ABCMdb

PMID: 10674713

Fujita A, Kurachi Y
Molecular aspects of ATP-sensitive K+ channels in the cardiovascular system and K+ channel openers.
Pharmacol Ther. 2000 Jan;85(1):39-53., [PubMed]

Sentences

No. Mutations Sentence Comment

565 ABCC8 p.Lys719Ala ABCC8 p.Lys1384Met Gribble et al. (1997b) found that the ATPi sensitivity of the SUR1/Kir6.2 channel was not modified by mutations on either or both of the two conserved lysine residues in the Walker A motifs in the first or the second NBF of SUR1 (K719A and K1384M, respectively). Login to comment 567 ABCC8 p.Asp854Asn ABCC8 p.Lys719Arg ABCC8 p.Lys719Met The high-affinity binding site was saturated with 10 ␮M ATPi in the absence of Mg2ϩ i. Substitution of the conserved lysine residue in the Walker A motif (K719R and K719M) or the aspartate residue in the Walker B motif (D854N) in the first NBF all abolished the high-affinity ATPi-binding, while the corresponding mutations in the second NBF did not cause any significant effect. Login to comment 568 ABCC8 p.Lys719Ala ABCC8 p.Asp854Asn ABCC8 p.Lys719Arg ABCC8 p.Lys719Met Because Ueda et al. (1997) and Gribble et al. (1997b) used different mutations (K719R, K719M, or D854N vs. K719A, respectively), it is not clear whether the ATPi binding found by Ueda et al. (1997) underlies the sensitization of Kir6.2 to ATPi by SUR1. Login to comment 569 ABCC8 p.Lys719Ala ABCC8 p.Lys1384Met Gribble et al. (1997b) found that the ATPi sensitivity of the SUR1/Kir6.2 channel was not modified by mutations on either or both of the two conserved lysine residues in the Walker A motifs in the first or the second NBF of SUR1 (K719A and K1384M, respectively). Login to comment 571 ABCC8 p.Asp854Asn ABCC8 p.Lys719Arg ABCC8 p.Lys719Met The high-affinity binding site was saturated with 10 mM ATPi in the absence of Mg21 i. Substitution of the conserved lysine residue in the Walker A motif (K719R and K719M) or the aspartate residue in the Walker B motif (D854N) in the first NBF all abolished the high-affinity ATPi-binding, while the corresponding mutations in the second NBF did not cause any significant effect. Login to comment 572 ABCC8 p.Lys719Ala ABCC8 p.Asp854Asn ABCC8 p.Lys719Arg ABCC8 p.Lys719Met Because Ueda et al. (1997) and Gribble et al. (1997b) used different mutations (K719R, K719M, or D854N vs. K719A, respectively), it is not clear whether the ATPi binding found by Ueda et al. (1997) underlies the sensitization of Kir6.2 to ATPi by SUR1. Login to comment 629 ABCC8 p.Lys719Ala ABCC8 p.Lys1384Met Gribble et al. (1997b) showed that either the K719A or K1384M mutation of r-SUR1 abolished the stimulatory effects of ADPi on the partial rundown SUR1/Kir6.2 channel, both in the presence and in the absence of ATPi. Login to comment 633 ABCC8 p.Lys719Ala ABCC8 p.Lys1384Met Gribble et al. (1997b) showed that either the K719A or K1384M mutation of r-SUR1 abolished the stimulatory effects of ADPi on the partial rundown SUR1/Kir6.2 channel, both in the presence and in the absence of ATPi. Login to comment