Relevant bibliographies by topics / Transient receptor potential melastatin channels

Academic literature on the topic 'Transient receptor potential melastatin channels'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Transient receptor potential melastatin channels"

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Kytikova, Oxana Yu, Tatyana P. Novgorodtseva, Yulia K. Denisenko, Denis E. Naumov, Tatyana A. Gvozdenko, and Juliy M. Perelman. "Thermosensory Transient Receptor Potential Ion Channels and Asthma." Biomedicines 9, no. 7 (July 14, 2021): 816. http://dx.doi.org/10.3390/biomedicines9070816.

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Asthma is a widespread chronic disease of the bronchopulmonary system with a heterogeneous course due to the complex etiopathogenesis. Natural-climatic and anthropogenic factors play an important role in the development and progression of this pathology. The reception of physical and chemical environmental stimuli and the regulation of body temperature are mediated by thermosensory channels, members of a subfamily of transient receptor potential (TRP) ion channels. It has been found that genes encoding vanilloid, ankyrin, and melastatin TRP channels are involved in the development of some asthma phenotypes and in the formation of exacerbations of this pathology. The review summarizes modern views on the role of high and low temperatures in airway inflammation in asthma. The participation of thermosensory TRP channels (vanilloid, ankyrin, and melastatin TRP channels) in the reaction to high and low temperatures and air humidity as well as in the formation of bronchial hyperreactivity and respiratory symptoms accompanying asthma is described. The genetic aspects of the functioning of thermosensory TRP channels are discussed. It is shown that new methods of treatment of asthma exacerbations caused by the influence of temperature and humidity should be based on the regulation of channel activity.
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Vriens, Joris, and Thomas Voets. "Transient Receptor Potential Melastatin 3 Channel." Biophysical Journal 100, no. 3 (February 2011): 109a. http://dx.doi.org/10.1016/j.bpj.2010.12.800.

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Nilius, Bernd, Grzegorz Owsianik, Thomas Voets, and John A. Peters. "Transient Receptor Potential Cation Channels in Disease." Physiological Reviews 87, no. 1 (January 2007): 165–217. http://dx.doi.org/10.1152/physrev.00021.2006.

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The transient receptor potential (TRP) superfamily consists of a large number of cation channels that are mostly permeable to both monovalent and divalent cations. The 28 mammalian TRP channels can be subdivided into six main subfamilies: the TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPP (polycystin), TRPML (mucolipin), and the TRPA (ankyrin) groups. TRP channels are expressed in almost every tissue and cell type and play an important role in the regulation of various cell functions. Currently, significant scientific effort is being devoted to understanding the physiology of TRP channels and their relationship to human diseases. At this point, only a few channelopathies in which defects in TRP genes are the direct cause of cellular dysfunction have been identified. In addition, mapping of TRP genes to susceptible chromosome regions (e.g., translocations, breakpoint intervals, increased frequency of polymorphisms) has been considered suggestive of the involvement of these channels in hereditary diseases. Moreover, strong indications of the involvement of TRP channels in several diseases come from correlations between levels of channel expression and disease symptoms. Finally, TRP channels are involved in some systemic diseases due to their role as targets for irritants, inflammation products, and xenobiotic toxins. The analysis of transgenic models allows further extrapolations of TRP channel deficiency to human physiology and disease. In this review, we provide an overview of the impact of TRP channels on the pathogenesis of several diseases and identify several TRPs for which a causal pathogenic role might be anticipated.
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Yang, Wei, Paul T. Manna, Jie Zou, Jianhong Luo, David J. Beech, Asipu Sivaprasadarao, and Lin-Hua Jiang. "Zinc Inactivates Melastatin Transient Receptor Potential 2 Channels via the Outer Pore." Journal of Biological Chemistry 286, no. 27 (May 20, 2011): 23789–98. http://dx.doi.org/10.1074/jbc.m111.247478.

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Zinc ion (Zn2+) is an endogenous allosteric modulator that regulates the activity of a wide variety of ion channels in a reversible and concentration-dependent fashion. Here we used patch clamp recording to study the effects of Zn2+ on the melastatin transient receptor potential 2 (TRPM2) channel. Zn2+ inhibited the human (h) TRPM2 channel currents, and the steady-state inhibition was largely not reversed upon washout and concentration-independent in the range of 30–1000 μm, suggesting that Zn2+ induces channel inactivation. Zn2+ inactivated the channels fully when they conducted inward currents, but only by half when they passed outward currents, indicating profound influence of the permeant ion on Zn2+ inactivation. Alanine substitution scanning mutagenesis of 20 Zn2+-interacting candidate residues in the outer pore region of the hTRPM2 channel showed that mutation of Lys952 in the extracellular end of the fifth transmembrane segment and Asp1002 in the large turret strongly attenuated or abolished Zn2+ inactivation, and mutation of several other residues dramatically changed the inactivation kinetics. The mouse (m) TRPM2 channels were also inactivated by Zn2+, but the kinetics were remarkably slower. Reciprocal mutation of His995 in the hTRPM2 channel and the equivalent Gln992 in the mTRPM2 channel completely swapped the kinetics, but no such opposing effects resulted from exchanging another pair of species-specific residues, Arg961/Ser958. We conclude from these results that Zn2+ inactivates the TRPM2 channels and that residues in the outer pore are critical determinants of the inactivation.
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Latorre, Ramon, Cristián Zaelzer, and Sebastian Brauchi. "Structure–functional intimacies of transient receptor potential channels." Quarterly Reviews of Biophysics 42, no. 3 (August 2009): 201–46. http://dx.doi.org/10.1017/s0033583509990072.

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AbstractAlthough a unifying characteristic common to all transient receptor potential (TRP) channel functions remains elusive, they could be described as tetramers formed by subunits with six transmembrane domains and containing cation-selective pores, which in several cases show high calcium permeability. TRP channels constitute a large superfamily of ion channels, and can be grouped into seven subfamilies based on their amino acid sequence homology: the canonical or classic TRPs, the vanilloid receptor TRPs, the melastatin or long TRPs, ankyrin (whose only member is the transmembrane protein 1 [TRPA1]), TRPN after the nonmechanoreceptor potential C (nonpC), and the more distant cousins, the polycystins and mucolipins. Because of their role as cellular sensors, polymodal activation and gating properties, many TRP channels are activated by a variety of different stimuli and function as signal integrators. Thus, how TRP channels function and how function relates to given structural determinants contained in the channel-forming protein has attracted the attention of biophysicists as well as molecular and cell biologists. The main purpose of this review is to summarize our present knowledge on the structure of channels of the TRP ion channel family. In the absence of crystal structure information for a complete TRP channel, we will describe important protein domains present in TRP channels, structure–function mutagenesis studies, the few crystal structures available for some TRP channel modules, and the recent determination of some TRP channel structures using electron microscopy.
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Badheka, Doreen, Istvan Borbiro, and Tibor Rohacs. "Transient receptor potential melastatin 3 is a phosphoinositide-dependent ion channel." Journal of General Physiology 146, no. 1 (June 29, 2015): 65–77. http://dx.doi.org/10.1085/jgp.201411336.

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Phosphoinositides are emerging as general regulators of the functionally diverse transient receptor potential (TRP) ion channel family. Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) has been reported to positively regulate many TRP channels, but in several cases phosphoinositide regulation is controversial. TRP melastatin 3 (TRPM3) is a heat-activated ion channel that is also stimulated by chemical agonists, such as pregnenolone sulfate. Here, we used a wide array of approaches to determine the effects of phosphoinositides on TRPM3. We found that channel activity in excised inside-out patches decreased over time (rundown), an attribute of PI(4,5)P2-dependent ion channels. Channel activity could be restored by application of either synthetic dioctanoyl (diC8) or natural arachidonyl stearyl (AASt) PI(4,5)P2. The PI(4,5)P2 precursor phosphatidylinositol 4-phosphate (PI(4)P) was less effective at restoring channel activity. TRPM3 currents were also restored by MgATP, an effect which was inhibited by two different phosphatidylinositol 4-kinase inhibitors, or by pretreatment with a phosphatidylinositol-specific phospholipase C (PI-PLC) enzyme, indicating that MgATP acted by generating phosphoinositides. In intact cells, reduction of PI(4,5)P2 levels by chemically inducible phosphoinositide phosphatases or a voltage-sensitive 5′-phosphatase inhibited channel activity. Activation of PLC via muscarinic receptors also inhibited TRPM3 channel activity. Overall, our data indicate that TRPM3 is a phosphoinositide-dependent ion channel and that decreasing PI(4,5)P2 abundance limits its activity. As all other members of the TRPM family have also been shown to require PI(4,5)P2 for activity, our data establish PI(4,5)P2 as a general positive cofactor of this ion channel subfamily.
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Zholos, Alexander. "Pharmacology of transient receptor potential melastatin channels in the vasculature." British Journal of Pharmacology 159, no. 8 (March 5, 2010): 1559–71. http://dx.doi.org/10.1111/j.1476-5381.2010.00649.x.

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Jiang, L. H. "Subunit interaction in channel assembly and functional regulation of transient receptor potential melastatin (TRPM) channels." Biochemical Society Transactions 35, no. 1 (January 22, 2007): 86–88. http://dx.doi.org/10.1042/bst0350086.

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Functional TRPM (transient receptor potential melastatin) ion channels are multimers, thought to be tetramers. Subunit interaction is the prerequisite step in channel assembly, and the specificity of subunit interaction is crucial in assembling channels with distinct functional properties. In addition, expression of short non-functional subunits and their interaction with full-length subunits serve as one of the post-translational mechanisms regulating the channel activity. This paper aims to provide an overview of the current knowledge of TRPM subunit interactions and their roles in assembly and functional regulation of the TRPM channels.
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Bishnoi, Mahendra, and Louis S. Premkumar. "Changes in TRP Channels Expression in Painful Conditions." Open Pain Journal 6, no. 1 (March 8, 2013): 10–22. http://dx.doi.org/10.2174/1876386301306010010.

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Over the last fifteen years after the successful cloning of the first nociceptive Transient Receptor Potential (TRP) channel, TRP Vanilloid 1, other members of the TRP channel family have been cloned, characterized and implicated in different modalities of pain. Tremendous progress has been made with regard to the specific role of these TRP channels in nociception using electrophysiological and molecular methods, along with behavioral models combined with gene disruption techniques. This review summarizes the evidence supporting the role of TRP channels (TRP Vanilloid 1, TRP Vanilloid 2, TRP Vanilloid 3, TRP Vanilloid 4, TRP Ankyrin 1, TRP Melastatin 2, TRP Melastatin 3, TRP Melastatin 8, TRP Mucolipin 3 and TRP Canonical 1, 6) involved in nociception. The review also highlights the current status and future avenues for developing TRP channel modulators as analgesic agents.
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Santoni, Giorgio, Federica Maggi, Maria Beatrice Morelli, Matteo Santoni, and Oliviero Marinelli. "Transient Receptor Potential Cation Channels in Cancer Therapy." Medical Sciences 7, no. 12 (November 30, 2019): 108. http://dx.doi.org/10.3390/medsci7120108.

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In mammals, the transient receptor potential (TRP) channels family consists of six different families, namely TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPML (mucolipin), TRPP (polycystin), and TRPA (ankyrin), that are strictly connected with cancer cell proliferation, differentiation, cell death, angiogenesis, migration, and invasion. Changes in TRP channels’ expression and function have been found to regulate cell proliferation and resistance or sensitivity of cancer cells to apoptotic-induced cell death, resulting in cancer-promoting effects or resistance to chemotherapy treatments. This review summarizes the data reported so far on the effect of targeting TRP channels in different types of cancer by using multiple TRP-specific agonists, antagonists alone, or in combination with classic chemotherapeutic agents, microRNA specifically targeting the TRP channels, and so forth, and the in vitro and in vivo feasibility evaluated in experimental models and in cancer patients. Considerable efforts have been made to fight cancer cells, and therapies targeting TRP channels seem to be the most promising strategy. However, more in-depth investigations are required to completely understand the role of TRP channels in cancer in order to design new, more specific, and valuable pharmacological tools.
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Dissertations / Theses on the topic "Transient receptor potential melastatin channels"

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Lucius, Alexander [Verfasser]. "Characterization of temperature-sensitive transient receptor potential channel melastatin 8 (TRPM8) in cultivated human ocular surface cells / Alexander Lucius." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1126503886/34.

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Wang, Qian, and 王倩. "Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206750.

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Autophagy is a major catabolic pathway for maintaining cell homeostasis through degradation and recycle of macromolecules and organelles. Autophagy can be activated under environmental stress conditions, including reactive oxygen species (ROS). TRPM2, a non-selective trans-membrane calcium channel, can be activated by ROS that, in turn, leads to intracellular 〖Ca〗^(2+) increase through 〖Ca〗^(2+) influx. It is well known that ROS regulates autophagy, and vice versa. Yet, the molecular mechanisms underlying the interplay between ROS and autophagy remain elusive. Here we studied the role of TRPM2-mediated 〖Ca〗^(2+) influx in interplay between ROS and autophagy. From our study, we found that ROS activated TRPM2 for 〖Ca〗^(2+) influx via ADPR to inhibit early autophagy induction, which ultimately led to apoptosis in TRPM2 expressing cancer cell lines. On the other hand, ROS induced autophagy, not apoptosis, for cell survival in cancer cell lines which do not express TRPM2, and autophagy inhibition, either by ATG5 knockdown or by treating cells with bafilomycin A1 (an autophagy inhibitor), converted cells to apoptosis upon ROS treatment. In addition, ROS dramatically changed mitochondrial morphology, increased mitochondrial 〖Ca〗^(2+) content, and abolished mitochondrial membrane potential in TRPM2 expressing cells. Moreover, we found that ROS-induced Ca2+ influx via TRPM2 actually activated calmodulin-dependent protein kinase II (CaMKII) to phosphorylate Ser295 on Beclin1. Phosphorylated Beclin1, in turn, decreased the association between Beclin1 and VPS34, but induced the binding between Beclin1 and BCL-2. In summary, our data demonstrated that the TRPM2/〖Ca〗^(2+)/CaMKII/ Beclin1 cascade is the molecular switch between autophagy and apoptosis in response to ROS. Since dysregulation of ROS and autophagy has been associated with a variety of human diseases, e.g. cancer, neurological disorders, heart diseases, and liver diseases, manipulating the TRPM2/〖Ca〗^(2+)/CaMKII/ Beclin1 cascade should provide novel treatment option for these diseases.
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Chen, Wenchun [Verfasser], and Bernhard [Gutachter] Nieswandt. "Studies on the role of calcium channels and the kinase domain of transient receptor potential melastatin-like 7 (TRPM7) in platelet function / Wenchun Chen. Gutachter: Bernhard Nieswandt." Würzburg : Universität Würzburg, 2014. http://d-nb.info/1111783284/34.

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Pimentel, Montero Fátima Elizabeth. "Modulation of transient receptor potential melastatin 8 by protein kinase C /." Available to subscribers only, 2005. http://proquest.umi.com/pqdweb?did=1075689361&sid=10&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Stokes, Alexander James. "Regulatory interactions of transient receptor potential channels." Thesis, University of Warwick, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418114.

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Cao, De-Shou. "Role of transient receptor potential (TRP) channels in nociception /." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1967913291&sid=2&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Cao, Deshou. "Role of Transient Receptor Potential (TRP) Channels in Nociception." OpenSIUC, 2009. https://opensiuc.lib.siu.edu/dissertations/71.

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Transient receptor potential (TRP) channels play an important role in sensory and nonsensory functions. TRPVanilloid 1 and TRPVanilloid 4 are proposed to be involved in inflammation-induced pain. TRPV1 is extensively studied and it is specifically involved in inflammatory thermal hypersensitivity. Mechanical hypersensitivity is one of the significant components of nociception. Several receptors have been proposed to underlie mechanosensation. The molecular entities responsible for mechanosensation are not fully understood. In this study, I have characterized the properties of TRPV4, a putative mechanosensitive ion channel expressed in dorsal root ganglion (DRG) neurons and nonsensory tissues. First, I have investigated the expression and function of TRPV4 and TRPV1 in the DRG neuronal cell bodies as well as their central terminals and determined the modulation by protein kinase C (PKC). Both TRPV4 and TRPV1 are expressed in DRG and laminae I and II of the spinal dorsal horn (DH). Ca2+ fluorescence imaging and whole-cell patch-clamp experiments showed that both capsaicin-induced TRPV1 response and 4alpha-phorbol 12, 13-didecanoate (4alpha-PDD)-induced TRPV4 response were observed in a proportion of the same DRG neurons, suggesting their co-expression. Incubation of DRG neurons with phorbol 12, 13-dibutyrate (PDBu), a PKC activator, resulted in a significantly greater potentiation of TRPV4 currents than TRPV1 currents. In HEK cells heterologously expressing TRPV4, PDBu potentiated TRPV4-mediated single-channel current activity. In patch-clamped DH neurons, the application of 4alpha-PDD at the first sensory synapse increased the frequency but not the amplitude of the miniature excitatory postsynaptic currents (mEPSCs), suggesting a presynaptic locus of action. 4alpha-PDD-induced increase in the frequency of mEPSC was further facilitated by PDBu. These results suggest that TRPV4 in the central terminals modulates synaptic transmission and is regulated by PKC. Second, I have studied the mechanosensitivity of TRPV4 in cell-attached patches by applying direct mechanical force via the patch pipette. In TRPV4 expressing HEK cells, the application of negative pressure evoked single-channel current activity in a reversible manner and the channel activity was enhanced after incubation with PDBu. TRPV4 has been shown to be activated by hypotonicity. Here I show that negative pressure exaggerated hypotonicity-induced single-channel current activity. However, in similar experimental conditions, cells expressing TRPV1 did not respond to mechanical force. TRP channels are also expressed in non-sensory regions and the role of these channels is not fully understood. Both TRPV4 and TRPV1 are expressed in the hippocampus. Using whole-cell patch-clamp techniques, I have found that 4alpha-PDD increased the frequency, but not the amplitude of mEPSCs in cultured hippocampal neurons, suggesting a presynaptic site of action. Interestingly, the application of capsaicin had no effect on synaptic transmission in hippocampal neuronal cultures. Finally, I have investigated the expression and function of TRP channels in diabetes because TRP channels have been shown to be involved in peripheral neuropathy as well as vascular complications in diabetes. ROS production plays a critical role in the progress of diabetes. I propose that lower levels of ROS up-regulate the expression TRP channels in the early stages of diabetes, leading to hyperalgesia, and higher levels of ROS or chronic exposure to ROS down-regulate TRP channels in the late stages of diabetes, resulting in hypoalgesia. I have found that the expression of TRPV1 and phospho p38 (p-p38) MAPK was increased in DRG of streptozotocin (STZ)-injected diabetic and non-diabetic hyperalgesic mice. An increase in TRPV1 and p-p38 MAPK levels was induced by STZ or H2O2 treatment in stably TRPV1 expressing HEK cells, suggesting the involvement of STZ-ROS-p38MAPK pathway. TRPV4 has been reported to be involved in vasodilatation by shear stress in blood vessels. Here, I have demonstrated that TRPV4 is expressed in lymphatic endothelial cells (LECs). Treatment with low concentration of H2O2 enhanced the expression of TRPV4 at mRNA and protein levels in LECs, suggesting that mild levels of ROS up-regulate TRPV4 expression. In diabetes, beta cell dysfunction is responsible for decreased insulin release. TRPV4 is expressed in RINm5F (beta cell line), islets and pancreas. It has been shown that hypotonicity induced insulin release in beta cell lines, which was mediated by activation of stretch-activated channels, raising the possibility of the involvement of TRPV4, a mechanosensitive channel. Therefore, I have studied the functional role of TRPV4 in beta cells. Incubation with 4alpha-PDD enhanced insulin release in RINm5F cells, suggesting TRPV4 regulates insulin secretion from pancreatic beta cells. Since TRPV4 expression levels are decreased in diabetes, insulin secretion from beta cells may be impaired. In summary, TRPV1, a thermosensitive channel, and TRPV4, a mechanosensitive channel, contribute to thermal and mechanical hyperalgesia, respectively in the early stage of DPN through their up-regulation by ROS-p38 MAPK and insulin/IGF-1 pathways. Due to the mechanical sensitivity of TRPV4 channel, the up-regulation in the early stage and down-regulation in the late stage may be involved in the development of vascular complications and regulation of insulin release in diabetes.
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Ogawa, Nozomi. "Detection of cellular redox status by transient receptor potential channels." 京都大学 (Kyoto University), 2016. http://hdl.handle.net/2433/215577.

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Pabbidi, Reddy M. "Role of transient receptor potential channels in diabetic peripheral neuropathy /." Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1456284721&sid=5&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Bomben, Valerie Christine. "Role of transient receptor potential canonical channels in glioma cell biology." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2010. https://www.mhsl.uab.edu/dt/2010p/bomben.pdf.

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Books on the topic "Transient receptor potential melastatin channels"

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Islam, Md Shahidul, ed. Transient Receptor Potential Channels. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0265-3.

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service), SpringerLink (Online, ed. Transient Receptor Potential Channels. Dordrecht: Springer Science+Business Media B.V., 2011.

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Flockerzi, Veit, and Bernd Nilius, eds. Transient Receptor Potential (TRP) Channels. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-34891-7.

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J, Abramowitz, Flockerzi Veit, and Nilius B, eds. Transient receptor potential (TRP) channels. Berlin: Springer, 2007.

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Nilius, Bernd, and Veit Flockerzi, eds. Mammalian Transient Receptor Potential (TRP) Cation Channels. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05161-1.

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Nilius, Bernd, and Veit Flockerzi, eds. Mammalian Transient Receptor Potential (TRP) Cation Channels. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2.

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Wang, Yizheng, ed. Transient Receptor Potential Canonical Channels and Brain Diseases. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1088-4.

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Szallasi, Arpad. TRP channels in health and disease: Implications for diagnosis and therapy. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Nilius, Bernd, and Veit Flockerzi. Transient Receptor Potential Channels. Springer, 2010.

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Islam, MD Shahidul. Transient Receptor Potential Channels. Springer, 2011.

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Book chapters on the topic "Transient receptor potential melastatin channels"

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Wakamori, Minoru, Takashi Yoshida, Takashi Kikuchi, Daisuke Kondoh, and Masashi Komatsu. "Melastatin Transient Receptor Potential Channel Type 5." In Interface Oral Health Science 2011, 341–45. Tokyo: Springer Japan, 2012. http://dx.doi.org/10.1007/978-4-431-54070-0_99.

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Hall, Hannah K., and David W. Koh. "Methods for Investigating Transient Receptor Potential Melastatin-2 (TRPM2): A Cation Channel Activated by ADP-Ribose and Involved in Cell Death." In Methods in Molecular Biology, 213–26. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2891-1_13.

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Lehen’kyi, V’yacheslav, and Natalia Prevarskaya. "Oncogenic TRP Channels." In Transient Receptor Potential Channels, 929–45. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_48.

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Hofherr, Alexis, and Michael Köttgen. "TRPP Channels and Polycystins." In Transient Receptor Potential Channels, 287–313. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_16.

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Kaleta, Marta, and Christopher Palmer. "TRP Channels in Yeast." In Transient Receptor Potential Channels, 315–21. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_17.

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Xiao, Rui, and X. Z. Shawn Xu. "C. elegans TRP Channels." In Transient Receptor Potential Channels, 323–39. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_18.

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Wolstenholme, Adrian J., Sally M. Williamson, and Barbara J. Reaves. "TRP Channels in Parasites." In Transient Receptor Potential Channels, 359–71. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_20.

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Islam, Md Shahidul. "TRP Channels of Islets." In Transient Receptor Potential Channels, 811–30. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_42.

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Li, Minghui, Yong Yu, and Jian Yang. "Structural Biology of TRP Channels." In Transient Receptor Potential Channels, 1–23. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_1.

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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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Conference papers on the topic "Transient receptor potential melastatin channels"

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Liu, Mingli. "Abstract 774: Regulation of autophagy and epigenetic modulator micro RNA by transient receptor potential melastatin 7 (TRPM7) channel in glioma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-774.

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Liu, Mingli. "Abstract 774: Regulation of autophagy and epigenetic modulator micro RNA by transient receptor potential melastatin 7 (TRPM7) channel in glioma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-774.

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Koh, David W., Daniel P. Powell, Steven D. Blake, Joy L. Hoffman, and Xiaoxing Feng. "Abstract 1717: Selective induction of breast adenocarcinoma cell death via inhibition of the transient receptor potential melastatin-2 (TRPM2) cation channel." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1717.

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Koh, David W., Steven D. Blake, and Daniel P. Powell. "Abstract 1269: Enhanced cytotoxicity in primary human metastatic melanoma cells via inhibition of the transient receptor potential melastatin-2 (TRPM2) channel." 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.am2016-1269.

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Botta, Davide, Andre' Ballesteros-Tato, Kyle Martin, Louise Hartson, Tirumalai Rangasamy, Thomas J. Mariani, Troy D. Randall, Debra A. Cockayne, Christopher S. Stevenson, and Frances E. Lund. "Deficiency Of The Transient Receptor Potential Melastatin 2 (TRPM2) Cation Channel Provides Protection Against Pulmonary Inflammation In A Murine Model Of Chronic Obstructive Pulmonary Disease (COPD)." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1305.

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Baxter, Matthew D., Maria G. Belvisi, and Mark A. Birrell. "The Role Of Transient Receptor Potential Melastatin 2 (TRPM2) In Murine Models Of Airway Inflammation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6411.

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Cheon, Dae Young, Joo-Hee Kim, Young-Suk Jang, Yong Il Hwang, Sunghoon Park, Dong-Gyu Kim, Seung-Hun Jang, and Ki-Suck Jung. "The activation of transient receptor potential melastatin 8 (TRPM8) receptors of bronchial epithelial cells induces airway inflammation in bronchial asthma." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3997.

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Kaoud, Tamer Saad, Jihyun Park, Clint D. J. Tavares, Shreya Mitra, Micael Cano, Chun-Chia Tseng, and Kevin N. Dalby. "Abstract 2722: Suppression of breast cancer cell migration by novel inhibitors that target transient receptor potential-melastatin-like 7 (Trpm7) kinase activity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2722.

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Toumpanakis, Dimitrios, Athanasia Chatzianastasiou, Vyronia Vassilakopoulou, Eleftheria Mizi, Stamatios Theocharis, and Theodoros Vassilakopoulos. "Transient receptor potential vanilloid 4 channels mediate resistive breathing-induced acute lung injury." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3298.

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Bonvini, Sara, Eric Dubuis, John Adcock, Michael Wortley, Mark Birrell, and Maria Belvisi. "Activation of transient receptor potential (TRP) channels by hypoosmolar solution: an endogenous mechanism of ATP release and afferent nerve activation." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa4410.

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