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A Novel TRPM2 Isoform Inhibits Calcium Influx and Susceptibility to Cell Death*
Exposure of TRPM2-S to HEK 293T cells inhibited susceptibility to cell death and onset of apoptosis induced by H2O2 in cells expressing TR PM2-L, and data demonstrate that TRPM 2-S is an important physiologic isoform ofTRPM2 and modulates channel activity and induction of cell death by oxidative stress through TRPM1-L. Expand
The Role of TRP Channels in Oxidative Stress-induced Cell Death
  • B. Miller
  • Biology, Medicine
  • The Journal of Membrane Biology
  • 17 April 2006
A dramatic increase in caspase 8, 9, 3, 7, and PARP cleavage was observed in TRPM2-expressing cells, demonstrating a downstream mechanism through which cell death is mediated, and physiologically important in oxidative stress-induced cell death. Expand
Regulation of the Transient Receptor Potential Channel TRPM2 by the Ca2+ Sensor Calmodulin*
It is suggested that Ca2+ entering through TRPM2 enhances interaction of CaM withTRPM2 at the IQ-like motif in the N terminus, providing crucial positive feedback for channel activation. Expand
Hydroxyurea enhances fetal hemoglobin production in sickle cell anemia.
Although examination of DNA synthesis in erythroid marrow cells in vitro revealed no decreased methylcytidine incorporation, Eco RI + Hpa II digestion of DNA revealed that hypomethylation of gamma-genes had taken place in vivo after treatment, suggesting that hydroxyurea is a potentially useful agent for the treatment of sickle cell anemia and that demethylation of the gamma-globin genes accompanies increased gamma- globin gene activity. Expand
TRPM2 is an ion channel that modulates hematopoietic cell death through activation of caspases and PARP cleavage.
The data show that one mechanism through which oxidative stress or TNF-alpha mediates cell death is activation of TRPM2, resulting in increased [Ca(2+)](i), followed by caspase activation and PARP cleavage, and this important cell death pathway is antagonized. Expand
Role of TRPM2 in cell proliferation and susceptibility to oxidative stress.
It is suggested that overexpression of TRPM2-S results in increased proliferation through phosphatidylinositol 3-kinase/Akt and ERK pathways, while overexposure of TR PM2-L confers protection against oxidative stress-induced cell death through FOXO3a and SOD. Expand
Regulation of TRP channel TRPM2 by the tyrosine phosphatase PTPL1.
Modulation of TRPM2 tyrosine phosphorylation is a mechanism through which PTPL1 may mediate resistance to cell death and inhibited the rise in [Ca(2+)](i) and the loss of cell viability, which follow H(2)O( 2) or TNFalpha treatment. Expand
TRPM2 mediates ischemic kidney injury and oxidant stress through RAC1.
It is demonstrated that TRPM2-dependent RAC1 activation increases oxidant stress and suggest that therapeutic approaches targeting TRPM1 and/or RAC2 may be effective in reducing ischemic kidney injury. Expand
TRP channels as mediators of oxidative stress.
Therapeutic approaches to modulate activation of specific TRP channels are likely to have an important impact in reducing tissue damage in a number of diseases resulting from oxidant stress including ischemia/reperfusion injury and diabetes. Expand
A Splice Variant of the Human Ion Channel TRPM2 Modulates Neuroblastoma Tumor Growth through Hypoxia-inducible Factor (HIF)-1/2α*
The data suggest that TRPM2 activity is important for tumor growth and for cell viability and survival following doxorubicin treatment and that interference with TR PM2-L function may be a novel approach to reduce tumor growth through modulation of HIF-1/2α, mitochondrial function, and mitophagy. Expand