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. 2006 Mar 6;103(11):4040–4045. doi: 10.1073/pnas.0510050103

Fig. 1.

Fig. 1.

CRAC channel function correlates with altered expression of STIM1. (A) Development of ICRAC in Jurkat T cells overexpressing either STIM1 (red) or control empty vector (black). Current at −80 mV or +80 mV (red open circles) was measured in 20 mM extracellular Ca2+; addition of 50 μM 2-APB is indicated by the bar. (B) I–V profile determined at the time of maximal current in A. (C) Average maximal current at −100 mV in STIM1-overexpressing cells (n = 3) and control-expressing Jurkat T cells (n = 3). (D) Western analysis comparing STIM1 expression levels in RBL cells after knockdown and reexpression of STIM1. (E). The I–V profile for ICRAC was determined in DVF after maximal activation in Ca2+ex in control (blue), rSTIM1 knockdown (black), or rSTIM1 knockdown/hSTIM1-reexpressing RBL (red) cells. (Inset) Inactivation with overexpression of STIM1 WT in DVF. (F) Comparison of the average maximal current in DVF for control (n = 3), rSTIM1 knockdown (n = 3), and hSTIM1-reexpressing RBL (n = 4) cells. (G) ICRAC measured in rSTIM1 knockdown RBL cells reexpressing exogenous hSTIM1. Fifty micromolar 2-APB, but not 5 μM 2-APB, blocks the current in DVF. (H) Nonstationary noise analysis of the current in DVF from G to determine single-channel conductance (see Materials and Methods).