ABCC7 p.Lys978Ala
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PMID: 17582383
[PubMed]
Melin P et al: "CFTR inhibition by glibenclamide requires a positive charge in cytoplasmic loop three."
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Sentence
Comment
2
Charge-neutralizing mutations K978A, K978Q, K978S abolished the inhibition of forskolin-activated CFTR chloride current by glibenclamide but not by CFTRinh-172.
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ABCC7 p.Lys978Ala 17582383:2:30
status: NEW77 We investigated the role of the charged residue K978 in the sequence ILNRFSKD of CL3 (Fig. 1B) described as a region physically close to the pore [29] and examined the interaction of glibenclamide with mutated EGFP-CFTR channels: K978A, K978Q, K978R, Fig. 2.
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ABCC7 p.Lys978Ala 17582383:77:230
status: NEW84 Similar effects in the presence of Fsk were recorded with cells expressing K978A, K978Q, K978R and K978S mutants CFTR.
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ABCC7 p.Lys978Ala 17582383:84:75
status: NEW96 To investigate the role of the charge of the side chain of K978 in glibenclamide resistance, different amino acid substitutions were examined: K978A, K978Q, K978R.
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ABCC7 p.Lys978Ala 17582383:96:143
status: NEW98 Fig. 4A presents the ratio Iglib/Ifsk, recorded at -100 mV, with 100 bc;M glibenclamide, for K978A, K978Q, K978R, K978S channels compared to CFTR-wt.
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ABCC7 p.Lys978Ala 17582383:98:96
status: NEW108 neutralizing mutations (K978A, K978Q) rendered channels insensitive to inhibition by glibenclamide as demonstrated by the time course of current recorded at +40 mV (Fig. 4B).
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ABCC7 p.Lys978Ala 17582383:108:24
status: NEW128 (B) Examples of time course of current densities (between +40 mVand -40 mV) from the charge neutralizing mutants CFTR-K978Q (a0;) and CFTR-K978A (ef;) in presence of Fsk 10 bc;M, and Fsk+Glib 100 bc;M, and Fsk+CFTRinh-172 10 bc;M.
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ABCC7 p.Lys978Ala 17582383:128:143
status: NEW138 This was the case for the mutations that neutralized the charge of the side chain of the residue 978 (K978A, K978Q, K978S).
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ABCC7 p.Lys978Ala 17582383:138:102
status: NEW