Overview:
KAT3B (also known as EP300) encodes the adenovirus E1A-associated cellular p300 transcriptional co-activator protein that functions as a histone acetyltransferase. KAT3B regulates transcription via chromatin remodeling and is important in the processes of cell proliferation and differentiation. KAT3B binding is a highly accurate process and can be used for identifying enhancers and their associated activities (1). KAT3B is also useful in the study of the role of tissue-specific enhancers in human biology and diseases on a genome wide scale. Defects in KAT3B gene are a cause of Rubinstein-Taybi syndrome that play a important role in epithelial cancer and act as a classic tumor suppressor gene (2).
Gene Aliases:
KAT3B; EP300; p300
Genbank Number:
NM_001429
References:
1. Visel, A. et.al: ChIP-seq accurately predicts tissue-specific activity of enhancers. Nature 457: 854-858, 2009.2. Gayther, S. A. et.al: Mutations truncating the EP300 acetylase in human cancers. Nature Genet. 24: 300-303, 2000.
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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."

