Functional expression of the Na-K-2Cl cotransporter NKCC2 in mammalian cells fails to confirm the dominant-negative effect of the AF splice variant.

Even though these increases in 86 Rb uptake are highly significant ( p < 0.005), 30–40% of bumetanide-sensitive 86 Rb uptakes probably occur through the endogenous NKCC1 of the HEK whose expression level and phosphorylation state ( Fig. 2 A ) are not affected by the expression of any fNKCC2 variant.

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However, although additional fluxes could be detected in stable fNKCC2B and -F cells these did not reach statistical significance.

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