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 paperweex plored thepossibility of utilizing the Saccharomyces cerevisiae strain B31 foridentification of the signal motifsthatregulatesurfaceexpressionofmembraneproteinsandforstudyingstructure–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) 2:

กิจกรรมของโพแทสเซียม (K +) ช่องวิกฤตขึ้นอยู่กับความหนาแน่นของพวกเขาในเยื่อหุ้มเซลล์ผิวซึ่งถูกควบคุมโดย dynamicprotein โปรตีนใน teractions ที่ teninvolve distincttrafficking สัญญาณใน cargoproteins.In paperweex นี้ plored thepossibility ของการใช้สายพันธุ์ Saccharomyces cerevisiae B31 foridentification ของสัญญาณ motifsthatregulatesurfaceexpressionofmembraneproteinsandforstudyingstructure–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.