Supplementary Materials for:

Ca²⁺ controls gating of voltage-gated calcium channels by releasing the β2e subunit from the plasma membrane

Dong-Il Kim, Hae-Jin Kweon, Yongsoo Park, Deok-Jin Jang, Byung-Chang Suh*

*Corresponding author. Email: bcsuh{at}dgist.ac.kr

This PDF file includes:

• Fig. S1. Stimulation of endogenous purinergic receptors with ATP triggers β2e translocation to the cytosol.
• Fig. S2. Oxo-M- and ATP-induced translocation of PH-RFP and β2e-GFP in cells transfected with M₁R and P2Y2 receptors.
• Fig. S3. IP3K-A prevents the ATP-induced translocation of β2e-mCherry.
• Fig. S4. Phosphorylation is not a key factor for translocation of β2e.
• Fig. S5. β2e-mediated CDI of Ca_v2.3 channels is independent of CaM.
• Fig. S6. Purinergic activation induces translocation of β2e in PIPKIγ-expressing cells.
• Fig. S7. Depolarization by 30 mM K⁺ has no effect on membrane PIP₂ distribution.
• Fig. S8. Lyn-tagged N-del-β2e is localized to the plasma membrane.

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Citation: D.-I. Kim, H.-J. Kweon, Y. Park, D.-J. Jang, B.-C. Suh, Ca²⁺ controls gating of voltage-gated calcium channels by releasing the β2e subunit from the plasma membrane. Sci. Signal. 9, ra67 (2016).

© 2016 American Association for the Advancement of Science