motifs/domains
| two coiled-coil (CC) domains, one in the N-terminus required for protein expression and function, and the other in the C-terminus, playing an important, but not exclusive, role in the TRPM2 channel assembly |
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seven putative transmembrane domains protein |
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a highly conserved TRP (EWKFHR) domain and a nudix NUDT9 (nucleoside diphosphate linked moiety X-type motif 9) homology domain near the C terminus |
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a N-x-x-D motif playing specific roles in TRPM8 and TRPM2, reflecting different requirements for voltage-dependent and voltage-independent channel gating |
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seven predicted membrane-spanning domain |
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C terminal MutT motif |
basic FUNCTION
| permeable non selective cation channel, enabling Ca2+ influx into cells |
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TRPM2-mediated Ca2+ influx induces chemokine production in monocytes that aggravates inflammatory neutrophil infiltration |
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mediates nuclear translocation of NFKB, and amplifies Erk signal via Pyk2 and Ras activation |
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implicated in cell death induced by oxidants |
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required for lipopolysaccharide-induced cytokine production in monocytes |
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essential for prostate cancer cell proliferation |
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fulfills an important role in oxidative stress signaling in immune and other cells, to which local extracellular acidosis is known to occur under physiological or pathological conditions and impose significant effects on their functions |
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calcium-permeable non-selective cation channel critically involved in aggravating reactive oxygen species (ROS)-induced inflammatory processes and has been implicated in cell death |
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TRPM2, TRPM4 and TRPM5 control insulin secretion levels by sensing intracellular Ca2+ increase, NAD metabolites, or hormone receptor activation |
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redox-sensitive channel, mediating cell death |
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imbalance of TRPM2 channel activity caused by excess copper or ROS may be one of the pathophysiological mechanisms for disruption of Ca2+ homeostasis in diabetes and neurodegenerative disorders |
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extracellular acidity limits Ca2+ influx through TRPM2 by driving the channels into a conformation similar to the C-type inactivated state |
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TRPM2 channels occupy a key role in cell proliferation and survival following oxidative stress in neuroblastoma |
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role of TRPM2 and TRPV1 cation channels in cellular responses to radiation-induced DNA damage |
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key factor that links oxidative stress to the NLRP3 inflammasome activation |
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crucial role of a positively charged amino acid residue at position 1110 for TRPM2 channel activity |
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TRPM2 channels protect the heart from ischemia/reperfusion (I/R) injury by ameliorating mitochondrial dysfunction and reducing reactive oxygen species levels |
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its activity is required for immune cell activation and insulin secretion and is responsible for postischemic neuronal cell death |
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is a simple ligand-gated channel that obeys an equilibrium gating mechanism uncoupled from its enzymatic activity |
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TRPM2 channel limits oxidative stress and preserves mitochondrial function |
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cardiac TRPM2-mediated Ca2+ influx is necessary to maintain mitochondrial function and protect against hypoxia-reoxygenation (H/R) injury |