Published 24 May 2004. doi:10.1083/jcb.20040511165357
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 165, Number 4, 593-593
Srinivasa Subramaniam,
Ute Zirrgiebel,
Oliver von Bohlen und Halbach,
Jens Strelau,
Christine Laliberté,
David R. Kaplan, and
Klaus Unsicker
Vol. 165, No. 3, May 10, 2004. Pages 357369.
This article originally appeared with errors in the legend to Fig. 7. The cyclohexamide (CHX) concentration should be 10 µg/ml, not 10 g/ml as published. The correct text is printed below.
Figure 7. Effect of antioxidants and protein synthesis inhibitor on neuronal degeneration and ERK/caspase-3 activation. At the time of potassium change (low K+), 5 mM N-acetyl cystein (N-AC), 50 U/ml superoxide dismutase (SOD), or 10 µg/ml cyclohexamide (CHX) was added; and triple staining and Western blot analysis were performed at the indicated time points. (A) The triple staining for the aforementioned groups at 24 h. ***P < 0.001, **P < 0.01, and *P < 0.05 compared with untreated cultures. (B) Western blot probed for total ERK (ERK), p-ERK, and caspase-3. (C) 5 mM N-AC, 50 U/ml SOD, and 10 µg/ml CHX were added immediately after potassium change, and cell extracts were assayed for caspase-3 activation; , untreated; blank, without cell extract. Error bars represent mean ± SEM from at least six experiments. (D) CHX does not act by binding to ERK and caspase-3. 10 µg/ml CHX was added at 0 and 12 h after the potassium switch. 20 µM U0126 was added at 12 h. The cell lysates were isolated after 13 h and processed for caspase-3 and ERK activation. Tubulin and total ERK blots reveal total protein loading.

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