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 Ca
2+ Entry.
Sci. Signal. 6, ra18 (2013).
© 2013 American Association for the Advancement of Science
