Supplementary Materials

Supplementary Materials for:

Ca2+ signals regulate mitochondrial metabolism by stimulating CREB-mediated expression of the mitochondrial Ca2+ uniporter gene MCU

Santhanam Shanmughapriya, Sudarsan Rajan, Nicholas E. Hoffman, Xueqian Zhang, Shuchi Guo, Jill E. Kolesar, Kevin J. Hines, Jonathan Ragheb, Neelakshi R. Jog, Roberto Caricchio, Yoshihiro Baba, Yandong Zhou, Brett A. Kaufman, Joseph Y. Cheung, Tomohiro Kurosaki, Donald L. Gill,* Muniswamy Madesh*

*Corresponding author. E-mail: madeshm{at}temple.edu (M.M.); dongill{at}psu.edu (D.L.G.)

This PDF file includes:

  • Fig. S1. KO of IP3Rs or CRAC channel components does not alter basal mitochondrial membrane potential (ΔΨm).
  • Fig. S2. Inhibitors of acidic intracellular compartments do not alter mitochondrial Ca2+ uptake in HEK293T cells.
  • Fig. S3. KO of IP3Rs or CRAC channel components reduces resting [Ca2+]m.
  • Fig. S4. KO of IP3Rs or CRAC channel components reduces mitochondrial Ca2+ uptake after IgM stimulation.
  • Fig. S5. Cytosolic Ca2+ dynamics in IP3R TKO, STIM1 KO, and Orai1,2 DKO lymphocytes after thapsigargin stimulation is similar in the presence or absence of ionomycin.
  • Fig. S6. KO of IP3Rs and CRAC channel components does not affect MCUR1 abundance.
  • Fig. S7. The abundance of MCU depends on STIM1.
  • Fig. S8. KD of MCU did not alter the expression or abundance of IP3R and CRAC channel components.
  • Fig. S9. pCREB is reduced in STIM1-deficient MEFs.
  • Fig. S10. The abundances of MCU and pCREB are similar after exposure of wild-type and KO DT40 cells to forskolin treatment.

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Citation: S. Shanmughapriya, S. Rajan, N. E. Hoffman, X. Zhang, S. Guo, J. E. Kolesar, K. J. Hines, J. Ragheb, N. R. Jog, R.Caricchio, Y. Baba, Y. Zhou, B. A. Kaufman, J. Y. Cheung, T. Kurosaki, D. L. Gill, M. Madesh, Ca2+ signals regulate mitochondrial metabolism by stimulating CREB-mediated expression of the mitochondrial Ca2+ uniporter gene MCU. Sci. Signal. 8, ra23 (2015).

© 2015 American Association for the Advancement of Science