ABCC7 p.Gly1349Ile
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PMID: 20861014
[PubMed]
Tsai MF et al: "Optimization of the degenerated interfacial ATP binding site improves the function of disease-related mutant cystic fibrosis transmembrane conductance regulator (CFTR) channels."
No.
Sentence
Comment
120
Interestingly, we found that non-conservative mutations L1346Q and S1347G (Fig. 3A) and G1349I greatly reduced the nucleotide-dependent activation of W401F/G551D channels.
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ABCC7 p.Gly1349Ile 20861014:120:88
status: NEW189 These mutations include W401G,W401I (Fig. 1, B-D), which eliminate a ring-ring stacking interaction, S1347G (supplemental Fig. S6), which may break a hydrogen bond between ATP and the NBD2 signature motif, and G1349I (supplemental Fig. S6), whose side chain likely protrudes into site 1 and causes a steric clash with ATP (22-24).
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ABCC7 p.Gly1349Ile 20861014:189:210
status: NEW