Relevant bibliographies by topics / TRPM2 and TRPM7

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Academic literature on the topic 'TRPM2 and TRPM7'

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Published: 14 March 2023

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Journal articles on the topic "TRPM2 and TRPM7"

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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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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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Du Preez, Stanley, Natalie Eaton-Fitch, Helene Cabanas, Donald Staines, and Sonya Marshall-Gradisnik. "Characterization of IL-2 Stimulation and TRPM7 Pharmacomodulation in NK Cell Cytotoxicity and Channel Co-Localization with PIP2 in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients." International Journal of Environmental Research and Public Health 18, no. 22 (November 12, 2021): 11879. http://dx.doi.org/10.3390/ijerph182211879.

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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multisystemic disorder responsible for significant disability. Although a unifying etiology for ME/CFS is uncertain, impaired natural killer (NK) cell cytotoxicity represents a consistent and measurable feature of this disorder. Research utilizing patient-derived NK cells has implicated dysregulated calcium (Ca2+) signaling, dysfunction of the phosphatidylinositol-4,5-bisphosphate (PIP2)-dependent cation channel, transient receptor potential melastatin (TRPM) 3, as well as altered surface expression patterns of TRPM3 and TRPM2 in the pathophysiology of ME/CFS. TRPM7 is a related channel that is modulated by PIP2 and participates in Ca2+ signaling. Though TRPM7 is expressed on NK cells, the role of TRPM7 with IL-2 and intracellular signaling mechanisms in the NK cells of ME/CFS patients is unknown. This study examined the effect of IL-2 stimulation and TRPM7 pharmacomodulation on NK cell cytotoxicity using flow cytometric assays as well as co-localization of TRPM7 with PIP2 and cortical actin using confocal microscopy in 17 ME/CFS patients and 17 age- and sex-matched healthy controls. The outcomes of this investigation are preliminary and indicate that crosstalk between IL-2 and TRMP7 exists. A larger sample size to confirm these findings and characterization of TRPM7 in ME/CFS using other experimental modalities are warranted.
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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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Müller, Isabel, Philipp Alt, Suhasini Rajan, Lena Schaller, Fabienne Geiger, and Alexander Dietrich. "Transient Receptor Potential (TRP) Channels in Airway Toxicity and Disease: An Update." Cells 11, no. 18 (September 17, 2022): 2907. http://dx.doi.org/10.3390/cells11182907.

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Our respiratory system is exposed to toxicants and pathogens from both sides: the airways and the vasculature. While tracheal, bronchial and alveolar epithelial cells form a natural barrier in the airways, endothelial cells protect the lung from perfused toxic compounds, particulate matter and invading microorganism in the vascular system. Damages induce inflammation by our immune response and wound healing by (myo)fibroblast proliferation. Members of the transient receptor potential (TRP) superfamily of ion channel are expressed in many cells of the respiratory tract and serve multiple functions in physiology and pathophysiology. TRP expression patterns in non-neuronal cells with a focus on TRPA1, TRPC6, TRPM2, TRPM5, TRPM7, TRPV2, TRPV4 and TRPV6 channels are presented, and their roles in barrier function, immune regulation and phagocytosis are summarized. Moreover, TRP channels as future pharmacological targets in chronic obstructive pulmonary disease (COPD), asthma, cystic and pulmonary fibrosis as well as lung edema are discussed.
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Islam, Md Shahidul. "Molecular Regulations and Functions of the Transient Receptor Potential Channels of the Islets of Langerhans and Insulinoma Cells." Cells 9, no. 3 (March 11, 2020): 685. http://dx.doi.org/10.3390/cells9030685.

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Insulin secretion from the β-cells of the islets of Langerhans is triggered mainly by nutrients such as glucose, and incretin hormones such as glucagon-like peptide-1 (GLP-1). The mechanisms of the stimulus-secretion coupling involve the participation of the key enzymes that metabolize the nutrients, and numerous ion channels that mediate the electrical activity. Several members of the transient receptor potential (TRP) channels participate in the processes that mediate the electrical activities and Ca2+ oscillations in these cells. Human β-cells express TRPC1, TRPM2, TRPM3, TRPM4, TRPM7, TRPP1, TRPML1, and TRPML3 channels. Some of these channels have been reported to mediate background depolarizing currents, store-operated Ca2+ entry (SOCE), electrical activity, Ca2+ oscillations, gene transcription, cell-death, and insulin secretion in response to stimulation by glucose and GLP1. Different channels of the TRP family are regulated by one or more of the following mechanisms: activation of G protein-coupled receptors, the filling state of the endoplasmic reticulum Ca2+ store, heat, oxidative stress, or some second messengers. This review briefly compiles our current knowledge about the molecular mechanisms of regulations, and functions of the TRP channels in the β-cells, the α-cells, and some insulinoma cell lines.
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Andriulė, Inga, Dalia Pangonytė, Asfree Gwanyanya, Dainius Karčiauskas, Kanigula Mubagwa, and Regina Mačianskienė. "Detection of TRPM6 and TRPM7 Proteins in Normal and Diseased Cardiac Atrial Tissue and Isolated Cardiomyocytes." International Journal of Molecular Sciences 23, no. 23 (November 28, 2022): 14860. http://dx.doi.org/10.3390/ijms232314860.

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Magnesium-sensitive transient receptor potential melastatin (TRPM) ion channels, TRPM6 and TRPM7, are present in several organs, but their roles in the heart remain unclear. Therefore, here, we studied the expression patterns of TRPM6 and TRPM7 in normal and diseased myocardium. Cardiac atrial tissue and cardiomyocytes were obtained from healthy pigs and undiseased human hearts as well as from hearts of patients with ischemic heart disease (IHD) or atrial fibrillation (AF). Immunofluorescence and ELISA were used to detect TRP proteins. TRPM6 and TRPM7 immunofluorescence signals, localized at/near the cell surface or intracellularly, were detected in pig and human atrial tissues. The TRP channel modulators carvacrol (CAR, 100 µM) or 2-aminoethoxydiphenyl borate (2-APB, 500 µM) decreased the TRPM7 signal, but enhanced that of TRPM6. At a higher concentration (2 mM), 2-APB enhanced the signals of both proteins. TRPM6 and TRPM7 immunofluorescence signals and protein concentrations were increased in atrial cells and tissues from IHD or AF patients. TRPM6 and TRPM7 proteins were both detected in cardiac atrial tissue, with relatively similar subcellular localization, but distinctive drug sensitivity profiles. Their upregulated expression in IHD and AF suggests a possible role of the channels in cardiac atrial disease.
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Özcan, SS, G. Gürel, and M. Çakır. "Gene expression profiles of transient receptor potential (TRP) channels in the peripheral blood mononuclear cells of psoriasis patients." Human & Experimental Toxicology 40, no. 8 (February 8, 2021): 1234–40. http://dx.doi.org/10.1177/0960327121991911.

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Psoriasis is a chronic autoimmune disease in which peripheral blood mononuclear cells (PBMCs) are involved in the pathological process. Transient receptor potential (TRP) channels expressed in immune cells have been shown to be associated with inflammatory diseases. We aimed to evaluate mRNA expression levels of TRP channels in PBMCs of patients with psoriasis. 30 patients with plaque psoriasis and 30 healthy age- and gender-matched control subjects were included in this study. mRNA expression levels of TRP channels in psoriasis patients were determined by Real-time polymerase chain reaction. A decreased TRPM4, TRPM7, TRPV3, TRPV4, and TRPC6 genes expression levels were found in the patient group compared to controls, respectively ( p = 0.045, p = 0.000, p = 0.000, p = 0.045, p = 0.009), whereas, an increased expression level was found in TRPM2 and TRPV1 genes in the patient group compared to controls ( p = 0.001 and p = 0.028). This is the first study showing the TRP channel mRNA expressions in PBMCs of psoriasis patients. Different expression patterns of TRP channels may have a role in pathogenesis of psoriasis.
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Scharenberg, Andrew M. "TRPM2 and TRPM7: channel/enzyme fusions to generate novel intracellular sensors." Pflügers Archiv - European Journal of Physiology 451, no. 1 (July 7, 2005): 220–27. http://dx.doi.org/10.1007/s00424-005-1444-0.

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Dissertations / Theses on the topic "TRPM2 and TRPM7"

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Bianchetti, Elena. "Cell death neuroprotection and repair mechanisms in a model of rat spinal cord injury in vitro." Doctoral thesis, SISSA, 2013. http://hdl.handle.net/20.500.11767/4099.

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Nowadays, new spinal cord injury (SCI) cases are frequently due to non traumatic causes, especially vascular disorders. A prerequisite to developing mechanism-based neuroprotective strategies for acute SCI is a full understanding of the early pathophysiological changes to prevent later disability and paralysis. The immediate damage spreads from the initial site through excitotoxicity and metabolic dysfunction (ischemia, free radicals and neuroinflammation) to surrounding tissue (secondary damage). Using an in vitro neonatal rat spinal cord model, an experimental protocol (pathological medium, PM) has been developed to mimic the profound metabolic perturbation (hypoxia, aglycemia, oxidative stress, acidosis, toxic free radicals) occurring in vivo after ischemic SCI, a condition surprisingly worsened by extracellular Mg2+ (1 mM). The current study sought to identify the cells affected by PM (with Mg2+), and the associated molecular death pathways in the spinal lumbar region which contains the locomotor networks. The results indicated that 1 h PM+Mg2+ application induced delayed pyknosis chiefly in the spinal white matter via overactivation of poly (ADP-ribose) polymerase 1 (PARP1), suggesting cell death mediated by the process of parthanatos and also via caspase 3-dependent apoptosis. Grey matter damage was less intense and concentrated in dorsal horn neurons and motoneurons which became nuclearimmunoreactive for the mitochondrial apoptosis-inducing factor. Moreover, TRPM2 channel expression was enhanced 24 h later in dorsal horn and motoneurons, while TRPM7 channel expression concomitantly decreased. Conversely, TRPM7 expression grew earlier (3 h) in white matter cells, while TRPM2 remained undetectable. Our results show that extracellular Mg2+ amplified the white matter cell death via parthanatos and apoptosis, and motoneuronal degeneration via PARP1-dependent pathways with distinct changes in their TRPM expression. In fact, the PARP-1 inhibitor PJ34, when applied 30 min after the moderate excitotoxic insult, could protect spinal networks controlling locomotion in more than 50 % of preparations. Interestingly, the drug per se strongly increased spontaneous network discharges without cell damage. Glutamate ionotropic receptor blockers suppressed this phenomenon reversibly. Our results suggest that pharmacological inhibition of PARP-1 could prevent damage to the locomotor networks if this procedure had been implemented early after the initial lesion and when the lesion was limited. PJ34 had also a positive effect on PM+Mg2+ treated spinal cords, especially in the white matter after 24 h, both alone or administered together with caspase-3 inhibitor. The neonatal rat in vitro SCI model was also useful to study the activation of endogenous spinal stem cells. We identified the ATF3 transcription factor as a novel dynamic marker for ependymal stem/progenitor cells (nestin, vimentin and SOX2 positive) located around the central canal of the neonatal or adult rat spinal cord. While quiescent ependymal cells showed cytoplasmic ATF3 expression, over 6-24 h in vitro these cells mobilized and acquired intense nuclear ATF3 staining. The migration of ATF3-nuclear positive cells preceded the strong proliferation of ependymal cells occurring after 24 h in vitro. Pharmacological inhibition of MAPK-p38 and JNK/c-Jun, upstream effectors of ATF3 activation, prevented the mobilization of ATF3 nuclear-positive cells. Excitotoxicity or ischemia-like conditions did not enhance migration of ependymal cells at 24 h. ATF3 is, therefore, suggested as a new biomarker of activated migrating stem cells in the rat spinal cord in vitro that represents an advantageous tool to study basic properties of endogenous stem cells.
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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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Drews, Anna-Dorothée [Verfasser], and Johannes [Akademischer Betreuer] Oberwinkler. "Elektrophysiologische Charakterisierung der murinen Ionenkanäle TRPM1 und TRPM3 und des TRPM Kanals von Drosophila melanogaster / Anna-Dorothée Drews. Betreuer: Johannes Oberwinkler." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2011. http://d-nb.info/1051095492/34.

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Klose, Chihab [Verfasser]. "Funktionelle Charakterisierung der Kationenkanäle TRPM3 und Melastatin (TRPM1) / Chihab Klose." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1029954984/34.

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Romero, Amanda Batista da Rocha. "Restrição dietética de magnésio associada à dieta hiperlipídica: implicações sobre a homeostase do mineral e sensibilidade à insulina." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/9/9132/tde-06122018-140629/.

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A resistência dos tecidos à ação da insulina é uma das principais complicações do excesso de peso. O aumento da gordura corporal, decorrente do consumo excessivo de nutrientes, é acompanhado por um quadro de inflamação crônica de baixa intensidade que está relacionado com a fisiopatologia da resistência à insulina. O magnésio (Mg) é um mineral envolvido com diversos processos fisiológicos e bioquímicos, especialmente aqueles relacionados ao metabolismo energético e ao controle glicêmico. Apesar de a deficiência deste mineral estar relacionada com condições pré-diabéticas, não está claro se a inadequação dietética promove alterações na sensibilidade à insulina e/ou se condições de resistência à insulina causam distúrbios na homeostase de Mg. O objetivo deste trabalho foi investigar os efeitos da restrição dietética de Mg e sua associação com o excesso de lipídios sobre a homeostase do mineral e a sensibilidade à insulina. Ratos Wistar, machos, com peso entre 97-123 g, permaneceram em gaiolas individuais por 24 semanas. Os animais receberam rações normolipídicas (CON, 7% de lipídios) ou hiperlipídicas (HL, 32% de lipídios), adequadas (CON e HL Mg; 500 mg de Mg/kg de ração; n = 6 para cada grupo) ou com restrição de Mg (Mg[50] e HL Mg[50]; 50 mg de Mg/kg de ração; n = 6 para cada grupo). O consumo da dieta HL promoveu maior acúmulo de tecido adiposo e maior ganho de peso corporal (p < 0,05). Os animais que consumiram rações com restrição de Mg apresentaram hipomagnesemia (p<0,01), menor excreção urinária (p < 0,01) e fecal (p < 0,001) de Mg e menor concentração óssea desse mineral (p < 0,001). No entanto, não foram observadas alterações no Mg muscular (p > 0,05). O grupo HL Mg[50] apresentou maior concentração de Mg no eritrócito quando comparado aos outros grupos. A restrição dietética de Mg, isoladamente, não promoveu alterações na sensibilidade à insulina (avaliada pelo teste de tolerância à insulina). Quando associada à dieta hiperlipídica, resultou em aumento da glicemia de jejum e em redução da sensibilidade à insulina, após 16 semanas (p < 0,01). Em nível molecular, a fosforilação da proteína quinase B (Akt) no músculo e no fígado foi significantemente menor no grupo HL Mg[50] (p < 0,05). A restrição dietética de Mg induziu ao aumento do conteúdo proteico dos canais TRPM6 e TRPM7 no rim, independentemente da sensibilidade à insulina. Os resultados deste estudo apontam que a deficiência de Mg tende a agravar as repercussões metabólicas do consumo de dietas hiperlipídicas na sensibilidade à insulina e que a resistência à insulina altera a compartimentalização do Mg.
Insulin resistance is one of the main complications of overweight. Increase body fat, due to excessive consumption of nutrients is accompanied by a chronic low-grade inflammation related to insulin resistance pathophysiology. Magnesium (Mg) is a mineral involved in many physiological and biochemical processes, especially those related to energy metabolism and glycemic control. Although Mg deficiency is related to pre-diabetic conditions, it is unclear whether dietary inadequacy promotes changes in insulin sensitivity and/or if conditions of insulin resistance cause disturbances in Mg homeostasis. This work aimed to investigate the effects of dietary Mg restriction and its association with high-fat diet on mineral homeostasis and insulin sensitivity. Male Wistar rat (97-123 g) remained in individual cages for 24 weeks. Animals received normolipid diet (CON, 7% lipid) or high-fat diet (HF, 32% lipid), adequate (CON and HF, 500 mg Mg / kg diet, n = 6 for each group) or Mg restricted (Mg[50] and HF Mg[50], 50 mg of Mg / kg of diet, n = 6 for each group). High-fat diet promoted a greater adipose tissue excess and body weight gain (p<0.05). Animals with Mg restricted diet had hypomagnesemia (p<0.01), lower Mg urinary (p<0.01) and faecal loss (p<0.001) and lower bone Mg concentration (p<0.001). However, no changes were observed in muscle Mg (p>0.05). HF Mg[50] group presented higher concentration of erythrocyte Mg when compared to the other groups. Singly, dietary Mg restriction did not induce changes in insulin sensitivity (as assessed by the insulin tolerance test). When associated with high-fat diet, dietary Mg restriction resulted in higher fasting glycemia and lower insulin sensitivity after 16 weeks (p<0.01). At the molecular level, protein kinase B (Akt) phosphorylation in muscle and liver was significantly lower in HFMg [50] group (p<0.05). Dietary Mg restriction induced increased protein content of renal TRPM6 and TRPM7 channels, regardless of insulin sensitivity. The results of this study indicate that Mg deficiency worsens metabolic effects of high-fat diet on insulin sensitivity. In addition, insulin resistance changes Mg compartmentalization.
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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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Ferioli, Silvia [Verfasser], and Barbara [Akademischer Betreuer] Conradt. "Cellular functions of the kinase-coupled TRPM6/TRPM7 channels / Silvia Ferioli ; Betreuer: Barbara Conradt." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1162840501/34.

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Eckstein, Eugenia [Verfasser], and Frank [Akademischer Betreuer] Zufall. "Trpm4 and Trpm5 in the murine olfactory system / Eugenia Eckstein ; Betreuer: Frank Zufall." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2019. http://d-nb.info/1203128940/34.

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Beesetty, Pavani. "Consequences of TRPM7 kinase inactivation in immune cells." Wright State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=wright1526406780596661.

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Miquel, Perrine. "Regulation of TRPM7 by Aldosterone." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104628.

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ABSTRACTTRPM7 (transient receptor potential melastatin), a member of the large TRP ion channel family, is ubiquitously expressed in cells and is constitutively active. It is comprised of six transmembrane domains that assemble into tetramers to form a central Mg2+ and Ca2+ permeable pore. TRPM7 and its homologue TRPM6 are some of the only channels known to carry Mg2+. Hypertension, a cardiovascular condition linked to low levels of intracellular Mg2+ is also associated with high levels of aldosterone. Previous results have demonstrated that aldosterone increases mRNA levels of TRPM7 whereas protein levels decreased in VSMCs. To understand if TRPM7 may be implicated in hypertension, we questioned whether aldosterone could regulate TRPM7 currents, and inquired for a possible underlying mechanism. Whole-cell patch clamp studies were conducted in inducible HEK-293 cells, stably expressing wild type TRPM7. We found that TRPM7 currents are enhanced after overnight stimulation with aldosterone compared to non-stimulated cells. When the mineralocorticoid receptor (hMR) is transfected two days prior aldosterone stimulation, this response is further increased. The introduction of 10mM BAPTA, a Ca2+ chelator, to the intracellular medium doubled the TRPM7 current in WT cells and also increased the response to aldosterone in cells transfected with the hMR receptor. Surprisingly, protein levels of TRPM7 do not vary, suggesting a redistribution of already existing channels to the membrane. SGK-1, a serine threonine kinase was suggested as a possible mediator of the response. In fact, when a specific blocker to SGK-1 is applied onto the cells, both current and total protein levels of TRPM7 are significantly decreased. Overall, these results demonstrate that aldosterone can regulate TRPM7 through an increase in total current. This response appears to be mediated by SGK-1 in a calcium sensitive manner.
RÉSUMÉTRPM7 (transient receptor potential melastatin), membre de la large famille des canaux ioniques des TRP, est exprimée de façon omniprésente dans toutes les cellules, et est active de façon constitutive. TRPM7 est composée de six domaines transmembranaires qui s'assemblent en tétramères pour former un pore central, perméable aux ions Mg2+ et Ca2+. TRPM7, et son homologue TRPM6, sont les seuls canaux ioniques connus pour le transport du Mg2+. L'hypertension, une maladie cardiovasculaire associée à de faibles niveaux en Mg2+ intracellulaire est aussi liée à de niveaux élevés d'aldosterone. Des recherches antérieures ont démontré que l'aldosterone augmente les niveaux d'ARNm de TRPM7 tandis que la quantité de protéines diminue dans les cellules vasculaires lisses du muscle. Afin de comprendre si TRPM7 peut être impliquée dans l'hypertension, nous nous sommes demandés si l'aldosterone pouvait réguler les courants associés à TRPM7, et si nous pouvions définir un mécanisme d'action qui pourrait expliquer une telle régulation. La technique du patch clamp a été utilisée sur des cellules HEK-293 inductibles exprimant de façon stable le phénotype humain de TRPM7. Nous avons trouvé que les courants de TRPM7 sont augmentés après une stimulation de nuit avec de l'aldosterone, comparé à des cellules non stimulées. Lorsque le récepteur humain mineralocorticoid (hMR) est transfecté deux jours avant la stimulation par l'aldosterone, la réponse en courant est rehaussée. L'ajout de 10mM de BAPTA, un chélateur du Ca2+, dans la solution intracellulaire permet de doubler la réponse en courant dans ces cellules, ainsi que d'augmenter la réponse à l'aldosterone dans les cellules transfectées avec le récepteur hMR. Etonnamment, les niveaux de protéines de TRPM7 ne sont pas affectés, suggérant une redistribution des canaux ioniques déjà existants à la membrane. SGK-1, une kinase membre de la famille des serine-threonines a été proposée comme un possible médiateur de la réponse a l'aldosterone. En effet, après l'application d'un bloquer spécifique pour le SGK-1, une diminution des courants ainsi que de la quantité de protéines associées à TRPM7 a été observée. De façon générale, ces résultats démontrent que l'aldosterone est capable de réguler TRPM7 à travers une augmentation des courants. Cette réponse, qui semble être sous l'influence de SGK-1, utilise un mécanisme sensible aux niveaux de calcium intracellulaire..
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Books on the topic "TRPM2 and TRPM7"

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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 "TRPM2 and TRPM7"

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Hermosura, Meredith C. "Alterations in TRPM2 and TRPM7 Functions in the Immune System Could Confer Susceptibility to Neurodegeneration." In Pathologies of Calcium Channels, 333–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_18.

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Faouzi, Malika, and Reinhold Penner. "TRPM2." In Handbook of Experimental Pharmacology, 403–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2_16.

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Fleig, Andrea, and Vladimir Chubanov. "TRPM7." In Handbook of Experimental Pharmacology, 521–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2_21.

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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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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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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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Oberwinkler, Johannes. "TRPM3." In Encyclopedia of Signaling Molecules, 5734–41. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101920.

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Kon, Tetsuo, and Takahisa Furukawa. "TRPM1." In Encyclopedia of Signaling Molecules, 5727–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101948.

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Irie, Shoichi, and Takahisa Furukawa. "TRPM1." In Handbook of Experimental Pharmacology, 387–402. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2_15.

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Oberwinkler, Johannes, and Stephan E. Philipp. "TRPM3." In Handbook of Experimental Pharmacology, 427–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2_17.

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Conference papers on the topic "TRPM2 and TRPM7"

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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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Kaoud, Tamer S., Jihyun Park, Shreya Mitra, Clint D. J. Tavares, Anna Tseng, and Kevin N. Dalby. "Abstract 4551: Identification of TRPM7 kinase inhibitors." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4551.

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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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Epshtein, Y., W. Chen, H. Wang, and J. R. Jacobson. "TRPM2 Augments Lung Endothelial Barrier Function After Radiation Via Sphinoglipid Signaling." 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.a5392.

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Kaoud, Tamer S., Xuemei Xie, Jihyun Park, Clint D. J. Tavares, Shreya Mitra, Micael Cano, Mohamed F. Radwan, Chandra Bartholomeusz, and Kevin N. Dalby. "Abstract A17: TRPM7 kinase domain is involved in breast tumor cell metastasis." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-a17.

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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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Shabanov, Gennadiy, and Aleksandr Rybchenko. "DEVELOPMENT OF EXPRESS DIAGNOSTICS OF COLD ENDURANCE AND PROPENSION TO BRONCHOPULUM DISEASES ON THE BASIS OF REGISTRATION OF BRAIN MICROVIBRATIONS." 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_5fe01d9cb71499.17311740.

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The paper explored the possibility of using the complex for registration and spectral analysis of microvibrations of the brain for mass examinations, professional selection of contingents working in difficult climatic conditions of the North and the Far East. Spectral characteristics of factors leading to increased expression of TRPM8 cold receptors were studied in the rhythms of brain activity using a menthol functional test. The results of the work can be used to identify people at risk of developing bronchopulmonary pathology.
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Lange, Ingo, and Dana-Lynn T. Koomoa. "Abstract 3781: MYCN-induced TRPM7 mediates calcium influx and promotes neuroblastoma cell migration." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3781.

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Hirschler-Laszkiewicz, Iwona Malgorzata, Shu-jen Chen, Lei Bao, JuFang Wang, Xue-Qian Zhang, Santhanam Shanmughapriya, Kerry Keefer, Muniswamy Madesh, Joseph Y. Cheung, and Barbara A. Miller. "Abstract 1458: TRPM2 modulates neuroblastoma cell survival through Pyk2, CREB and MCU activation." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1458.

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Liu, Mingli. "Abstract 3128: TRPM7 regulates glioma cell proliferation and migration through different function domains." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3128.

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