The activity of potassium(K+) chann

The activity of potassium(K+) channels critically depends ontheirdensityonthecellsurfacemembrane,whichisregulatedbydynamicprotein–proteininteractionsthatofteninvolvedistincttrafficking
signalsonthecargoproteins.InthispaperweexploredthepossibilityofutilizingtheSaccharomyces
cerevisiaestrainB31foridentification ofthesignalmotifsthatregulatesurfaceexpressionofmembraneproteinsandforstudyingstructure–functionrelationshipsofK
+
channels.B31cellslacktheK
+
effluxsystemandwerereportedtoshowoverloadedK
+
-mediatedgrowthinhibitioninhighK
+
media
uponheterologousexpressionofamammalianinwardlyrectifyingK
+
channel(Kir2.1).Weshowthat
whiletheexpressionofwild-typeKir2.1channelinhibitsthegrowthofB31cellsinhighK
+
media,the
humandisease-causingmutationsofKir2.1thatabolishK
+
conduction(V302M)orsurfacetrafficking
(314/315)fullyrestoresthegrowth.Theexpressionoftwo-pore-domainK
+
channelKCNK3orKCNK9
alsoinhibitedthegrowthofB31inhighK
+
mediawhileC-terminalmutationsthatreducetheir14-3-3
protein-dependentcellsurfacetraffickingrestoredthegrowthofB31.Finally,theexpressionofKir2.1
channelsthatwereC-terminallyfusedwithknownsequencemotifsincluding ERretention/retrieval
signalsandanendocytosissignalallowedthegrowthofB31inhighK
+
media.TheseresultsdemonstratethepotentialofB31yeaststrainasauniquebiologicaltooltoscreentherandompeptidelibraries
fornovelsequencesignalsthatdown-regulatesurfaceexpressionofmembraneproteins,aswellasto
systematicallyidentifythestructuraldeterminantsforcellsurfacetraffickingand/orionconductance
ofK
+
channels.

ผลลัพธ์ (ไทย) 1:

กิจกรรมของช่อง potassium(K+) เหลือขึ้น ontheirdensityonthecellsurfacemembrane, whichisregulatedbydynamicprotein-proteininteractionsthatofteninvolvedistincttraffickingsignalsonthecargoproteins InthispaperweexploredthepossibilityofutilizingtheSaccharomycescerevisiaestrainB31foridentification ofthesignalmotifsthatregulatesurfaceexpressionofmembraneproteinsandforstudyingstructure-functionrelationshipsofK+ช่องทางการ B31cellslacktheK+effluxsystemandwerereportedtoshowoverloadedK+-mediatedgrowthinhibitioninhighK+สื่อuponheterologousexpressionofamammalianinwardlyrectifyingK+channel(Kir2.1) Weshowthatwhiletheexpressionofwild-typeKir2.1channelinhibitsthegrowthofB31cellsinhighK+สื่อ การhumandisease-causingmutationsofKir2.1thatabolishK+orsurfacetrafficking นำ (V302M)fullyrestoresthegrowth (314/315) DomainK Theexpressionoftwo รูขุมขน+channelKCNK3orKCNK9alsoinhibitedthegrowthofB31inhighK+mediawhileC-terminalmutationsthatreducetheir14-3-3โปรตีน dependentcellsurfacetraffickingrestoredthegrowthofB31.Finally,theexpressionofKir2.1channelsthatwereC-terminallyfusedwithknownsequencemotifsincluding ERretention/เรียกsignalsandanendocytosissignalallowedthegrowthofB31inhighK+สื่อ TheseresultsdemonstratethepotentialofB31yeaststrainasauniquebiologicaltooltoscreentherandompeptidelibrariesfornovelsequencesignalsthatdown-regulatesurfaceexpressionofmembraneproteins, aswellastosystematicallyidentifythestructuraldeterminantsforcellsurfacetraffickingand/orionconductanceofK+ช่องทางการ

ผลลัพธ์ (ไทย) 2:

กิจกรรมของโพแทสเซียม (K +) ช่องวิกฤตขึ้น ontheirdensityonthecellsurfacemembrane,whichisregulatedbydynamicprotein–proteininteractionsthatofteninvolvedistincttrafficking
signalsonthecargoproteins.InthispaperweexploredthepossibilityofutilizingtheSaccharomyces
cerevisiaestrainB31foridentification ofthesignalmotifsthatregulatesurfaceexpressionofmembraneproteinsandforstudyingstructure–functionrelationshipsofK
+
channels.B31cellslacktheK
+
effluxsystemandwerereportedtoshowoverloadedK
+
-mediatedgrowthinhibitioninhighK
+
media
uponheterologousexpressionofamammalianinwardlyrectifyingK
+
channel(Kir2.1).Weshowthat
whiletheexpressionofwild-typeKir2.1channelinhibitsthegrowthofB31cellsinhighK
+
media,the
humandisease-causingmutationsofKir2.1thatabolishK
+
conduction(V302M)orsurfacetrafficking
(?314/315)fullyrestoresthegrowth.Theexpressionoftwo-pore-domainK
+
channelKCNK3orKCNK9
alsoinhibitedthegrowthofB31inhighK
+
mediawhileC-terminalmutationsthatreducetheir14-3-3
protein-dependentcellsurfacetraffickingrestoredthegrowthofB31.Finally,theexpressionofKir2.1
channelsthatwereC-terminallyfusedwithknownsequencemotifsincluding ERretention/retrieval
signalsandanendocytosissignalallowedthegrowthofB31inhighK
+
media.TheseresultsdemonstratethepotentialofB31yeaststrainasauniquebiologicaltooltoscreentherandompeptidelibraries
fornovelsequencesignalsthatdown-regulatesurfaceexpressionofmembraneproteins,aswellasto
systematicallyidentifythestructuraldeterminantsforcellsurfacetraffickingand/orionconductance
ofK
+
channels.