Nitric Oxide, reversed the antinociceptive action of Riparin IV, suggesting, in part, the participation of nitric oxide pathway at the mechanism of action. The results showed that this substance did not alter the locomotor activity at the open field test, neither diminished the number of falls at the rota Rod test, discharging the possibility of sedation or incoordination by Riparin IV. In summary, the results showed that Riparin IV has an action in animal models of nociception, possibly involving the receptors TRPV1, TRPM8, glutamatergic receptors and the nitric oxide pathway.
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Viñuela-Fernández, Ignacio. "Equine laminitis pain and modulatory mechanisms at a potential analgesic target, the TRPM8 ion channel." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/8728.

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Chronic neuropathic pain, resulting from dysfunction of the nervous system, is a clinical concern in both humans and animal patients. Neuropathic pain is characterised by spontaneous pain, hypersensitivity, manifested as hyperalgesia and allodynia, and refractoriness to conventional analgesics such as non-steroidal anti-inflammatory drugs, thus representing an unmet therapeutic need. Equine laminitis is a disease that involves the disruption of the dermoepidermal junction within the hoof, leading to severe pain and lameness, with poor responsiveness to anti-inflammatory therapy. We developed a Quantitative Sensory Testing method, using a novel hydraulically-powered feedbackcontrolled hoof tester, in order to provide an objective tool for the assessment of mechanical hyperalgesia in laminitic horses. Hoof Compression Thresholds of laminitic horses were significantly lower than those of normal horses and variance component analysis of the data confirmed the reliability of the method. In order to investigate mechanisms underlying laminitis pain, we performed histological studies of peripheral nerves innervating the hoof. Electron micrographic analysis of the digital nerve of laminitic horses revealed a significant reduction in the number of unmyelinated and myelinated fibres together with abnormal morphology. Additionally, cell bodies of sensory neurons innervating the hoof in cervical C8 dorsal root ganglia showed an upregulated expression of the nerve injury marker activating transcription factor-3 (ATF3), neuropeptide Y (NPY), and the TRPM8 channel; each of which has been associated with laboratory models of neuropathic pain. Previous work has shown that, in a rodent model of neuropathic pain, the TRPM8 channel is upregulated in sensory neurons and its activation by cool temperature, menthol or icilin leads to reversal of the hypersensitive pain state. Further investigation of TRPM8-channel mediated analgesia was aimed at uncovering the molecular mechanisms involved in the activation of this system in sensitised states. It was hypothesised that serotonin, released following inflammation and nerve damage, can enhance TRPM8 channel activity through peripheral 5-HT1B receptors. Calcium fluorometry carried out in HEK293 cells transfected with the TRPM8 channel and the 5-HT1B receptor revealed that coadministration of a 5-HT1B receptor agonist facilitated the activation of the TRPM8 channel by icilin. Moreover, it appears that this effect is mediated through phospholipase D1 (PLD1), possibly leading to increased production of phosphatidylinositol (4,5-) bisphosphate (PIP2), a known positive modulator of TRPM8 channel activity. In vitro co-immunoprecipitation studies suggested that the TRPM8 channel, the 5-HT1B receptor and PLD1 physically interact with each other, further providing a molecular basis for their functional co-operation. Calcium imaging carried out in cultured rat DRG cells showed that the 5-HT1B receptor-mediated enhancement of icilin responses at the TRPM8 channel also occurs in sensory cells and is reversed by inhibition of PLD1. Moreover, TRPM8 and the 5-HT1B receptor appear to be physically associated in vivo as shown by their co-immunoprecipitation from spinal cord homogenates. Assessment of nociceptive behavioural reflexes following intrathecal injection of selective pharmacological agents provided further support for the idea of 5-HT1B receptor facilitation of TRPM8 channel responses in vivo. In addition to providing novel evidence of a neuropathic component to equine laminitis and validation of a novel QST method for pain assessment in horses, this study reveals for the first time a physical and functional interaction between the 5-HT1B receptor and the TRPM8 channel.
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Bidaux, Gabriel. "Caractérisation du canal calcique TRPM8 dans la physiopathologie de la prostate humaine." Lille 1, 2006. https://pepite-depot.univ-lille.fr/LIBRE/Th_Num/2006/50376-2006-Bidaux.pdf.

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Seconde cause de mortalité par cancer chez l'individu de sexe masculin, le cancer de la prostate présente une incidence croissante liée à l'augmentation de l'espérance de vie dans les pays développés. Les variations pathologiques d'homéostasie calcique sont connues pour participer à l'évolution du cancer de la prostate. Cette thèse porte sur l'étude du canal ionique TRPM8 dont l'expression est spécifique de la prostate et augmente dans les cellules cancéreuses. Nos résultats montrent que l'expression de TRPM8 est finement régulée par le récepteur aux androgènes dans les cellules épithéliales apicales de la prostate et que son apparition coïncide avec la différenciation terminale de ces cellules. Nous démontrons que le canal est fonctionnel dans le plasmalemme des cellules épithéliales apicales, mais aussi dans la membrane du réticulum endoplasmique. Finalement, en corrélant ces travaux avec d'autres réalisés sur des cellules cancéreuses de la prostate, nous avons proposé un modèle d'évolution de l'activité du canal TRPM8 au cours de la différenciation et de l'oncogenèse des cellules de la prostate. Nous avons, d'autre part, mis en évidence l'existence d'isoformes de TRPM8 dont certaines sont des canaux ioniques fonctionnels alors que d'autres sont des petites protéines tronquées agissant comme sous-unités régulatrices du canal TRPM8. Pour finir, nous avons caractérisé une voie d'activation du canal TRPM8 par la phospholipase A2 indépendante du calcium et nous avons réalisé une étude pharmacologique démontrant l'activation de TRPM8 par une classe de molécules dérivées de l'iciline.
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Books on the topic "TRPM8"

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Lei, Ya-Ting. TRPM5 Channels Contribute to Persistent Neural Activity and Working Memory. [New York, N.Y.?]: [publisher not identified], 2013.

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Odone, Alberto. Materiali TRPM II Periodo 1-2. Independently Published, 2021.

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Grimm, Christian. Molekulare Und Funktionelle Charakterisierung Des Melastatin-Verwandten Trp-Kationenkanals Trpm3. Logos Verlag Berlin, 2004.

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Yum, Jennie. Role of the PDZ-binding motif of TRPM7 in mediating calcium-dependent cellular degeneration induced by chemical anoxia. 2006.

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Book chapters on the topic "TRPM8"

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Almaraz, Laura, Jan-Albert Manenschijn, Elvira de la Peña, and Félix Viana. "TRPM8." In Handbook of Experimental Pharmacology, 547–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2_22.

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Olivares, Erick, and Patricio Orio. "Mathematical Modeling of TRPM8 and the Cold Thermoreceptors." In TRP Channels in Sensory Transduction, 209–23. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18705-1_10.

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Liu, Yi, and Ning Qin. "TRPM8 in Health and Disease: Cold Sensing and Beyond." In Transient Receptor Potential Channels, 185–208. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_10.

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Langille, Neil F., and Daniel B. Horne. "Discovery and Development of AMG 333: A TRPM8 Antagonist for Migraine." In ACS Symposium Series, 125–54. Washington, DC: American Chemical Society, 2019. http://dx.doi.org/10.1021/bk-2019-1332.ch006.

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McKemy, David D. "TRPM8 Channels as Potential Therapeutic Targets for Pain, Analgesia, and Thermoregulation." In Methods in Pharmacology and Toxicology, 141–58. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-077-9_8.

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Guinamard, Romain, Laurent Sallé, and Christophe Simard. "The Non-selective Monovalent Cationic Channels TRPM4 and TRPM5." In Transient Receptor Potential Channels, 147–71. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_8.

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Pirali, Tracey, Ubaldina Galli, Marta Serafini, Alessia Griglio, Armando A. Genazzani, and Gian Cesare Tron. "Drug Discovery for Soft Drugs on TRPV1 and TRPM8 Channels Using the Passerini Reaction." In Methods in Molecular Biology, 207–21. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9446-5_13.

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Colsoul, Barbara, Miklos Kecskes, Koenraad Philippaert, Aurelie Menigoz, and Rudi Vennekens. "The Ca2+-Activated Monovalent Cation-Selective Channels TRPM4 and TRPM5." In Methods in Pharmacology and Toxicology, 103–25. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-077-9_6.

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Zakharian, Eleonora. "Inorganic Polyphosphate Is an Essential Structural and Functional Component of the Mammalian Ion Channel TRPM8." In Inorganic Polyphosphates in Eukaryotic Cells, 207–15. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41073-9_13.

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Guinamard, Romain, Christophe Simard, and Laurent Sallé. "TRPM4." In Encyclopedia of Signaling Molecules, 5741–49. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101882.

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Conference papers on the topic "TRPM8"

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Borodin, Evgeniy. "SEARCH FOR POTENTIAL LIGANDS FOR TRPM8 WITH THE HELP OF COMPUTER DESIGN." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9b2fdca3.97577371.

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A search was carried out for potential ligands to TRPM8 - a representative of the family of cationic channels with a transient receptor potential involved in the development of bronchial hypersensitivity and the occurrence of bronchospasm in response to low temperatures. We used a structural design and molecular docking using the autodock software package (http://autodock.scripps.edu/), which allows automated testing of many potential ligands for TRPM8. Docking was carried out with tyrosine 745 (Y745) amino acid residue as a critical residue for channel sensitivity to menthol, a classic TRPM8 agonist. The selection of potential candidates for the role of drugs intended for the treatment of bronchial cold hyperreactivity using in silico methods can be supplemented by testing their biological activity in vitro experiments with cell and tissue cultures and in vivo with experimental animals.
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Timkin, Pavel, E. Timofeev, A. Chupalov, and Evgeniy Borodin. "ANALYSIS AND SELECTION OF LIGANDS FOR TRPM8 USING HARD DOCKING AND MACHINE LEARNING." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9b233509.17835494.

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In this work, using the in-silico experiment modeling method, the receptor and its ligands were docked in order to obtain the data necessary to study the possibility of using machine learning and hard intermolecular docking methods to predict potential ligands for various receptors. The protein TRPM8 was chosen, which is a member of the TRP superfamily of proteins and its classic agonist menthol as a ligand. It is known that menthol is able to bind to tyrosine 745 of the B chain. To carry out all the manipulations, we used the Autodock software and a special set of graphic tools designed to work with in silico models of chemicals. As a result of all the manipulations, the menthol conformations were obtained that can bind to the active center of the TRPM8 receptor.
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Naumov, D., O. Kotova, D. Gassan, E. Afanaseva, E. Sheludko, and J. Perelman. "TRPM8 Polymorphism Affects Post-bronchodilator Lung Function In Asthma." 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.a7396.

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Naumov, Denis, Dina Gassan, Olesya Kotova, Elizaveta Sheludko, Evgeniya Afanaseva, Juliy Perelman, Yana Gorchakova, Qi Li, and Xiangdong Zhou. "Effect of systemic glucocorticoids on TRPM8 expression in asthma patients." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1122.

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Naumov, Denis, Dina Gassan, Olesya Kotova, Anna Prikhodko, Juliy Perelman, and Victor Kolosov. "TRPM8 polymorphism as an independent factor of bronchial obstruction in asthma." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa1271.

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Maher, Sarah, Mark Birrell, Sara Bonvini, Michael Wortley, Eric Dubuis, Fisnik Shala, Victoria Jones, et al. "Beneficial effects of menthol are mediated via a TRPM8-independent mechanism." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa3254.

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Asuthkar, Swapna, and Eleonora Zakharian. "Abstract 1165: TRPM8 is avidly targeted for degradation in prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1165.

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Naumov, Denis, Olesya Kotova, Dina Gassan, Elizaveta Sheludko, Evgeniya Afanaseva, Tatyana Maltseva, and Ivana Sugaylo. "Role of TRPM8 polymorphisms in predisposition to COPD development in smokers." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1128.

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Naumov, Denis, Dina Gassan, Olesya Kotova, Evgeniya Afanaseva, Elizaveta Sheludko, Ivana Sugaylo, and Juliy Perelman. "Effect of TRPA1 and TRPM8 polymorphisms on lung function in COPD." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1129.

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Тимкин, П. Д., Э. А. Тимофеев, А. П. Чупалов, and Е. А. Бородин. "Предсказание потенциальных лигандов для TRPM8 методами машинного обучения и межмолекулярного докинга." In Актуальные проблемы химии и биологии. Федеральное государственное бюджетное учреждение науки Тихоокеанский институт биоорганической химии им. Г.Б. Елякова Дальневосточного отделения Российской академии наук, 2020. http://dx.doi.org/10.47471/17_2020_09_07_10_24.

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