A key role for TRPM7 channels in anoxic neuronal death.

By M. Aarts, K. Iihara, Wenlin Wei, Z. Xiong, M. Arundine, Waldy Cerwinski, J. Macdonald, M. Tymianski. Cell, 2003

806 citations recorded by the source corpus.

Subfields: Nutrition and Dietetics, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/7bcc0c75926401a43fc7cbab860b828c28aa515b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Nutrition and Dietetics

1. B. Nilius
2. G. Owsianik
3. T. Voets
4. D. Julius

In Sensory Systems

1. B. Nilius
2. G. Owsianik
3. T. Voets
4. D. Clapham
5. M. Delling
6. Ramsey Delling Clapham
7. I. S. Ramsey
8. John A. Peters

Citations in the corpus

• Necrotic death as a cell fate. (2006, background): “In mammalian cells, Ca2+ has been shown to enter cells via voltage-sensitive L-type Ca2+ channels (Fryer et al. 1999), transient receptor potential (TRP) cation channels (Aarts et al. 2003), or ASIC (Xiong et al. 2004).”
• NMDA Receptor Subunits Have Differential Roles in Mediating Excitotoxic Neuronal Death Both In Vitro and In Vivo (2007, background): “Increasing evidence supports the fact that some of the non-NMDA receptormediated mechanisms, while secondary to NMDA receptor activation, may contribute significantly to brain damage, particularly after severe stroke insults (Aarts et al., 2003; Xiong et al., 2004).”
• An introduction to TRP channels. (2006, background): “TRPM7 may be regulated by reactive oxygen species to mediate anoxia-induced cell death in brain (151) and has been reported to be required for cell viability (152).”
• Transient receptor potential cation channels in disease. (2007, background): “Cases of anoxic neuronal death have been described that include the involvement of TRPM7 in cellular damage due to an imbalance of the normal physiological processes (1).”
• Excitotoxicity and stroke: identifying novel targets for neuroprotection. (2014, positive): “, 2007), and this inhibition likely accounts for the depression of synaptic NMDAR activity following oxygen– glucose deprivation (Aarts et al., 2003).”
• Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival (2008, background): “and allows Ca 2+ entry by activating the melastatin subfamily of TRP channel”
• TRP Channels (2012, neutral): “By directly patch clamping the LEL membrane, wild TRPML1 was shown to function as a cation channel and lysosomes (Fig.”
• Neuroprotection in ischemia: blocking calcium-permeable acid-sensing ion channels. (2004, background): “D). gated Ca2 channels (Aarts et al., 2003).”