Extended Data Fig. 5: Effect of protein kinase inhibition or activation on digoxin-mediated REV-ERBα protein level decrease.
Representative WES analysis (related to quantified data in Fig. 4) are shown. REV-ERBα protein level in synchronized AC16 cells treated with REV-ERBα protein levels were quantified after a 6 hour-treatment with or without digoxin and with or without enzyme inhibitors: (a) PP2 (20 µM, Src kinase inhibitor), (b) ZSTK474 (10 µM, PI3 kinase inhibitor), (c) SCH772984 (10 µM, ERK 1&2 inhibitor), (d) MK2206 (1 µM, AKT1/2/3 kinase inhibitor), (e) KN93 (10 µM, CAMK 2&4 inhibitor), (f) PD98059 (10 µM, MEK 1&2 inhibitor), (g) RP-8-pCPT-cGMPS (20 µM, PKG1&2), (h) CRT0066101 (5 µM, PKD inhibitor), (i) PF-4708671 (10 µM, P70S6K1 inhibitor), (j) BAY11-7082 (10 µM, LUBAC and UPS inhibitor), (k) HOIPIN8 (10 µM, LUBAC-HOIP specific inhibitor), (l) TPCA-1 (20 nM, IKKβinhibitor), (m) TPCA-1 (5 µM, IKKβ/α inhibitor) (n) amlexanox (1 µM, IKKε & TBK1 inhibitor). HSP90α was used as a protein loading control.
