Results from a co-localisation study of the L51H KCNE1 mutant using a resident ER marker calnexin showed WT proteins co localising well in the ER but there is also lots of KCNE1 at the cell membrane, what did the L51H mutant cell show?
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Card 17
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Why does the L51H KCNE1 mutation lead to problems with repolarization in myocytes?
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Card 18
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True or false, evidence has indicated that KCNE1 protein mutations such as L51H also impairs K+ transport via Kv1.4 channels?
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Card 19
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What neurotransmitter is responsible for acting on beta-2 adrenoreceptors via G-proteins to increase cAMP which activates Iks and increases the density of the currents thus increasing heart rates
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Card 20
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Why does the increase in Iks current density result in increased heart rate?
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Card 21
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Why do many LQT patients die playing sports or jumping into cold water?
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Card 22
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When an increase in heart rate is no longer required how is the KCNQ1/KCNE1 complex inactivated to return heart rate to normal?
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Card 23
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What impact on currents does adding cAMP and OA (a PP1 inhibitor) to cells with KCNQ1 proteins but not KCNE1 proteins?
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Card 24
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W87R KCNE1 mutants do show an increase in Iks currents in the presence of cAMP and have no impact on regulation so what impairment is seen in this genotype?
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Card 25
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D76N KCNE1 mutations are very strong mutations with few channels in the PM and thus small K currents and show no sensitivity to CAMP. What happens when sufferers exercise?
