Product Specifications:
Item#1121-G: Murine anti-gp120 HIV-1 Monoclonal Antibody (Cross Reactive) Conjugated to Colloidal Gold
Antibody: IgG1
Concentration: See vial
Mass/vial: N/A
Diluent: 10mM Tris, pH8;5% BSA;0.05% PEG; 0.02% NaN3
Storage: 4°C
Stability: At least 6 months at 4°C Minimum
Dilution: 1 : 50
Application: Dot Blot Assays, Immunohistocytology, Cell Surface Binding.
Description: High affinity murine anti-gp120 HIV-1 mAb conjugated to Colloidal Gold (approx. 30nm mean diameter).
Coupling Ratio: OD 520nm = 15; protein content approximately 50µg.
Specificity: Binds to V3-loop of HIV-1 gp120/gp160. Cross reactive with MN, IIIB, RF, SF2 and other primary HIV-1 isolates. Cell surface binding was performed with HIV-1 infected lymphocytes enriched from human PBL’s.
Biological Activity: Not determined.
Application and Instructions for use:
Recommended dilutions for use are approximate values. A dose dependent response assay should be performed to determine the optimal concentration for use in specific applications. Dot Blot assays may be performed at 10-100ng of gp120 in solid phase (membrane bound). Immunohistochemical studies may be performed in 1:50 to 1:100 dilution range of gold conjugate.
ebiomall.com
>
>
>
>
>
>
>
>
>
>
>
>
硝酸根从根向地上部茎的长距离运输过程中首先要进行木质部的装载。台湾科学家发现NRT1.5是一个低亲和且依赖于pH的双向转运蛋白,位于质膜并在靠近木质部的中柱鞘细胞中表达,对于硝酸根在木质部的装载具有重要作用。
所以NRT1.5是双向性的转运蛋白
代谢通路:目前在通路数据库(PATHWAY database) 中代谢通路是建立得最好的,有大约90个参考代谢途径的图形。每个参考代谢途径是一个由酶或EC号组成的网络。
QianWang,JessamyTiffen,CharlesG.Bailey,MelanieL.Lehman,WilliamRitchie,LadanFazli,CynthiaMetierre,Yue(Julie)Feng,EstelleLi,MartinGleave,GrantBuchanan,ColleenC.Nelson,JohnE.J.Rasko,JeffHolst
Correspondenceto:JeffHolst,PhD,OriginsofCancerLaboratory,LockedBag6,Newtown,NSW2042Australia.(e-mail:j.holst@centenary.org.au).
BackgroundL-typeaminoacidtransporters(LATs)uptakeneutralaminoacidsincludingL-leucineintocells,stimulatingmammaliantargetofrapamycincomplex1signalingandproteinsynthesis.LAT1andLAT3areoverexpressedatdifferentstagesofprostatecancer,andtheyareresponsIBLeforincreasingnutrientsandstimulatingcellgrowth.
MethodsWeexaminedLAT3proteinexpressioninhumanprostatecancertissuemicroarrays.LATfunctionwasinhibitedusingaleucineanalog(BCH)inandrogen-dependentand-independentenvironments,withgeneexpressionanalyzedbymicroarray.APC-3xenograftmousemodelwasusedtostudytheeffectsofinhibitingLAT1andLAT3expression.ResultswereanalyzedwiththeMann-WhitneyUorFisherexacttests.Allstatisticaltestsweretwo-sided.
ResultsLAT3proteinwasexpressedatallstagesofprostatecancer,withastatisticallysignificantdecreaseinexpressionafter4–7monthsofneoadjuvanthormonetherapy(4–7monthmean=1.571;95%confidenceinterval=1.155to1.987vs0month=2.098;95%confidenceinterval=1.962to2.235;P=.0187).InhibitionofLATfunctionledtoactivatingtranscriptionfactor4–mediatedupregulationofaminoacidtransportersincludingASCT1,ASCT2,and4F2hc,allofwhichwerealsoregulatedviatheandrogenreceptor.LATinhibitionsuppressedM-phasecellcyclegenesregulatedbyE2Ffamilytranscriptionfactorsincludingcriticalcastration-resistantprostatecancerregulatorygenesUBE2C,CDC20,andCDK1.InsilicoanalysisofBCH-downregulatedgenesshowedthat90.9%arestatisticallysignificantlyupregulatedinmetastaticcastration-resistantprostatecancer.Finally,LAT1orLAT3knockdowninxenograftsinhibitedtumorgrowth,cellcycleprogression,andspontaneousmetastasisinvivo.
ConclusionInhibitionofLATtransportersmayprovideanoveltherapeutictargetinmetastaticcastration-resistantprostatecancer,viasuppressionofmammaliantargetofrapamycincomplex1activityandM-phasecellcyclegenes.
L-typeaminoacidtransporters(LATs)supplycellswithlargeneutralaminoacids,whicharenotonlyrequiredforproteinsynthesisbutalsocontributetovarioussignalingpathways.Intracellularleucinelevelsaresensedbytheleucyl-transferRNAsynthetase,previouslyknowntocatalyzetheadenosinetriphosphate–dependentligationofL-leucinetotransferRNAduringproteinsynthesis(1,2).Leucyl-transferRNAsynthetaseactivatestheRagguanosinetriphosphatasecomplexandbindstoRaptortoactivatemammaliantargetofrapamycincomplex1(mTORC1)signalingonthesurfaceoflysosomes(1–3).Inthiswayleucineisnotonlyanessentialaminoacidbutactsasarate-limitingsignalingmoleculeinthemTORC1pathway.
Incellsdeprivedofaminoacids,thereisanaccumulationofunchargedtransferRNA,whichbindstoandactivatesthegeneralcontrolnonrepressed2(GCN2)kinase.Inturn,GCN2phosphorylatesthetranslationinitiationfactor2α(eIF2α)onserine51,triggeringtranslationalupregulationofactivatingtranscriptionfactor(ATF)4(4).ATF4itselfupregulatestheexpressionofaminoacidtransportersasameansofrestoringintracellularaminoacidlevels(5).Therefore,understandinghowaminoacidtransportersregulateintracellularleucinelevels,andgeneratingnovelinhibitorsofthesetransporters,mayleadtopotentsuppressorsofmTORC1signaling.
ThetwodistinctfamiliesofLATsare1)solutecarrier7(SLC7)members(LAT1/SLC7A5andLAT2/SLC7A8),whichmediateNa+-independentneutralaminoacidexchangeasheterodimerswiththe4F2cell-surfaceantigenheavychain(4F2hc/SLC3A2/CD98)glycoprotein(6,7);and2)SLC43proteins(LAT3/SLC43A1andLAT4/SLC43A2)thatmediateNa+-independentuniportofneutralaminoacids(8,9).AlthoughtheexpressionofeachLATmembervariesdramaticallyindifferenttissues,thesetransportersarecommonlyupregulatedincancer.IncreasedLAT1expressionhasbeendetectedinlungcancer,coloncancer,breastcancer,headandneckcancer,genitalcancers,andsofttissuesarcomas(10–12).WeandothershaveshownthatLAT1andLAT3areoverexpressedinprostatecancer(11–14),withLAT1expressionincreasedinmetastasiscomparedwithprimarycancer(10,12).
WehypothesizedthatinhibitionofLAT1andLAT3mayofferaneffectivetherapeuticapproachforprostatecancer.

