ABCC8 p.Ala286Gly
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PMID: 18996847
[PubMed]
Garneau L et al: "Hydrophobic interactions as key determinants to the KCa3.1 channel closed configuration. An analysis of KCa3.1 mutants constitutively active in zero Ca2+."
No.
Sentence
Comment
110
Results obtained with the V275C/A286G mutant are also included to illustrate the effect of MTSEAϩ on a nonconstitutively active channel, despite Ala286 facing the channel pore.
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ABCC8 p.Ala286Gly 18996847:110:32
status: NEW119 D, constitutive activation was not seen with the V275C/A286G mutant, although Ala286 is facing the channel pore just like Ala279 and Val282 .
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ABCC8 p.Ala286Gly 18996847:119:55
status: NEW123 The continuous application of MTSEAϩ onto the V275C/A286G mutant in Ca2ϩ free conditions (Fig. 5D) did not result in a detectable current inhibition (I0 ϭ IEGTA) confirming that V275C/A286G is not constitutively active.
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ABCC8 p.Ala286Gly 18996847:123:58
status: NEWX
ABCC8 p.Ala286Gly 18996847:123:202
status: NEW124 Furthermore, the absence of inhibition in this case cannot be attributed to cysteines at position 275 not being accessible to MTSEAϩ for the V275C/A286G mutant, because the subsequent addition of Ca2ϩ failed to initiate current activation, thus indicating covalent modification of V275C.
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ABCC8 p.Ala286Gly 18996847:124:153
status: NEW212 D, an identical perfusion protocol applied to the V275C/A286G mutant failed to provide evidence of an MTSEAϩ -induced inhibition of I0, in accordance with V275C/A286G being closed in the absence of Ca2ϩ .
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ABCC8 p.Ala286Gly 18996847:212:56
status: NEWX
ABCC8 p.Ala286Gly 18996847:212:167
status: NEW