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Cell culture, animal models, and patient samples established that TRPM2 expression/function is important for dopaminergic neuronal survival and is increased in neurotoxin models that mimic Parkinson's Disease.
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These findings explain the molecular mechanism of concerted TRPM2 gating by adenosine diphosphate (ADP)-ribose and Ca(2+) and provide insights into the gating mechanism of other TRP channels.
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Data suggest that TRPM2 plays roles in viability of gastric cancer cell line and in survival of gastric cancer patients; TRPM2 appears to regulate autophagy, mitophagy (mitochondrial degradation), and apoptosis; TRPM2 modulates autophagy through a c-Jun N-terminal kinase (JNK)-dependent mechanism.
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TRPM2 overexpression in a PDAC cell line (PANC1) promoted cell proliferation, invasion and metastatic ability. TRPM2 represents a potential therapeutic target and prognostic marker for patients with PDAC.
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The expression of TRPM2-AS was higher in most HCC tissues and was significantly correlated with tumor size, AJCC stage, tumor differentiation, and the prognosis of HCC patients. Interfering TRPM2-AS expression using siRNA significantly inhibited cell proliferation and promoted cell apoptosis in two HCC cell lines.
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Results reveal a novel, potentially druggable signalling pathway for FFA-induced beta-cell death. The cascade involves NOX-2-dependent production of ROS, activation of TRPM2 channels, rise in mitochondrial Zn(2+), Drp-1 recruitment and abnormal mitochondrial fission.
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TRPM2 is essential for the survival and migration of squamous cell cancer cells.
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Results provide compelling evidence to support a role for nitrosative stress in linking the TRPM2 turnover with the disturbance of autophagy in brain pericyte injury.
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oxidative stress activates the TRPM2-Ca(2+)-CAMK2 cascade to phosphorylate BECN1 resulting in autophagy inhibition
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We conclude from these studies that inhibition of ROS production, and the subsequent abrogation of TRPM2-mediated Ca(2+) influx, is the primary mechanism underlying RE-1's inhibitory effect on LNs-induced inflammasome activation.
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oxidative stress activated the TRPM2-CaMKII cascade to further induce intracellular ROS production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential
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The work summarized here shows that TRPM2 channels protect cardiac myocytes from ischaemia-reperfusion injury and tumour cells from doxorubicin toxicity, and demonstrates that the mechanisms involve preservation of mitochondrial bioenergetics and modulation of ROS
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Activation of TRPM2 channels, however, caused intracellular release of not only Ca(2+) but also of Zn(2+) Intriguingly, elevation of intracellular Zn(2+) faithfully reproduced all of the effects of H2O2, whereas Ca(2+) showed opposite effects. Interestingly, H2O2 caused increased trafficking of Zn(2+)-enriched lysosomes to the leading edge of migrating cells, presumably to impart polarisation of Zn(2+) location.
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neutrophils sense reactive oxygen species via the TRPM2 channel to arrest migration at their target site.
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The inhibitory function of oxidant sensing by TRPM2 requires the oxidation of Cys549, which then induces TRMP2 binding to formyl peptide receptor 1 (FPR1) and subsequent FPR1 internalization and signaling inhibition
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findings demonstrate the important function of TRPM2 in modulation of cell survival through mitochondrial ROS, and the potential of targeted inhibition of TRPM2 as a therapeutic approach to reduce cellular bioenergetics, tumor growth, and enhance susceptibility to chemotherapeutic agents.
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Study demonstrate that PRL is necessary for the survival of (retinal pigment epithelium) RPE under normal and advancing age conditions and, identified SIRT2 and TRPM2 as molecular targets for the antioxidant and antiapoptotic actions of PRL in the RPE.
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TRPM2 has a role in the DNA damage response of T cell leukemia cells in a BCL-2 dependent manner
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Data show that HEK293 cells expressing low levels of receptor potential melastatin 2 (TRPM2) channel were more susceptible to silica nanoparticles (NPs) than those expressing high levels of TRPM2.
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This is expected to provide a basis for inhibiting TRPM2 for the improved treatment of breast cancer, which potentially includes treating breast tumors that are resistant to chemotherapy due to their evasion of apoptosis.
