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Figure 5: Regulation of CFTR activation. R domain phosphorylation followed by ATP binding at the NBD1 site enables the cycling mechanism to proceed [Figure 6]. In the CFTR model, the ATP molecule has adopted functions other than just powering the cycle as it is also required for activating the NBD1 site as well being the hydrolytic ligand in the gating cycle. However, the ATP concentrations within a cell are high enough for constant activation of the channel, thereby making these regulatory steps essential in preventing futile cycling.

Figure 5: Regulation of CFTR activation. R domain phosphorylation followed by ATP binding at the NBD1 site enables the cycling mechanism to proceed [Figure 6]. In the CFTR model, the ATP molecule has adopted functions other than just powering the cycle as it is also required for activating the NBD1 site as well being the hydrolytic ligand in the gating cycle. However, the ATP concentrations within a cell are high enough for constant activation of the channel, thereby making these regulatory steps essential in preventing futile cycling.