TRPM2 Cation Channels, Oxidative Stress and Neurological Diseases: Where Are We Now?
Explore this paper's citation graph
Summary
TRPM2 channels in neuronal cells can be gated by either ADPR or H2O2, and it seems to that the exact relationship between TR PM2 channels activation and neuronal cell death still remains to be determined.
- Type
- review
- Published
- 2011-03-01
- Cited by
- 154
- References
- 70
- OpenAlex
- https://openalex.org/W1972085322
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:11367924
Keywords
TRPM2, Transient receptor potential channel, Oxidative stress, Flufenamic acid, Chemistry
References
- Molecular mechanisms of vitamin E on intracellular signalling pathways in brain.
- The Ca2+ release-activated Ca2+ current (ICRAC) mediates store-operated Ca2+ entry in rat microglia
- Inhibition of the transient receptor potential cation channel TRPM2 by 2‐aminoethoxydiphenyl borate (2‐APB)
- ADP-ribose gating of the calcium-permeable LTRPC2 channel revealed by Nudix motif homology
- N-(p-amylcinnamoyl)anthranilic acid (ACA): a phospholipase A(2) inhibitor and TRP channel blocker.
- TRPM3 is expressed in sphingosine‐responsive myelinating oligodendrocytes
- Ca2+‐dependent induction of TRPM2 currents in hippocampal neurons
- A critical role of TRPM2 in neuronal cell death by hydrogen peroxide.
- Calmodulin signaling via the IQ motif
- Differential expression of TRPM2 and TRPV4 channels and their potential role in oxidative stress-induced cell death in organotypic hippocampal culture.
- Role of an N-Terminal Splice Segment in the Activation of the Cation Channel TRPM2 by ADP-Ribose and Hydrogen Peroxide
- Second messenger function and the structure–activity relationship of cyclic adenosine diphosphoribose (cADPR)
- Cell death in the injured brain: roles of metallothioneins.
- Letter: Macronumbers of microorganisms.
- Guam amyotrophic lateral sclerosis-parkinsonism-dementia linked to a plant excitant neurotoxin.
- Transient Receptor Potential Melastatin 2 Expression is Increased Following Experimental Traumatic Brain Injury in Rats
- Acute action of rotenone on nigral dopaminergic neurons – involvement of reactive oxygen species and disruption of Ca2+ homeostasis
- Flufenamic acid is a pH-dependent antagonist of TRPM2 channels.
- Amyloid β‐peptide(1–42) and hydrogen peroxide‐induced toxicity are mediated by TRPM2 in rat primary striatal cultures
- TRPM channels, calcium and redox sensors during innate immune responses.
Cited by
- Calcium signaling in glioma cells--the role of nucleotide receptors.
- Particulates Initiate Immune Response Via Inducing Oxidative Stress-Mediated NLRP3 Inflammasome Activation
- [NAD+-converting enzymes in neuronal and glial cells: CD38 as a novel target for neuroprotection].
- Endothelial dysfunction and amyloid-β-induced neurovascular alterations
- Amlodipine besylate and amlodipine camsylate prevent cortical neuronal cell death induced by oxidative stress
- Hydrogen peroxide modulates synaptic transmission in ventral horn neurons of the rat spinal cord
- Role of TRPM2 cation channels in dorsal root ganglion of rats after experimental spinal cord injury
- Cerium and Yttrium Oxide Nanoparticles Against Lead-Induced Oxidative Stress and Apoptosis in Rat Hippocampus
- TRPM2 mediates the lysophosphatidic acid-induced neurite retraction in the developing brain
- Effects of Selenium on Calcium Signaling and Apoptosis in Rat Dorsal Root Ganglion Neurons Induced by Oxidative Stress
- Aminoethoxydiphenyl Borate and Flufenamic Acid Inhibit Ca2+ Influx Through TRPM2 Channels in Rat Dorsal Root Ganglion Neurons Activated by ADP-Ribose and Rotenone
- Reduction in traumatic brain injury-induced oxidative stress, apoptosis, and calcium entry in rat hippocampus by melatonin: Possible involvement of TRPM2 channels
- Perinatal Exposure to Lead: Reduction in Alterations of Brain Mitochondrial Antioxidant System with Calcium Supplement
- Ascorbic acid protects against colistin sulfate-induced neurotoxicity in PC12 cells
- Homocysteine and cytosolic GSH depletion induce apoptosis and oxidative toxicity through cytosolic calcium overload in the hippocampus of aged mice: involvement of TRPM2 and TRPV1 channels.
- Neuroprotection Induced by N-acetylcysteine and Selenium Against Traumatic Brain Injury-Induced Apoptosis and Calcium Entry in Hippocampus of Rat
- Redox Regulation of Transient Receptor Potential Channels
- Involvement of apoptosis and calcium accumulation through TRPV1 channels in neurobiology of epilepsy.
- Molecular role of catalase on oxidative stress-induced Ca2+ signaling and TRP cation channel activation in nervous system
- TRPM2 channel protective properties of N-acetylcysteine on cytosolic glutathione depletion dependent oxidative stress and Ca2+ influx in rat dorsal root ganglion.
Related papers
- Transient Receptor Potential Melastatin 2:an Ion Channel for Oxidative Stress Sensing.
- Two Decades of Evolution of Our Understanding of the Transient Receptor Potential Melastatin 2 (TRPM2) Cation Channel
- In with the TRP Channels: Intracellular Functions for TRPM1 and TRPM2
- Regulation of the Transient Receptor Potential Channel TRPM2 by the Ca2+ Sensor Calmodulin*
- Transient receptor potential melastatin 2 channels in neurological disorders: Mechanisms and animal models
- TRPM2: a multifunctional ion channel for oxidative stress sensing.
- TRPM2 in the Brain: Role in Health and Disease
- The transient receptor potential melastatin-2 (TRPM2) channel and inflammation
- TRPM2: a multifunctional ion channel for calcium signalling