LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death.
By Y. Hara, M. Wakamori, M. Ishii, E. Maeno, M. Nishida, Takashi Yoshida, Hisanobu Yamada, S. Shimizu, E. Mori, J. Kudoh and 5 more. Molecules and Cells, 2002
817 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Sensory Systems
View Paper: https://www.semanticscholar.org/paper/ed91b86b73008b103359e0cdae5167446047cf1c
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Citations in the corpus
- The TRP Superfamily of Cation Channels (2005, background): “The alteration in redox state appears to activate TRPM2 through binding of β-NAD+ (nicotinamide adenine dinucleotide) to the NUDT9 domain (174).”
- Stress response, cell death and signalling: the many faces of reactive oxygen species (2003, background): “…directly or indirectly through a calmodulin-regulated NAD kinase (Pou De Crescenzo et al. 2001, Sagi and Fluhr 2001) and because calcium channels are redox regulated (Hamilton and Reid 2000, Hara et al. 2002, Lecourieux et al. 2002), an initial perturbation of either signature can alter both.”
- Reactive Oxygen Species in Inflammation and Tissue Injury (2014, neutral): “(164) demonstrated that TRPM2 is a Ca(2) + permeable cation channel and can be activated by H2O2 via”
- An introduction to TRP channels. (2006, background): “0 antagonist (56, 75, 126) I HEK, SCG 2-APB TRPV1 114-249μM 1.”
- A key role for TRPM7 channels in anoxic neuronal death. (2003, methodology): “As previously observed, neurons exmodulation by ROS (Hara et al., 2002; Wehage et al., posed to 1 hr OGD in the absence of MCN succumbed 2002), and we have shown that siRNA targeted against by 24 hr, whereas those treated with MCN survived TRPM7 may also inhibit TRPM2 mRNA (Figure 7C).”