Product Description
Many types of venom contain components that activate complement.A major component of cobra venom is CVF which binds to the victim’s factor B and this is then activated by factor D forming CVF,Bb.CVF, Bb is a serine protease specific for the victim’s C3 and often C5 as well.The activity of this C3/C5 convertase is not affected by the complement regulatory proteins in blood and the complex is extremely stable (half-life approximately 7 hours) (Morgan, B.P. ed. (2000); Law, S.K.A. and Reid, K.B.M. (1995); Nolan, K.F. and Reid, K.B.M. (1993)).It is thought that the release of C3a is important for dilation of the blood vessels near the bite and this aids dispersion of the other venom components.C5a release provides a systemic activation of numerous immune cells and inflammatory reactions.CVF from naja naja kaouthia produces an enzyme that cleaves both human C3 and C5.The affinity of the naja naja kaouthia CVF for C5 is so high that it primarily consumes C5 first, then C3.
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OUR (A150) COBRA VENOM FACTOR IS SOLD IN THE U.S.A ONLY
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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."

