Censoring the editor in transient forebrain ischemia.
A molecular explanation for why some neurons are more vulnerable than others to ischemic injury has long remained elusive. In this issue of Neuron, Peng et al. propose that CREB-dependent downregulation of the RNA editing enzyme ADAR2, resulting in defective Q/R editing of AMPA receptor GluR2 subunits and increased availability of calcium and zinc-permeable death-promoting AMPA receptors, underlies the vulnerability of some neuronal populations to ischemia.
Kittler
Josef T
JT
Department of Physiology, University College London, London WC1E 6BT, United Kingdom.
D000243:Adenosine Deaminase / Q000378:metabolism*; D000818:Animals; D050882:CREB-Binding Protein / Q000502:physiology*; D002118:Calcium; D016923:Cell Death / Q000502:physiology; D006801:Humans; D002546:Ischemic Attack, Transient / Q000473:pathology*; D009474:Neurons / Q000502:physiology*; D017393:RNA Editing; D016601:RNA-Binding Proteins; D015032:Zinc
D016601:RNA-Binding Proteins; D050882:CREB-Binding Protein; C567955:ADARB1 protein, human; D000243:Adenosine Deaminase; D015032:Zinc; D002118:Calcium