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. Author manuscript; available in PMC: 2017 Dec 5.
Published in final edited form as: Adv Exp Med Biol. 2017;963:337–358. doi: 10.1007/978-3-319-50044-7_20

Figure 3. Regulation of p90RSK-SENP2 to increase EC dysfunction by athero-prone flow.

Figure 3

p90RSK is uniquely activated by athero-prone (d-flow) flow. SENP2 contains several NLS and NES domains, and we found that p90RSK activation induces SENP2 nuclear export by phosphorylation of SENP2 Thr368 and direct binding to SENP2 aa131–300. This SENP2 nuclear export subsequently up-regulates SUMO modulation of nuclear p53 and ERK5, and increase apoptosis and EC inflammation, respectively. In addition, the increase of ERK5 SUMOylation decreases eNOS expression.