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Sci. Signal., 19 March 2013
[DOI: 10.1126/scisignal.2003425]

Supplementary Materials for:

STIM1 Controls Endothelial Barrier Function Independently of Orai1 and Ca2+ Entry

Arti V. Shinde, Rajender K. Motiani, Xuexin Zhang, Iskandar F. Abdullaev, Alejandro P. Adam, José C. González-Cobos, Wei Zhang, Khalid Matrougui, Peter A. Vincent, Mohamed Trebak*

*Corresponding author. E-mail: mtrebak{at}albany.edu

This PDF file includes:

  • Fig. S1. Effect of different STIM1 siRNAs on the thrombin-mediated decrease in TER in HUVECs.
  • Fig. S2. STIM1 knockdown does not affect basal endothelial monolayer resistance.
  • Fig. S3. STIM1 knockdown, but not Orai1 knockdown, inhibited the decrease in TER of HDMECs in response to thrombin.
  • Fig. S4. Low concentrations of Gd3+ completely abrogate Ca2+ entry in response to thrombin in HDMECs.
  • Fig. S5. The effects of thapsigargin on TER are distinct from those of thrombin and are SOCE-independent.
  • Fig. S6. STIM1 knockdown in HUVECs increased basal phosphorylation of FAK and paxillin.
  • Fig. S7. Effectiveness of TRPC1, TRPC4, or TRPC6 knockdown in HUVECs.
  • Fig. S8. MLCK knockdown in HUVECs and HDMECs has no effect on the thrombin-induced decrease in TER.
  • Table S1. Antibodies used in the study with corresponding dilutions.
  • Table S2. Sequences of the primers and siRNA sequences used throughout the study.

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Citation: A. V. Shinde, R. K. Motiani, X. Zhang, I. F. Abdullaev, A. P. Adam, J. C. González-Cobos, W. Zhang, K. Matrougui, P. A. Vincent, M. Trebak, STIM1 Controls Endothelial Barrier Function Independently of Orai1 and Ca2+ Entry. Sci. Signal. 6, ra18 (2013).

© 2013 American Association for the Advancement of Science


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