JPET #132308 1 Estrogen Receptor Independent Neuroprotection Via Protein Phosphatase Preservation and Attenuation of Persistent ERK1/2 Activation

Abstract

The mechanism of estrogen-mediated neuroprotection is not yet clear. Estrogens have a variety of modes of action including transducing signaling events such as activation and/or suppression of the MAPK pathway. We have previously shown protein phosphatases to be involved in 17β-estradiol mediated neuroprotection. In the present study, we assessed the role of estrogen-receptors (ER) in estrogen-mediated neuroprotection from oxidative/excitotoxic stress and the consequential effects on MAPK signaling. Okadaic acid and calyculin A, non-specific serine/threonine phosphatase inhibitors, were exposed to cells at various concentrations in the presence or absence of 17α-estradiol, the enantiomer of 17β-estradiol,

Cite this paper

@inproceedings{Yi2007JPET1, title={JPET #132308 1 Estrogen Receptor Independent Neuroprotection Via Protein Phosphatase Preservation and Attenuation of Persistent ERK1/2 Activation}, author={Kun Yi and Zu Yun Cai and Douglas F Covey and James William Simpkins and JPET}, year={2007} }