The activity of potassium(K+) chann

The activity of potassium(K+) channels critically depends on their density on the cell surface membrane,which is regulated by dynamicprotein–protein in teractions that of teninvolve distincttrafficking signals on the cargoproteins.In this paperweexploredthepossibilityof utilizing the Saccharomyces
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.