
Source | Human 293 Cells | M.W. | 37-40 kDa | CAS No. | |
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Structural Info | |||||
Formulation | Lyophilized in sterile filtered solution of PBS. | ||||
Reconstitution | Before reconstitution, a brief spin is recommend todrive down any material dislodged from the bottom of the tube. The lyophilized protein should bereconstituted in sterile H2O to a desired concentration. | ||||
Stability | The lyophilized protein is stable for at least oneyear if stored at -80 °C. Reconstituted protein is stable for at least four weeks at 4 °C,but should be stored in aliquots at -80 °C for longer term. Avoidrepeated freeze and thaw. | ||||
Purity | Greater than 90% as determined by SDS-PAGE analysis | ||||
Biological Activity | The activity was determined by using a TCF reporter gene assay in cultured human cells.The IC50 ranges from 100 - 500 ng/ml in the inhibition of 100 ng/mL WNT-3a activity.Activity in other assays | ||||
Country of Origin | USA |
DKK-1, Dickkopf-related protein-1, is a member of the DKKprotein family which includes DKK-1 through DDK-4. DKK was originally identified as ahead-forming molecule in Xenopus. Mechanisticstudies showed that DKK-1 inhibits the Wnt /β-catenin signaling pathway byforming inhibitory complexes with co-receptor LRP5/6. Inhibition of Wnt/β-catenin signaling isessential for posterior patterning and anterior development in vertebrates, supportedby the discovery that DKK-1 knock-out mice lack head formation. StemRDexpressed recombinant human DKK-1 in human 293 cells as a 37-40 kDaglycoprotein containing 235 amino-acid residues. It is purified by a series of chromatography including HPLC.
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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."

