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1、ThePI3KAktmTpathwayplaysanimptantroleinapoptosis.ActivatedPI3Kgeneratesphosphatidylinositol345triphosphatewhichrecruitsPDK1Aktserinethreoninekinaseattheplasmamembrane.ThisresultsinactivationofAkt.Aktactivatesmultipledown

2、streamtargetsincludingthemTpathway.AktinthispatywayisflankedbytwotumsuppresssPTENTSC1TSC2heterodimer.Variousrecepttyrosinekinases(RTKs)suchashumanepidermalgrowthfactrecept2(HER2)epidermalgrowthfactrecept(EGFR)insulinlike

3、growthfactreceptvularendothelialgrowthfactreceptactivatethegrowthsurviveofcellsinthemannerofmobilizingtheintracellularPI3Ksignalingpathway[1236].ThecarcinogenicroleofthePI3Kpathwayfirstlycameintothenoticesincemutationind

4、ucedabnmalcellularsignalingwasassociatedwithmalignantproliferationgrowth[58].IncreasingevidenceindicatedthatPI3Ksignalingpathwaywasusuallyfoundtobedisderedinmanykindsofcancers.THEPI3KFAMILYMEMBERSAllPI3Kfamilymembershave

5、theabilitytophosphylatethe3hydroxylgroupofphosphoinositides[9].280kDaserinethreoninekinasedownstreamofAkt.mTisthenuclearcatalyticsubunitoftwocomplexes:mTC1mTC2[66].mTC1iscomprisedofmTRaptmLST8PRAS40(amTinhibit).Thiscompl

6、expresentedclassicfeaturesofmTasanutrientenergysensproteinsynthesisconditioner[162229304651].TheactivatedmTC1showedanegativefeedbackinhibitiononPI3Ksignaling[61].DifferentfrommTC1activatedmTC2couldinducethephosphylationo

7、fAktatserine473servingasapositivefeedbackonPI3Ksignalingcade[53].PI3KPAINRecentlyseverallinesofevidencesuggestedtheinvolvementofPI3Ksignalingcadesintheregulationofcentralperipheralsensitization.TheincreasedactivationofAk

8、twasoftenfoundinDRGdsalhnneurons[11484957596069].CrespondinglyintrathecallyinjectionofPI3Kinhibitssuppressednerveinjuryinduced(Xuetal.2007)chemicalinduced[114860]hyperalgesia.FurthermespinallyinhibitionofmTbyrapamycinsho

9、wedwellantinociceptiveeffectinsomeanimalpainmodels[518284550].ItsuggestedthatPI3Kpathwaymightbeapotentialtargetfthedevelopmentofnovelanalgesics.PI3KPROTEINSYNTHESISWhatsmeinyounganimalsabigmountofnewproteinsynthesisarere

10、quiredinthenervoussystemdevelopmentprocesseslikeaxonguidancesynapsefmation[784167].ItwasreptedthatBDNFinducedtranslationoftheHomer2GluR1mRNAsinsynaptoneurosomescouldbewellinhibitedbyusingthespecificPI3K–mTkinaseinhibitsr

11、apamycinLY294002[55].ThusthePI3KAktmTrelatedmRNAtranslationproteinexpressionseemstobemesignificant.PI3KNEURALPLASTICITYOntheotherhinadultanimalhumanbeingnewproteinsynthesisalsoplaysimptantrolesinmanyaspectssuchasthemodul

12、ationoflongtermsynapticplasticity(LTP)whichisassociatedwithlearningmemyaswellaspainsensationmentionedabove[6].Specificallyithasbeenfoundthatthelocalproteinsynthesisinneurosynapseisessentialfthefunctionmphologyofnervoussy

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