2004
DOI: 10.1172/jci200421478
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Bim, Bad, and Bax: a deadly combination in epileptic seizures

Abstract: Several Bcl-2 family members, including Bim, may contribute to programmed cell death by inducing mitochondrial cytochrome c release, which activates caspase-9 and then caspase-3, the “executioner” of the cell. In this issue of the JCI, Shinoda and collaborators show the key role of Bim in epileptic seizure–induced neuronal injury and identify the contribution of transcription factors responsible for seizure-induced Bim upregulation

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Cited by 10 publications
(14 citation statements)
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“…PEBP4 also promotes the activation of AKT [9,16,17]. Activated AKT phosphorylates Bad, a member of Bcl-2 family, leading to the binding of Bad to the chaperone 14-3-3, which blocks the dimer formation of Bad and Bcl-2 or Bcl-xL, and prohibits Bad from promoting cell apoptosis [18]. The activated AKT can phosphorylate NF-κB and activate its transcriptional function, which promotes cell survival by enhancing the expression of a pro-survival member of the Bcl-2 family, Bcl-xL [19].…”
Section: Discussionmentioning
confidence: 99%
“…PEBP4 also promotes the activation of AKT [9,16,17]. Activated AKT phosphorylates Bad, a member of Bcl-2 family, leading to the binding of Bad to the chaperone 14-3-3, which blocks the dimer formation of Bad and Bcl-2 or Bcl-xL, and prohibits Bad from promoting cell apoptosis [18]. The activated AKT can phosphorylate NF-κB and activate its transcriptional function, which promotes cell survival by enhancing the expression of a pro-survival member of the Bcl-2 family, Bcl-xL [19].…”
Section: Discussionmentioning
confidence: 99%
“…Activated Akt can phosphorylate the Bcl-2 family member Bad and induce the interaction between Bad and the 14-3-3 chaperone. Therefore, the formation of dimers between Bad and Bcl-2 or Bcl-xL is blocked so that Bad cannot exert its pro-apoptotic function [23]. Akt can phosphorylate NF-κB and activate its transcriptional activity, thus promoting expression of the pro-survival protein Bcl-xL (also in the Bcl-2 family) to promote cell survival [24].…”
Section: Discussionmentioning
confidence: 99%
“…JNK can function to suppress tumors, which may be due to its role in tumor immune surveillance for regulating CD8 + T cells or may be related to the apoptotic functions of JNK activation [24]. The activation of AKT can phosphorylate the Bcl-2 family member Bad, which leads to the binding of the chaperone protein (Chaperone) 14-3-3, the subsequent blockade of Bad and Bcl-2 or Bcl-xL dimer formation, and inhibition of Bad-mediated apoptosis [25]. AKT can phosphorylate NF-κB, which activates its transcription function to promote the expression of Bcl-xL and Bcl-2 family members and subsequent cell survival [26].…”
Section: Discussionmentioning
confidence: 99%