Overview:
SMAD3isadirectmediatoroftranscriptionalactivationbytheTGFreceptor.TheactivityofSMAD3isregulatedbytheTGFreceptors,andSMAD3isphosphorylatedandassociatedwiththeligand-boundreceptorcomplex.TGFstimulationleadstophosphorylationandactivationofSMAD3,whichformacomplexwithSMAD4thataccumulateinthenucleusandregulatetranscriptionoftargetgenessuchasCDKinhibitor(1).SMAD3containingaC-terminaltruncationactsasadominant-negativeinhibitorofthenormalTGFresponse.SMAD3isamajorphysiologicsubstrateoftheG1cyclin-dependentkinasesCDK4andCDK2(2).
GeneAliases:
MADH3,JV15-2,HSPC193,HsT17436,MGC60396,KFZP586N0721,DKFZp686J10186
GenbankNumber:
NM_005902
References:
1.Inman,G.J.etal:NucleocytoplasmicshuttlingofSmads2,3,and4permitssensingofTGF-betareceptoractivity.Molec.Cell10:283-294,2002.2.Matsuura,I.etal:Cyclin-dependentkinasesregulatetheantiproliferativefunctionofSmads.Nature430:226-231,2004.
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本人目前需从电鳗放电器官中提取乙酰胆碱受体蛋白,提纯需要的步骤和电鳗器官都可以提供,有没有提供外包提纯服务的公司或者实验室。
算上其他生物24种
大概是记不太清了
NaturalProteinStopsDeadlyHumanBrainCancerInMice
ScientistsfromJohnsHopkinsandfromtheUniversityofMilanhaveeffectivelyproventhattheycaninhibitlethalhumanbraincancersinmiceusingaproteinthatselectivelyinducespositivechangesintheactivityofcellsthatbehavelikecancerstemcells.ThereportispublishedinNature.
Themostcommontypeofbraincancer-glioblastoma-ismarkedbythepresenceofthesestem-cell-likebraincells,which,insteadoftriggeringthereplacementofdamagedcells,formcancertissue.Stemcells,unlikeallothercellsinthebody,arecapableofformingalmostanykindofcellwhentheright"signals"triggertheirdevelopment.
Fortheirtreatmentexperiment,theresearchersreliedonaclassofproteins,bonemorphogenicproteins,thatcauseneuralstem-cell-likeclusterstolosetheirstemcellproperties,whichinturnstopstheirABIlitytodivide.
Firsttheypretreatedhumanglioblastomacellswithbonemorphogenicprotein4(BMP4),theninjectedthesetreatedcellsintomousebrains.Inmiceinjectedwithcellsthatwerenotpretreated,large,invasivecancersgrew.InthemicewithBMP4-treatedcells,nocancersgrewatall.Threetofourmonthsafterinjection,allmicethatgotuntreatedcellsdied,andnearlyallmicewithBMP4-treatedcellswerealive.
Next,thescientistsdeliveredslow-releaseBMP4-containing"beads"directlyintomousebrainswithimplantedglioblastomacells.Micethatgotemptybeadsdevelopedlargemalignanttumorsanddied.MicewithBMP4beadssurvivedmuchlonger,and80percentsurvivedfourmonthsaftercancercellimplants.
"OurideaistotreatpatientswithBMP4orsomethinglikeitrightaftersurgerytoremoveglioblastomainhopesofpreventingtheregrowthofthecancerandimprovingsurvivaltime,"saysAlessandroOlivi,M.D.,directoroftheDivisionofNeurosurgicalOncologyatHopkinsandacontributortothestudy.
OlivisaysclinicalstudiesusingBMP4couldbeginwithinayearand,ifsuccessful,drugtherapiescouldbeavailabletothepublicwithinthreetofouryears.
"ThiswasproofoftheideathatBMPscouldstopglioblastomabydepletingthestem-cell-likepopulationthatfeedsit,"saysHenryBrem,M.D.,chairmanoftheDepartmentofNeurosurgeryatHopkinsandacollaboratorinthestudy."Thisopensexcitingdoorstofutureresearchintotreatmentsandtherapiesforsuchadevastatingdisease."

