Supplementary Materials

Supplementary Materials for:

Membrane depolarization activates BK channels through ROCK-mediated β1 subunit surface trafficking to limit vasoconstriction

M. Dennis Leo, Xue Zhai, Padmapriya Muralidharan, Korah P. Kuruvilla, Simon Bulley, Frederick A. Boop, Jonathan H. Jaggar*

*Corresponding author. Email: jjaggar{at}uthsc.edu

This PDF file includes:

  • Fig. S1. Effect of different antagonists on depolarization- and SNP-induced changes in the surface abundance of BKα and β1 protein.
  • Fig. S2. Depolarization-induced surface trafficking of β1 subunits in human cerebral arteries.
  • Fig. S3. Overexpression of β1 subunits in HEK293 cells and colocalization analysis of BKα-β1 FRET with WGA.
  • Fig. S4. Effect of Rab11A shRNA or Rab11A dominant-negative mutant on Rab11A abundance and surface BKα protein.
  • Fig. S5. Regulation of surface BKα protein by antagonists and CaV1.2 and BKα proteins by CaV1.2 siRNA.
  • Fig. S6. Effect of ROCK 1 or ROCK2 knockdown and HA1100 on respective protein abundance.
  • Fig. S7. Rab11A knockdown does not alter vasoconstriction by membrane depolarization or myogenic tone.

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Citation: M. D. Leo, X. Zhai, P. Muralidharan, K. P. Kuruvilla, S. Bulley, F. A. Boop, J. H. Jaggar, Membrane depolarization activates BK channels through ROCK-mediated β1 subunit surface trafficking to limit vasoconstriction. Sci. Signal. 10, eaah5417 (2017).

© 2017 American Association for the Advancement of Science