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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: J Mol Cell Cardiol. 2009 Jun 21;47(3):400–410. doi: 10.1016/j.yjmcc.2009.06.010

Figure 2. Capacitative Ca2+ entry (CCE) controls nuclear translocation of NFATc1 after store depletion with thapsigargin.

Figure 2

A: Representative CCE trace induced by 2 mM [Ca2+]o in CPAE cells with depleted Ca2+ stores. Cells were pre-treated with 10 μM thapsigargin (TG) under Ca2+-free conditions to deplete the ER of Ca2+ (not shown). Application of 2 mM [Ca2+]o for 5 min resulted in Ca2+-influx (grey trace), which induced nuclear translocation of NFATc1 (black trace). B: Summary data: CCE alone was sufficient to induce nuclear translocation of NFATc1-GFP in CPAE cells. This effect was dependent on CCE duration (black columns). CsA inhibited CCE-induced nuclear translocation of NFAT. Store depletion alone (TG, [Ca2+]o = 0) without CCE failed to initiate NFAT translocation (grey columns). *, statistically significant (P < 0.05) compared to control.