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Статті в журналах з теми "Transient receptor potential melastatin channels"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

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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Анотація:

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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2

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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3

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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Анотація:

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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4

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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5

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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Анотація:

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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6

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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Анотація:

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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7

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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8

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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Анотація:

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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9

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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Анотація:

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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10

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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Анотація:

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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11

Inoue, Koichi, Deborah Branigan, and Zhi-Gang Xiong. "Zinc-induced Neurotoxicity Mediated by Transient Receptor Potential Melastatin 7 Channels." Journal of Biological Chemistry 285, no. 10 (January 4, 2010): 7430–39. http://dx.doi.org/10.1074/jbc.m109.040485.

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12

Kraft, Robert, and Christian Harteneck. "The mammalian melastatin-related transient receptor potential cation channels: an overview." Pflügers Archiv - European Journal of Physiology 451, no. 1 (May 14, 2005): 204–11. http://dx.doi.org/10.1007/s00424-005-1428-0.

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13

Earley, Scott. "Vanilloid and Melastatin Transient Receptor Potential Channels in Vascular Smooth Muscle." Microcirculation 17, no. 4 (March 8, 2010): 237–49. http://dx.doi.org/10.1111/j.1549-8719.2010.00026.x.

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14

Antunes, Tayze T., Glaucia E. Callera, Ying He, Alvaro Yogi, Alexey G. Ryazanov, Lillia V. Ryazanova, Alexander Zhai, Duncan J. Stewart, Alvin Shrier, and Rhian M. Touyz. "Transient Receptor Potential Melastatin 7 Cation Channel Kinase." Hypertension 67, no. 4 (April 2016): 763–73. http://dx.doi.org/10.1161/hypertensionaha.115.07021.

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15

de Baaij, Jeroen H. F., Maxime G. Blanchard, Marla Lavrijsen, Jens Leipziger, René J. M. Bindels, and Joost G. J. Hoenderop. "P2X4 receptor regulation of transient receptor potential melastatin type 6 (TRPM6) Mg2+ channels." Pflügers Archiv - European Journal of Physiology 466, no. 10 (January 12, 2014): 1941–52. http://dx.doi.org/10.1007/s00424-014-1440-3.

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16

Johnson, Christopher D., Donal Melanaphy, Andrew Purse, Susan A. Stokesberry, Paula Dickson, and Alexander V. Zholos. "Transient receptor potential melastatin 8 channel involvement in the regulation of vascular tone." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 6 (June 2009): H1868—H1877. http://dx.doi.org/10.1152/ajpheart.01112.2008.

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Анотація:

The transient receptor potential melastatin 8 (TRPM8) channel has been characterized as a cold and menthol receptor expressed in a subpopulation of sensory neurons but was recently identified in other tissues, including the respiratory tract, urinary system, and vasculature. Thus TRPM8 may play multiple functional roles, likely to be in a tissue- and activation state-dependent manner. We examined the TRPM8 channel presence in large arteries from rats and the functional consequences of their activation. We also aimed to examine whether these channels contribute to control of conscious human skin blood flow. TRPM8 mRNA and protein were detected in rat tail, femoral and mesenteric arteries, and thoracic aorta. This was confirmed in single isolated vascular myocytes by immunocytochemistry. Isometric contraction studies on endothelium-denuded relaxed rat vessels found small contractions on application of the TRPM8-specific agonist menthol (300 μM). However, both menthol and another agonist icilin (50 μM) caused relaxation of vessels precontracted with KCl (60 mM) or the α-adrenoceptor agonist phenylephrine (2 μM) and a reduction in sympathetic nerve-mediated contraction. These effects were antagonized by bromoenol lactone treatment, suggesting the involvement of Ca2+-independent phospholipase A2 activation in TRPM8-mediated vasodilatation. In thoracic aorta with intact endothelium, menthol-induced inhibition of KCl-induced contraction was enhanced. This was unaltered by preincubation with either Nω-nitro-l-arginine methyl ester (l-NAME; 100 nM), a nitric oxide synthase inhibitor, or the ACh receptor antagonist atropine (1 μM). Application of menthol (3% solution, topical application) to skin caused increased blood flow in conscious humans, as measured by laser Doppler fluximetry. Vasodilatation was markedly reduced or abolished by prior application of l-NAME (passive application, 10 mM) or atropine (iontophoretic application, 100 nM, 30 s at 70 μA). We conclude that TRPM8 channels are present in rat artery vascular smooth muscle and on activation cause vasoconstriction or vasodilatation, dependent on previous vasomotor tone. TRPM8 channels may also contribute to human cutaneous vasculature control, likely with the involvement of additional neuronal mechanisms.

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17

Nassini, Romina, Silvia Benemei, Camilla Fusi, Gabriela Trevisan, and Serena Materazzi. "Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy." Open Pain Journal 6, no. 1 (March 8, 2013): 127–36. http://dx.doi.org/10.2174/1876386301306010127.

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Chemotherapy-Induced Peripheral Neuropathy (CIPN) is a common dose-limiting side effect of many chemotherapeuticdrugs, including platinum-based compounds (e.g., cisplatin and oxaliplatin), taxanes (e.g., paclitaxel), vinca alkaloids (e.g., vincristine), and the first-in-class proteasome inhibitor, bortezomib. Among the various sensory symptoms of CIPN, paresthesia, dysesthesia, spontaneous pain, and mechanical and thermal hypersensitivity are prominent. Inflammation, oxidative stress, loss of intraepidermal nerve fibers, modifications of mitochondria, and various ion channels alterations are part of the several mechanisms contributing to CIPN. Because attempts to mitigate chemotherapeutic- induced acute neuronal hyperexcitability and the subsequent peripheral neuropathy have yielded unsatisfactory results, a more in-depth understanding of the mechanism(s) responsible for the neurotoxic action of anticancer drugs is required. Some members of the transient receptor potential (TRP) family of channels, as the TRPV1 and TRPV4 (vanilloid), TRPA1 (ankyrin) and TRPM8 (melastatin) are expressed on the plasma membrane of primary sensory neurons (nociceptors), where they are activated by an unprecedented series of physical and chemical stimuli. There is evidence that TRPV1, TRPV4, TRPA1 and TRPM8 are prominent contributors of mechanical and thermal hypersensitivity in models of CIPN. In particular, in vitro and in vivo studies have pointed out the unique role of TRPA1 and oxidative stress in the mechanism responsible for cold and mechanical hyperalgesia in rodent models of CIPN.

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18

Wang, Xin, Chiara W. Piccolo, Bruce M. Cohen, and Edgar A. Buttner. "Transient Receptor Potential Melastatin (TRPM) Channels Mediate Clozapine-induced Phenotypes inCaenorhabditis elegans." Journal of Neurogenetics 28, no. 1-2 (February 25, 2014): 86–97. http://dx.doi.org/10.3109/01677063.2013.879717.

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19

Yang, Wei, Paul T. Manna, Jie Zou, Jianhong Luo, David J. Beech, Asipu Sivaprasadarao, and Linhua Jiang. "Zinc Inactivates Melastatin Transient Receptor Potential 2 Channels via the Outer Pore." Biophysical Journal 102, no. 3 (January 2012): 343a. http://dx.doi.org/10.1016/j.bpj.2011.11.1882.

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20

Himmel, Nathaniel J., Jamin M. Letcher, Akira Sakurai, Thomas R. Gray, Maggie N. Benson, and Daniel N. Cox. "Drosophila menthol sensitivity and the Precambrian origins of transient receptor potential-dependent chemosensation." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1785 (September 23, 2019): 20190369. http://dx.doi.org/10.1098/rstb.2019.0369.

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Анотація:

Transient receptor potential (TRP) cation channels are highly conserved, polymodal sensors which respond to a wide variety of stimuli. Perhaps most notably, TRP channels serve critical functions in nociception and pain. A growing body of evidence suggests that transient receptor potential melastatin (TRPM) and transient receptor potential ankyrin (TRPA) thermal and electrophile sensitivities predate the protostome–deuterostome split (greater than 550 Ma). However, TRPM and TRPA channels are also thought to detect modified terpenes (e.g. menthol). Although terpenoids like menthol are thought to be aversive and/or harmful to insects, mechanistic sensitivity studies have been largely restricted to chordates. Furthermore, it is unknown if TRP-menthol sensing is as ancient as thermal and/or electrophile sensitivity. Combining genetic, optical, electrophysiological, behavioural and phylogenetic approaches, we tested the hypothesis that insect TRP channels play a conserved role in menthol sensing. We found that topical application of menthol to Drosophila melanogaster larvae elicits a Trpm - and TrpA1 -dependent nocifensive rolling behaviour, which requires activation of Class IV nociceptor neurons. Further, in characterizing the evolution of TRP channels, we put forth the hypotheses that three previously undescribed TRPM channel clades (basal, αTRPM and βTRPM), as well as TRPs with residues critical for menthol sensing, were present in ancestral bilaterians. This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.

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21

Fliegert, R., A. Gasser, and A. H. Guse. "Regulation of calcium signalling by adenine-based second messengers." Biochemical Society Transactions 35, no. 1 (January 22, 2007): 109–14. http://dx.doi.org/10.1042/bst0350109.

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cADPR [cyclic ADPR (ADP-ribose)], NAADP (nicotinic acid–adenine dinucleotide phosphate) and ADPR belong to the family of adenine-containing second messengers. They are metabolically related and are all involved in the regulation of cellular Ca2+ homoeostasis. Activation of specific plasma membrane receptors is connected to cADPR formation in many cell types and tissues. In contrast receptor-mediated formation of NAADP and ADPR has been shown only in a few selected cellular systems. The intracellular Ca2+ channel triggered by cADPR is the RyR (ryanodine receptor); in the case of NAADP, both activation of RyR and a novel Ca2+ channel have been proposed. In contrast, ADPR opens the non-specific cation channel TRPM2 [TRP (transient receptor potential) melastatin 2] that belongs to the TRP family of ion channels.

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22

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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Анотація:

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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23

Steinman, Joe, Andrea Ovcjak, Zhengwei Luo, Xinyang Zhang, Luiz Roberto Britto, Jeffrey T. Henderson, Hong-Shuo Sun, and Zhong-Ping Feng. "Transient receptor potential melastatin 2 channels in neurological disorders: Mechanisms and animal models." Advanced Neurology 1, no. 1 (April 8, 2022): 1–18. http://dx.doi.org/10.36922/an.v1i1.3.

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Анотація:

Transient receptor potential melastatin 2 (TRPM2) is a calcium-permeable ion channel implicated in neurodegenerative disorders and conditions. It is activated in response to reactive oxygen species (ROS) and thereby alters Ca2+ homeostasis and initiates pathways that lead to apoptosis and cell dysfunction. This review summarizes the current role of TRPM2 in neurological disorders, including Parkinson’s disease, Alzheimer’s disease, ischemia, traumatic brain injury, and depressive disorders (bipolar disease and depression). It describes the distribution and function of the TRPM2 channel across the brain and highlights common mechanisms between diseases. Specific animal and cell culture studies using TRPM2 inhibitors or genetic knockouts are discussed, including strategies to reduce the effect of ROS in disease through TRPM2 inhibition.

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24

Gavva, Narender R., Carl Davis, Sonya G. Lehto, Sara Rao, Weiya Wang, and Dawn XD Zhu. "Transient Receptor Potential Melastatin 8 (TRPM8) Channels are Involved in Body Temperature Regulation." Molecular Pain 8 (January 2012): 1744–8069. http://dx.doi.org/10.1186/1744-8069-8-36.

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25

Miller, Barbara A., JuFang Wang, Iwona Hirschler-Laszkiewicz, Erhe Gao, Jianliang Song, Xue-Qian Zhang, Walter J. Koch, et al. "The second member of transient receptor potential-melastatin channel family protects hearts from ischemia-reperfusion injury." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 7 (April 1, 2013): H1010—H1022. http://dx.doi.org/10.1152/ajpheart.00906.2012.

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The second member of the transient receptor potential-melastatin channel family (TRPM2) is expressed in the heart and vasculature. TRPM2 channels were expressed in the sarcolemma and transverse tubules of adult left ventricular (LV) myocytes. Cardiac TRPM2 channels were functional since activation with H2O2 resulted in Ca2+ influx that was dependent on extracellular Ca2+, was significantly higher in wild-type (WT) myocytes compared with TRPM2 knockout (KO) myocytes, and inhibited by clotrimazole in WT myocytes. At rest, there were no differences in LV mass, heart rate, fractional shortening, and +dP/d t between WT and KO hearts. At 2–3 days after ischemia-reperfusion (I/R), despite similar areas at risk and infarct sizes, KO hearts had lower fractional shortening and +dP/d t compared with WT hearts. Compared with WT I/R myocytes, expression of the Na+/Ca2+ exchanger (NCX1) and NCX1 current were increased, expression of the α1-subunit of Na+-K+-ATPase and Na+ pump current were decreased, and action potential duration was prolonged in KO I/R myocytes. Post-I/R, intracellular Ca2+ concentration transients and contraction amplitudes were equally depressed in WT and KO myocytes. After 2 h of hypoxia followed by 30 min of reoxygenation, levels of ROS were significantly higher in KO compared with WT LV myocytes. Compared with WT I/R hearts, oxygen radical scavenging enzymes (SODs) and their upstream regulators (forkhead box transcription factors and hypoxia-inducible factor) were lower, whereas NADPH oxidase was higher, in KO I/R hearts. We conclude that TRPM2 channels protected hearts from I/R injury by decreasing generation and enhancing scavenging of ROS, thereby reducing I/R-induced oxidative stress.

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Kim, Taek-Keun, Joo Hyun Nam, Won-Gyun Ahn, Nam-Ho Kim, Hwa-Yong Ham, Chang-Won Hong, Ju-Suk Nam, et al. "Lys1110 of TRPM2 is critical for channel activation." Biochemical Journal 455, no. 3 (October 10, 2013): 319–27. http://dx.doi.org/10.1042/bj20130303.

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Mandadi, S., S. T. Nakanishi, Y. Takashima, A. Dhaka, A. Patapoutian, D. D. McKemy, and P. J. Whelan. "Locomotor networks are targets of modulation by sensory transient receptor potential vanilloid 1 and transient receptor potential melastatin 8 channels." Neuroscience 162, no. 4 (September 2009): 1377–97. http://dx.doi.org/10.1016/j.neuroscience.2009.05.063.

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Zouharova, Monika, Petr Herman, Kateřina Hofbauerová, Jiri Vondrasek, and Kristyna Bousova. "TRPM6 N-Terminal CaM- and S100A1-Binding Domains." International Journal of Molecular Sciences 20, no. 18 (September 9, 2019): 4430. http://dx.doi.org/10.3390/ijms20184430.

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Transient receptor potential (TRPs) channels are crucial downstream targets of calcium signalling cascades. They can be modulated either by calcium itself and/or by calcium-binding proteins (CBPs). Intracellular messengers usually interact with binding domains present at the most variable TRP regions—N- and C-cytoplasmic termini. Calmodulin (CaM) is a calcium-dependent cytosolic protein serving as a modulator of most transmembrane receptors. Although CaM-binding domains are widespread within intracellular parts of TRPs, no such binding domain has been characterised at the TRP melastatin member—the transient receptor potential melastatin 6 (TRPM6) channel. Another CBP, the S100 calcium-binding protein A1 (S100A1), is also known for its modulatory activities towards receptors. S100A1 commonly shares a CaM-binding domain. Here, we present the first identified CaM and S100A1 binding sites at the N-terminal of TRPM6. We have confirmed the L520-R535 N-terminal TRPM6 domain as a shared binding site for CaM and S100A1 using biophysical and molecular modelling methods. A specific domain of basic amino acid residues (R526/R531/K532/R535) present at this TRPM6 domain has been identified as crucial to maintain non-covalent interactions with the ligands. Our data unambiguously confirm that CaM and S100A1 share the same binding domain at the TRPM6 N-terminus although the ligand-binding mechanism is different.

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Woo, Seung Kyoon, Min Seong Kwon, Alexander Ivanov, Volodymyr Gerzanich, and J. Marc Simard. "The Sulfonylurea Receptor 1 (Sur1)-Transient Receptor Potential Melastatin 4 (Trpm4) Channel." Journal of Biological Chemistry 288, no. 5 (December 19, 2012): 3655–67. http://dx.doi.org/10.1074/jbc.m112.428219.

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30

HEINER, Inka, Jörg EISFELD, Christian R. HALASZOVICH, Edith WEHAGE, Eberhard JÜNGLING, Christof ZITT, and Andreas LÜCKHOFF. "Expression profile of the transient receptor potential (TRP) family in neutrophil granulocytes: evidence for currents through long TRP channel 2 induced by ADP-ribose and NAD." Biochemical Journal 371, no. 3 (May 1, 2003): 1045–53. http://dx.doi.org/10.1042/bj20021975.

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An early key event in the activation of neutrophil granulocytes is Ca2+ influx. Members of the transient receptor potential (TRP) channel family may be held responsible for this. The aim of the present study is to analyse the expression pattern of TRP mRNA and identify characteristic currents unambiguously attributable to particular TRP channels. mRNA was extracted from human neutrophils, isolated by gradient centrifugation and also by magnetically labelled CD15 antibodies. The presence of mRNA was demonstrated using reverse transcriptase–PCR in neutrophils (controlled to be CD5-negative) as well as in human leukaemic cell line 60 (HL-60) cells, for the following TRP species: the long TRPC2 (LTRPC2), the vanilloid receptor 1, the vanilloid receptor-like protein 1 and epithelial Ca2+ channels 1 and 2. TRPC6 was specific for neutrophils, whereas only in HL-60 cells were TRPC1, TRPC2, TRPC3, melastatin 1 and melastatin-related 1 found. Patch-clamp measurements in neutrophils revealed non-selective cation currents evoked by intracellular ADP-ribose and by NAD+. Both these modes of activation have been found to be characteristic of LTRPC2. Furthermore, single-channel activity was resolved in neutrophils and it was indistinguishable from that in LTRPC2-transfected HEK-293 cells. The results provide evidence that LTRPC2 in neutrophil granulocytes forms an entry pathway for Na+ and Ca2+, which is regulated by ADP-ribose and the redox state.

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Chelaru, Nicoleta-Raluca, Andrei Chiosa, Andrei Sorop, Andreea Spiridon, Florentina Cojocaru, Dan Domocos, Dana Cucu, Irinel Popescu, and Simona-Olimpia Dima. "The Association between TRP Channels Expression and Clinicopathological Characteristics of Patients with Pancreatic Adenocarcinoma." International Journal of Molecular Sciences 23, no. 16 (August 12, 2022): 9045. http://dx.doi.org/10.3390/ijms23169045.

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Pancreatic adenocarcinoma (PDAC) has low survival rates worldwide due to its tendency to be detected late and its characteristic desmoplastic reaction, which slows the use of targeted therapies. As such, the discovery of new connections between genes and the clinicopathological parameters contribute to the search for new biomarkers or targets for therapy. Transient receptor potential (TRP) channels are promising tools for cancer therapy or markers for PDAC. Therefore, in this study, we selected several genes encoding TRP proteins previously reported in cellular models, namely, Transient Receptor Potential Cation Channel Subfamily V Member 6 (TRPV6), Transient receptor potential ankyrin 1 (TRPA1), and Transient receptor potential cation channel subfamily M (melastatin) member 8 (TRPM8), as well as the TRPM8 Channel Associated Factor 1 (TCAF1) and TRPM8 Channel Associated Factor 2 (TCAF2) proteins, as regulatory factors. We analyzed the expression levels of tumors from patients enrolled in public datasets and confirmed the results with a validation cohort of PDAC patients enrolled in the Clinical Institute Fundeni, Romania. We found significantly higher expression levels of TRPA1, TRPM8, and TCAF1/F2 in tumoral tissues compared to normal tissues, but lower expression levels of TRPV6, suggesting that TRP channels have either tumor-suppressive or oncogenic roles. The expression levels were correlated with the tumoral stages and are related to the genes involved in calcium homeostasis (Calbindin 1 or S100A4) or to proteins participating in metastasis (PTPN1). We conclude that the selected TRP proteins provide new insights in the search for targets and biomarkers needed for therapeutic strategies for PDAC treatment.

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Smith, Amy C., Kiril L. Hristov, Qiuping Cheng, Wenkuan Xin, Shankar P. Parajuli, Scott Earley, John Malysz, and Georgi V. Petkov. "Novel role for the transient potential receptor melastatin 4 channel in guinea pig detrusor smooth muscle physiology." American Journal of Physiology-Cell Physiology 304, no. 5 (March 1, 2013): C467—C477. http://dx.doi.org/10.1152/ajpcell.00169.2012.

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Members of the transient receptor potential (TRP) channel superfamily, including the Ca2+-activated monovalent cation-selective TRP melastatin 4 (TRPM4) channel, have been recently identified in the urinary bladder. However, their expression and function at the level of detrusor smooth muscle (DSM) remain largely unexplored. In this study, for the first time we investigated the role of TRPM4 channels in guinea pig DSM excitation-contraction coupling using a multidisciplinary approach encompassing protein detection, electrophysiology, live-cell Ca2+ imaging, DSM contractility, and 9-phenanthrol, a recently characterized selective inhibitor of the TRPM4 channel. Western blot and immunocytochemistry experiments demonstrated the expression of the TRPM4 channel in whole DSM tissue and freshly isolated DSM cells with specific localization on the plasma membrane. Perforated whole cell patch-clamp recordings and real-time Ca2+ imaging experiments with fura 2-AM, both using freshly isolated DSM cells, revealed that 9-phenanthrol (30 μM) significantly reduced the cation current and decreased intracellular Ca2+ levels. 9-Phenanthrol (0.1–30 μM) significantly inhibited spontaneous, 0.1 μM carbachol-induced, 20 mM KCl-induced, and nerve-evoked contractions in guinea pig DSM-isolated strips with IC50 values of 1–7 μM and 70–80% maximum inhibition. 9-Phenanthrol also reduced nerve-evoked contraction amplitude induced by continuous repetitive electrical field stimulation of 10-Hz frequency and shifted the frequency-response curve (0.5–50 Hz) relative to the control. Collectively, our data demonstrate the novel finding that TRPM4 channels are expressed in guinea pig DSM and reveal their critical role in the regulation of guinea pig DSM excitation-contraction coupling.

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Wykes, Rob C. E., Moonhee Lee, S. Mark Duffy, Weidong Yang, Elizabeth P. Seward, and Peter Bradding. "Functional Transient Receptor Potential Melastatin 7 Channels Are Critical for Human Mast Cell Survival." Journal of Immunology 179, no. 6 (September 4, 2007): 4045–52. http://dx.doi.org/10.4049/jimmunol.179.6.4045.

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34

Kim, Byung Joo. "Effects of Dangkwisoo-San, Ginger and Curcumin on Transient Receptor Potential Melastatin 7 Channels." Journal of Korean Medicine for Obesity Research 18, no. 1 (June 30, 2018): 10–18. http://dx.doi.org/10.15429/jkomor.2018.18.1.10.

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35

MacDonald, John F., and Michael F. Jackson. "Transient Receptor Potential Channels of the Melastatin Family and Ischemic Responses of Central Neurons." Stroke 38, no. 2 (February 2007): 665–69. http://dx.doi.org/10.1161/01.str.0000251671.77351.e2.

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36

Starkus, John G., Peter Poerzgen, Kristine Layugan, Kelly Galbraith Kawabata, Jun-Ichi Goto, Sayuri Suzuki, George Myers, et al. "Scalaradial Is a Potent Inhibitor of Transient Receptor Potential Melastatin 2 (TRPM2) Ion Channels." Journal of Natural Products 80, no. 10 (October 11, 2017): 2741–50. http://dx.doi.org/10.1021/acs.jnatprod.7b00515.

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37

Matsumoto, Kenjiro, Kanako Takagi, Atsumi Kato, Takuya Ishibashi, Yasuo Mori, Kimihito Tashima, Atsushi Mitsumoto, Shinichi Kato, and Syunji Horie. "Role of transient receptor potential melastatin 2 (TRPM2) channels in visceral nociception and hypersensitivity." Experimental Neurology 285 (November 2016): 41–50. http://dx.doi.org/10.1016/j.expneurol.2016.09.001.

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38

Kim, Byung Joo. "The role of ginseng total saponin in transient receptor potential melastatin type 7 channels." Animal Cells and Systems 16, no. 5 (October 2012): 376–84. http://dx.doi.org/10.1080/19768354.2012.680495.

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39

Hecquet, Claudie, and Asrar Malik. "Role of H2O2-activated TRPM2 calcium channel in oxidant-induced endothelial injury." Thrombosis and Haemostasis 101, no. 04 (2009): 619–25. http://dx.doi.org/10.1160/th08-10-0641.

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SummaryThe transient receptor potential (melastatin) 2 (TRPM2), is an oxidant-activated non-selective cation channel that is widely expressed in mammalian tissues including the vascular endothelium. Oxidative stress, through the generation of oxygen meta-bolites including H2O2, stimulates intracellular ADP-ribose formation which, in turn, opens TRPM2 channels. These channels act as an endogenous redox sensor for mediating oxidative stress/ROS-induced Ca2+ entry and the subsequent specific Ca2+-dependent cellular reactions such as endothelial hyper-permeability and apoptosis. This review summarizes recent findings on the mechanism by which oxidants induce TRPM2 activation, the role of these channels in the signalling vascular endothelial dysfunctions, and the modulation of oxidant-induced TRPM2 activation by PKCα and phospho-tyrosine phosphates L1.

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40

Hristov, Kiril L., Amy C. Smith, Shankar P. Parajuli, John Malysz, Eric S. Rovner, and Georgi V. Petkov. "Novel regulatory mechanism in human urinary bladder: central role of transient receptor potential melastatin 4 channels in detrusor smooth muscle function." American Journal of Physiology-Cell Physiology 310, no. 7 (April 1, 2016): C600—C611. http://dx.doi.org/10.1152/ajpcell.00270.2015.

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Transient receptor potential melastatin 4 (TRPM4) channels are Ca2+-activated nonselective cation channels that have been recently identified as regulators of detrusor smooth muscle (DSM) function in rodents. However, their expression and function in human DSM remain unexplored. We provide insights into the functional role of TRPM4 channels in human DSM under physiological conditions. We used a multidisciplinary experimental approach, including RT-PCR, Western blotting, immunohistochemistry and immunocytochemistry, patch-clamp electrophysiology, and functional studies of DSM contractility. DSM samples were obtained from patients without preoperative overactive bladder symptoms. RT-PCR detected mRNA transcripts for TRPM4 channels in human DSM whole tissue and freshly isolated single cells. Western blotting and immunohistochemistry with confocal microscopy revealed TRPM4 protein expression in human DSM. Immunocytochemistry further detected TRPM4 protein expression in DSM single cells. Patch-clamp experiments showed that 9-phenanthrol, a selective TRPM4 channel inhibitor, significantly decreased the transient inward cation currents and voltage step-induced whole cell currents in freshly isolated human DSM cells. In current-clamp mode, 9-phenanthrol hyperpolarized the human DSM cell membrane potential. Furthermore, 9-phenanthrol attenuated the spontaneous phasic, carbachol-induced and nerve-evoked contractions in human DSM isolated strips. Significant species-related differences in TRPM4 channel activity between human, rat, and guinea pig DSM were revealed, suggesting a more prominent physiological role for the TRPM4 channel in the regulation of DSM function in humans than in rodents. In conclusion, TRPM4 channels regulate human DSM excitability and contractility and are critical determinants of human urinary bladder function. Thus, TRPM4 channels could represent promising novel targets for the pharmacological or genetic control of overactive bladder.

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41

Kim, Byung Joo, Sung-Young Kim, Sanghoon Lee, Ju-Hong Jeon, Hirofumi Matsui, Young Kyu Kwon, Seon Jeong Kim, and Insuk So. "The role of transient receptor potential channel blockers in human gastric cancer cell viability." Canadian Journal of Physiology and Pharmacology 90, no. 2 (February 2012): 175–86. http://dx.doi.org/10.1139/y11-114.

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Transient receptor potential cation channel, subfamily M, receptor 7 (TRPM7) is a ubiquitous divalent-selective ion channel with its own kinase domain. Human gastric cancer cells express the TRPM7 channel, and the presence of this channel is essential for cell survival. Recent studies have suggested that 5-lipoxygenase (5-LOX) inhibitors are potent blockers of the TRPM7 channels. The aim of this study was to show the effects of 5-LOX inhibitors on the growth and survival of gastric cancer cells. Among 5-LOX inhibitors, nordihydroguaiaretic acid (NDGA), 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA861), and 3-[1-(p-chlorobenzyl)-5-(isopropyl)-3-tert-butylthioindol-2-yl]-2,2-dimethylpropanoic acid (MK886) were potent blockers of TRPM7-like currents in gastric cancer cells and also induced cell death. However, zileuton was ineffective in suppressing TRPM7-like current activity and inducing cell death. Moreover, a specific transient receptor potential cation channel, subfamily C, member 3 (TRPC3) inhibitor, a pyrazole compound (Pyr3), and a specific melastatin TRP (TRPM4) inhibitor, 9-phenanthrol, did not affect TRPM7-like currents or induce cell death. We conclude that TRPM7 has an important role in the growth and survival of gastric cancer cells and a likely potential target for the pharmacological treatment of gastric cancer.

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42

Gerka-Stuyt, John, Adrian Au, Neal S. Peachey, and Kumar N. Alagramam. "Transient Receptor Potential Melastatin 1: A Hair Cell Transduction Channel Candidate." PLoS ONE 8, no. 10 (October 11, 2013): e77213. http://dx.doi.org/10.1371/journal.pone.0077213.

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Blanchard, Maxime G., Jeroen H. F. de Baaij, Sjoerd A. J. Verkaart, Anke L. Lameris, Christine Basmadjian, Qian Zhao, Laurent Désaubry, René J. M. Bindels, and Joost G. J. Hoenderop. "Flavaglines Stimulate Transient Receptor Potential Melastatin Type 6 (TRPM6) Channel Activity." PLOS ONE 10, no. 3 (March 16, 2015): e0119028. http://dx.doi.org/10.1371/journal.pone.0119028.

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44

LeGay, Christina M., Evgueni Gorobets, Mircea Iftinca, Rithwik Ramachandran, Christophe Altier, and Darren J. Derksen. "Natural-Product-Derived Transient Receptor Potential Melastatin 8 (TRPM8) Channel Modulators." Organic Letters 18, no. 11 (May 12, 2016): 2746–49. http://dx.doi.org/10.1021/acs.orglett.6b01222.

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45

Toth, Balazs I., Joris Vriens, Debapriya Ghosh, and Thomas Voets. "Cellular Regulation of Transient Receptor Potential Melastatin 3 (TRPM3) Channel Activity." Biophysical Journal 106, no. 2 (January 2014): 334a. http://dx.doi.org/10.1016/j.bpj.2013.11.1913.

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46

Oh, Hyun Geun, Yoon Sun Chun, Yonjung Kim, Sung Hee Youn, Sora Shin, Myoung Kyu Park, Tae-Wan Kim, and Sungkwon Chung. "Modulation of transient receptor potential melastatin related 7 channel by presenilins." Developmental Neurobiology 72, no. 6 (May 14, 2012): 865–77. http://dx.doi.org/10.1002/dneu.22001.

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47

Touyz, Rhian M. "Transient receptor potential melastatin 6 and 7 channels, magnesium transport, and vascular biology: implications in hypertension." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 3 (March 2008): H1103—H1118. http://dx.doi.org/10.1152/ajpheart.00903.2007.

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Magnesium, an essential intracellular cation, is critically involved in many biochemical reactions involved in the regulation of vascular tone and integrity. Decreased magnesium concentration has been implicated in altered vascular reactivity, endothelial dysfunction, vascular inflammation, and structural remodeling, processes important in vascular changes and target organ damage associated with hypertension. Until recently, very little was known about mechanisms regulating cellular magnesium homeostasis, and processes controlling transmembrane magnesium transport had been demonstrated only at the functional level. Two cation channels of the transient receptor potential melastatin (TRPM) cation channel family have now been identified as magnesium transporters, TRPM6 and TRPM7. These unique proteins, termed chanzymes because they possess a channel and a kinase domain, are differentially expressed, with TRPM6 being found primarily in epithelial cells and TRPM7 occurring ubiquitously. Vascular TRPM7 is modulated by vasoactive agents, pressure, stretch, and osmotic changes and may be a novel mechanotransducer. In addition to its magnesium transporter function, TRPM7 has been implicated as a signaling kinase involved in vascular smooth muscle cell growth, apoptosis, adhesion, contraction, cytoskeletal organization, and migration, important processes involved in vascular remodeling associated with hypertension and other vascular diseases. Emerging evidence suggests that vascular TRPM7 function may be altered in hypertension. This review discusses the importance of magnesium in vascular biology and implications in hypertension and highlights the transport systems, particularly TRPM6 and TRPM7, which may play a role in the control of vascular magnesium homeostasis. Since the recent identification and characterization of Mg2+-selective transporters, there has been enormous interest in the field. However, there is still a paucity of information, and much research is needed to clarify the exact mechanisms of magnesium regulation in the cardiovascular system and the implications of aberrant transmembrane magnesium transport in the pathogenesis of hypertension and other vascular diseases.

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48

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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49

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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50

Szollosi, Andras. "Two Decades of Evolution of Our Understanding of the Transient Receptor Potential Melastatin 2 (TRPM2) Cation Channel." Life 11, no. 5 (April 27, 2021): 397. http://dx.doi.org/10.3390/life11050397.

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The transient receptor potential melastatin (TRPM) family belongs to the superfamily of TRP ion channels. It consists of eight family members that are involved in a plethora of cellular functions. TRPM2 is a homotetrameric Ca2+-permeable cation channel activated upon oxidative stress and is important, among others, for body heat control, immune cell activation and insulin secretion. Invertebrate TRPM2 proteins are channel enzymes; they hydrolyze the activating ligand, ADP-ribose, which is likely important for functional regulation. Since its cloning in 1998, the understanding of the biophysical properties of the channel has greatly advanced due to a vast number of structure–function studies. The physiological regulators of the channel have been identified and characterized in cell-free systems. In the wake of the recent structural biochemistry revolution, several TRPM2 cryo-EM structures have been published. These structures have helped to understand the general features of the channel, but at the same time have revealed unexplained mechanistic differences among channel orthologues. The present review aims at depicting the major research lines in TRPM2 structure-function. It discusses biophysical properties of the pore and the mode of action of direct channel effectors, and interprets these functional properties on the basis of recent three-dimensional structural models.

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