Overview:
PFKFB3 or 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 is a potent activator of a key regulatory enzyme in the glycolysis pathway called phosphofructokinase. Phosphofructokinase regulates the steady-state concentration of fructose-2,6-bisphosphate, a potent activator of key regulatory enzyme of the glycolysis pathway. PFKFB3 is bifunctional, although the phosphatase activity is low due to a mutation in an active site which can be upregulated after phosphorylation by protein kinases (1). PFKFB3 may be responsible for sustaining the high glycolytic flux of rapidly proliferating leukemia cells and may represent a molecular target for chemotherapeutic intervention (2).
Gene Aliases:
IPFK2; PFK2
Genbank Number:
NM_004566
References:
1. Sakakibara, R.et.al: Characterization of a human placental fructose-6-phosphate,2-kinase/fructose-2,6-bisphosphatase. J. Biochem. 122: 122-128, 1997.2. Chesney, J. et.al: An inducible gene product for 6-phosphofructo-2-kinase with an AU-rich instability element: role in tumor cell glycolysis and the Warburg effect. Proc. Nat. Acad. Sci. 96: 3047-3052, 1999.
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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."

