Apr 5, 2010 · We show that the Bcl-2 homology domain 3 (BH3)–only protein Bim, a proapoptotic Bcl-2 family member, is activated in multiple excitotoxicity paradigms, mediates excitotoxic apoptosis, and inhibits delayed Ca 2+ deregulation, mitochondrial depolarization, and apoptosis-inducing factor translocation.

Apr 27, 2012 · We have previously shown that ATP depletion and activation of AMP-activated protein kinase (AMPK) during excitotoxic injury induces neuronal apoptosis by transcription of the pro-apoptotic...

AMPK, a highly conserved serine/threonine protein kinase, serves as a master sensor and regulator of energy balance and controls many cellular processes, such as autophagy, cell death, and inflammation to maintain cellular homeostasis (Peixoto et al., 2017).

We recently reported that AMP-activated protein kinase (AMPK) contributes to zinc-induced neuronal death by inducing Bim, a pro-apoptotic Bcl-2 homology domain 3-only protein, in a liver kinase B1 (LKB1)-dependent manner.

Mechanistically, direct binding of penfluridol and PFKL inhibits glucose consumption, lactate and ATP production, leads to nuclear translocation of FOXO3a and subsequent transcriptional activation of BIM in an AMPK-dependent manner.

In the present study, we demonstrate that Ang II activation of AMPK leads to transcriptional regulation of the proapoptotic BH3-only protein Bim in PAEC. Ang II-induced phosphorylation of AMPKβ1/2 causes disassociation of AMPK from Cdk4, upstream of Cdk4 hyperphosphorylation of Rb and its subsequent dissociation from E2F1, thus allowing E2F1 ...

Feb 6, 2019 · Pharmacological activation of AMPK enhances the BIM load in MYC-overexpressing cells (red arrow), which together with inhibition of BCL-2/X L triggers apoptosis.

Apr 5, 2010 · In this study, we demonstrate that even a transient decrease in cellular bioenergetics and an associated activation of adenosine monophosphate-activated protein kinase (AMPK) is necessary for the activation of excitotoxic apoptosis.

pro-longed AMPK activation is sufficient to induce bim gene expression and to trigger a bim-dependent cell death. Collectively, our data demonstrate that A. PK activation and the BH3-only protein Bim couple transient energy depletion to stress-induced neuronal a.

Activation of caspase-3 is induced by liver kinase B1 (LKB1)-AMP-activated kinase (AMPK)-Bim cascade signaling and induction of p75NTR receptors and p75NTR-associated Death Executor. Thus, zinc excitotoxicity is a mechanism of neuronal …