SNX-482 hasbeenisolatedfromthevenomoftheSpiderHysterocratesgigas(Africantarantula). SNX-482 modulatestheR-type currentassociatedwiththeclassα1Ecalciumchannel(Cav2.3 fromtheCACNA1Egene). SNX-482 antagonizeschannelactivationbyinducingadepolarizingshiftintheactivationpotential,thuspreventingthechannelfromundergoingnormalmembranedepolarization. SNX-482 actsrapidlyandmaintainsitseffect.
Description:
AAsequence: Gly-Val-Asp-Lys-Ala-Gly-Cys7-Arg-Tyr-Met-Phe-Gly-Gly-Cys14-Ser-Val-Asn-Asp-Asp-Cys20-Cys21-Pro-Arg-Leu-Gly-Cys26-His-Ser-Leu-Phe-Ser-Tyr-Cys33-Ala-Trp-Asp-Leu-Thr-Phe-Ser-Asp-OH
Disulfidebonds: Cys7-Cys21,Cys14-Cys26 andCys20-Cys33
Length(aa): 41
Formula: C192H274N52O60S7
MolecularWeight: 4496.42Da
Appearance:Whitelyophilizedsolid
Solubility: waterandsalinebuffer
CASnumber: 203460-30-4
Source: Synthetic
Purityrate: >95%
Reference:
TheCav2.3calciumchannelantagoNISTSNX-482reducesdorsalhornneuronalresponsesinaratmodelofchronicneuropathicpain
Neuropathicpainisadifficultstatetotreat,characterizedbyalterationsinsensoryprocessingthatcanincludeallodynia(touch-evokedpain).Evidenceexistsfornervedamage-inducedplasticityinbothtransmission&modulatorysystems,includingchangesinvoltage-dependentcalciumchannel(VDCC)expression&function;however,theroleofCa(v)2.3calciumchannelshasnotclearlybeendefined.Here,theeffectsofSNX-482,aselectiveCa(v)2.3antagonist,onsensorytransmissionatthespinalcordlevelhavebeeninvestigatedintherat.Thespinalnerveligation(SNL)modelofchronicneuropathicpain[Kim&Chung,(1992)Pain,50,355-363]wasusedtoinducemechanicalallodynia,astestedontheipsilateralhindpaw.Invivoelectrophysiologicalmeasurementsofdorsalhornneuronalresponsestoinnocuous&noxiouselectricalandnaturalstimuliweremadeafterSNL&comparedtosham-operatedanimals.SpinalSNX-482(0.5-4microg/50microL)exerteddose-relatedinhibitionsofnoxiousC-fibre-andAdelta-fibre-mediatedneuronalresponsesinconditionsofneuropathy,butnotinsham-operatedanimals.MeasuresofspinalcordhyperexcitABIlity&nociceptionweremostsusceptIBLetoSNX-482.Incontrast,non-noxiousAbeta-mediatedresponseswerenotaffectedbySNX-482.Moreover,responsestoinnocuousmechanical&alsothermalstimuliweremoresensitivetoSNX-482inSNLthancontrolanimals.ThisstudyisthefirsttodemonstrateanantinociceptiveroleforSNX-482-sensitivechannelsindorsalhornneuronsduringneuropathy.ThesedataareconsistentwithplasticityinCa(V)2.3calciumchannelexpressionandsuggestapotentialselectivetargettoreducenociceptivetransmissionduringconditionsofnervedamage.
MatthewsEA., etal.(2007)TheCav2.3calciumchannelantagonistSNX-482reducesdorsalhornneuronalresponsesinaratmodelofchronicneuropathicpain. EurJNeurosci. PMID17610575
SNX482selectivelyblocksP/QCa2+channelsanddelaystheinactivationofNa+channelsofchromaffincells
TheeffectsofthetoxinSXN482onCa2+channelcurrents(ICa),Na+currents(INa),andK+currents(IK)havebeenstudiedinbovineadrenalmedullarychromaffincellsvoltage-clampedat-80mV.Currentswereelicitedbydepolarisingpulsesto0-10mV(ICaandINa)orto+60mV(IK).SNX482blockedICainaconcentration-dependentmanner.Theinhibitioncurveexhibitedtwophases.Thefirsthigh-affinityphasecomprised28%ofthewhole-cellcurrent&exhibitedanIC50of30.2nM.Thesecondlow-affinityphasecomprisedover70%ofICa&hadanIC50of758.6nM.Blockadewasrapidandfullyreversibleuponwashoutofthetoxin.OcclusionexperimentsshowedadditivityofblockadeexertedbynifedipineplusSNX482(0.3microM)andbyomega-conotoxinGVIAplusSNX482.Incontrast,blockadeexertedbycombinedomega-agatoxinIVAplusSNX482(about50%ofthewholecell)didnotshowadditivity.At0.3microMandhigherconcentrations,SNX482delayedtheinactivationofINa.Thetimeconstant(tau)forinactivationofINaincontrolconditionsdoubledinthepresenceof0.5microMSNX482.At0.3microM,SNX482didnotaffectIK.Ourdatademonstratethat:(i)SNX482selectivelyblocksP/QCa2+channelsatsubmicromolarconcentrations;(ii)thetoxinpartiallyblocksNa+channels;(iii)SNX482delaystheinactivationofNa+channels.TheseresultsrevealnovelpropertiesofSNX482andcastdoubtsontheclaimedselectivity&specificityofthetoxintoblocktheR-typeCa2+channel.
ArroyoG, etal.(2003)SNX482selectivelyblocksP/QCa2+channelsanddelaystheinactivationofNa+channelsofchromaffincells, EurJPharmacol. PMID:12954354
InteractionofSNX482withdomainsIIIandIVinhibitsactivationgatingofalpha(1E)(Ca(V)2.3)calciumchannels
Bourinet,E., etal. (2001)InteractionofSNX482withdomainsIIIandIVinhibitsactivationgatingofalpha(1E)(Ca(V)2.3)calciumchannels, Biophys. PMID11423396
SelectivepeptideantagonistoftheclassEcalciumchannelfromthevenomofthetarantulaHysterocratesgigas
WedescribethefirstpotentandselectiveblockeroftheclassECa2+channel.SNX-482,anovel41aminoacidpeptidepresentinthevenomoftheAfricantarantula,Hysterocratesgigas,wasidentifiedthroughitsabilitytoinhibithumanclassECa2+channelsstablyexpressedinamammaliancellline.AnIC50of15-30nMwasobtainedforblockoftheclassECa2+channel,usingeitherpatchclampelectrophysiologyorK+-evokedCa2+flux.Atlownanomolarconcentrations,SNX-482alsoblockedanativeresistantorR-typeCa2+currentinratneurohypophysealnerveterminals,butconcentrationsof200-500nMhadnoeffectonR-typeCa2+currentsinseveraltypesofratcentralneurons.ThepeptidehasthesequenceGVDKAGCRYMFGGCSVNDDCCPRLGCHSLFSYCAWDLTFSD-OHandishomologoustothespiderpeptidesgrammatoxinS1Aandhanatoxin,bothpeptideswithverydifferentionchannelblockingselectivities.NoeffectofSNX-482wasobservedonthefollowingionchannelactivities:Na+orK+currentsinseveralculturedcelltypes(upto500nM);K+currentthroughclonedpotassiumchannelsKv1.1andKv1.4expressedinXenopusoocytes(upto140nM);Ca2+fluxthroughL-andT-typeCa2+channelsinananteriorpituitarycellline(GH3,upto500nM);andBa2+currentthroughclassACa2+channelsexpressedinXenopusoocytes(upto280nM).AweakeffectwasnotedonCa2+currentthroughclonedandstablyexpressedclassBCa2+channels(IC50>500nM).TheuniqueselectivityofSNX-482suggestsitsusefulnessinstudyingthediversity,function,andpharmacologyofclassEand/orR-typeCa2+channels.
Newcomb,R., etal. (1998)SelectivepeptideantagonistoftheclassEcalciumchannelfromthevenomofthetarantulaHysterocratesgigas, Biochemistry. PMID:9799496
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常用流动相加酸碱后PH的总结，希望大家能够提供一点自己测过的结果，谢谢先
1.直接用固体磷酸钠配制成50mM的磷酸钠溶液，再调pH到7.4；（我们试着用这个做了下，发现挂不上柱）
2.配置磷酸钠盐缓冲液：按NaH2PO4：Na2HPO4以19：81的摩尔比配制成pH7.4的缓冲液？（附一张百度出来的配方
）
3.如果是磷酸钠盐缓冲液，可以直接将50mM的NaH2PO4的水溶液用NaOH调成pH7.4吗？
再者，2和3这两个方法配制的磷酸钠盐缓冲液有什么区别？最终效果是一样的吗？如果不一样，有什么理论的知识支撑呢？个人感觉是分析化学中酸碱理论中的缓冲液那里的知识。求帮忙解答这些疑问。
另外，我还想问一下，pH对于Ni柱对His-tagged的蛋白的分离纯化影响大吗？是怎么影响的？谢谢大家了！
有了源数据之后把源数据按照大小排列，
选中源数据区域-->ALT+A1-->选中图标区右键-->更改图表类型-->散点图
因为是考察不同PH对药物的影响，样品又不好改变其PH值，这种情况怎么办？希望有经验的高手指教。
我的流动相是甲醇-水（90：10）
谢谢赐教！
请进子版按格式发贴，自行修改，谢谢。
由弱酸及其盐、弱碱及其盐组成的混合溶液，能在一定程度上抵消、减轻外加强酸或强碱对溶液酸碱度的影响，从而保持溶液的pH值相对稳定。这种溶液称为缓冲溶液。
:)
我在做一细菌不同酸碱度生长状况时,发现这些奇怪现象:pH=3的培养基灭菌(TSB液体培养基)灭菌后pH上升到到9.2!而原来pH=9.0的降到8.7(基本没多少变化),请问各位大侠,这是什么原因?
一般做不同酸碱度生长实验时,该如何才能防止pH在湿热灭菌后基本不变化?
是否可以理解为纯化水得PH范围为6.3-7.6？能否直接用pH计测量？谢谢!
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