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. 2020 Oct 14;21(20):7579. doi: 10.3390/ijms21207579

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Prostratin and GRC-2 induce PKC-δ/PKD-dependent ERK activation. (A) A549 cells were treated with DMSO, prostratin (3 μM), or GRC-2 (300 nM) for indicated periods. Minus (-) indicates no treatment and plus (+) indicates treatment with prostratin or GRC-2. Cells were harvested and subjected to immunoblotting for ERK, p21, p27, cyclin B1, CDK1, and p-cdc25c. (B) PKC-δ-, PKD-, or PKC-α knockdown cells were treated with DMSO, prostratin, or GRC-2 for 0.5 h (ERK) and 6 h (p21 and p27), respectively, followed by immunoblotting.