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. 2009 May 29;284(22):14875–14880. doi: 10.1074/jbc.C109.000869

FIGURE 1.

FIGURE 1.

Bioelectric and expession patterns of TMEMs and CFTR neonatal tracheas. A, tracheal bioelectrics of WT (solid bars, n = 7), Tmem16a+/– (hatched bars, n = 28), and Tmem16a–/– pups (open bars, n = 7). Unstim. indicates the unstimulated Isc before drug application. Then, amiloride (Amil) 10–4 m was added apically, and the magnitude of the resulting change is shown. The residual Isc is the Isc remaining after amiloride application. Then, UTP (UTP 10–4) was added apically followed by apical forskolin (Forsk)10–5 m, and then bumetanide 10–4 (Bumet) was added basolaterally. The UTP response differed (**, p ≤ 0.01) from the other two groups, *, p ≤ 0.05 versus +/+ and +/–. Data are means ± S.E. (error bars). B, expression of mRNA from TMEM isoforms in epithelium and mesenchyme isolated from trachea at postnatal day 1. Tracheae were separated into sections, RNA was isolated, and RT-PCR was performed as described under “Experimental Procedures.” Whole adult trachea and lung were used as positive controls for Tmem16 a, Tmem16f, Tmem16j, and Tmem16k. For Tmem16b, mouse eye and brain were used because Tmem16b was not detected in adult trachea or lung (not shown). Blank = water control; MW = molecular weight marker. Approximate sizes of products are given (in bp). C, tracheal bioelectrics of WT (solid bars, n = 29) and CF (open bars, n = 31) pups. Drug additions and symbols are the same as in panel A, with the exception that forskolin was added before UTP. **, p ≤ 0.01 from WT. Data are means ± S.E (error bars).