Bax shuttling after rotenone treatment of neuronal primary cultures: effects on cell death phenotypes.

@article{Gill2009BaxSA,
  title={Bax shuttling after rotenone treatment of neuronal primary cultures: effects on cell death phenotypes.},
  author={Martin B. Gill and Jose Regino Perez-Polo},
  journal={Journal of neuroscience research},
  year={2009},
  volume={87 9},
  pages={2047-65}
}
Neonatal (P7) brain hypoxia-ischemia (HI) induces intracellular Bax protein shifts to the nucleus, mitochondria, and endoplasmic reticulum (ER), where it triggers the activation of the respective cell death signaling cascades. When compared with HI-treated rat pups, 100% O(2) resuscitation of HI-treated rat pups increases HI-induced ER Bax levels, ER-mediated cell death signaling, and resultant lesion volume and inflammation due to increased necrotic-like cell death. To better characterize the… CONTINUE READING

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