These authors contributed equally to this study.
Proteomic analysis of cPKCβII-interacting proteins involved in HPC-induced neuroprotection against cerebral ischemia of mice
Version of Record online: 1 MAR 2011
© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry
Journal of Neurochemistry
Volume 117, Issue 2, pages 346–356, April 2011
How to Cite
Bu, X., Zhang, N., Yang, X., Liu, Y., Du, J., Liang, J., Xu, Q. and Li, J. (2011), Proteomic analysis of cPKCβII-interacting proteins involved in HPC-induced neuroprotection against cerebral ischemia of mice. Journal of Neurochemistry, 117: 346–356. doi: 10.1111/j.1471-4159.2011.07209.x
- Issue online: 1 APR 2011
- Version of Record online: 1 MAR 2011
- Accepted manuscript online: 3 FEB 2011 12:00PM EST
- Received November 28, 2010; revised manuscript received/accepted January 28, 2011.
Figure S1. HPC inhibited the decrease of cPKCβII membrane translocation both in the ischemic core and penumbra of cortex following MCAO-induced ischemia. (a) Representative results of western blot showed the changes in cPKCβII membrane translocation and protein expression level in the ischemic core (I) and peri-infarct region (P) of control and HPC mice following MCAO. (b) Quantitative analysis demonstrated that cPKCβII membrane translocation decreased significantly, but HPC could inhibit the decrease of cPKCβII membrane translocation both in I and P of mouse cortex after MCAO. *p < 0.05 vs. S of control group, #p < 0.05 vs. S, I, P or C of control group, n = 5 per group. S, cortex of sham operated mice; C, contralateral cortex to MCAO-induced ischemic hemisphere.
Figure S2. Distribution of identified cPKCβII-interacting proteins in brain of HPC mice. The categorizations of molecular (a) and biological (b) functions were based on the information provided by the online resource PANTHER classification system.
Table S1. Identification of cPKCβII-interacting proteins by MALDI-TOF MS both in particulate and cytosolic fraction of mouse brain.
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