ABCC7 p.Glu267Cys
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PMID: 25190805
[PubMed]
Wang W et al: "An electrostatic interaction at the tetrahelix bundle promotes phosphorylation-dependent cystic fibrosis transmembrane conductance regulator (CFTR) channel opening."
No.
Sentence
Comment
127
As we showed in Fig. 2 the single E267C and K1060C mutations reduced CFTR channel activity especially after PKI addition but not to the extent of the charge-reversal substitutions.
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ABCC7 p.Glu267Cys 25190805:127:34
status: NEW128 Subsequent exposure of E267C-CFTR to MTSET rapidly and markedly inhibited the post-PKI current which was reversed by bath addition of DTT (Fig. 4A).
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ABCC7 p.Glu267Cys 25190805:128:23
status: NEW131 To test this idea we exposed E267C-CFTR channels to the poorly hydrolyzable AMP-PNP in the continued presence of ATP prior to MTSET addition (Fig. 4D).
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ABCC7 p.Glu267Cys 25190805:131:29
status: NEW133 E267C-CFTR channels also were strongly activated by AMP-PNP but remained sensitive to subsequent treatment with MTSET followed by DTT (Fig. 4D).
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ABCC7 p.Glu267Cys 25190805:133:0
status: NEW136 These findings support the idea that the accessibility of E267C to thiol modification is reduced in the open channel conformation(s) as would be expected if this position is buried in a helix bundle upon channel opening.
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ABCC7 p.Glu267Cys 25190805:136:58
status: NEW212 A positively charged thiol modifier strongly inhibits E267C-CFTR currents in an activity-dependent manner but modestly stimulates K1060C-CFTR currents.
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ABCC7 p.Glu267Cys 25190805:212:54
status: NEW213 A, E267C-CFTR macropatch record showing strong and rapid inhibition of this cysteine mutant by bath addition of 30 òe;M MTSET and reversal of this inhibition by 5 mM DTT.
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ABCC7 p.Glu267Cys 25190805:213:3
status: NEW220 D, E267C-CFTR macropatch record showing that MTSET inhibition was very slow when added after the current was stimulated with 2 mM AMP-PNP.
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ABCC7 p.Glu267Cys 25190805:220:3
status: NEW235 In addition, the rate of inhibition of the E267C mutant by this reagent was slowed markedly by AMP-PNP, a poorly hydrolysable ATP analog that prolongs open channel bursts and stabilizes the NBD dimer.
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ABCC7 p.Glu267Cys 25190805:235:43
status: NEW