简介：Versicanbelongstothefamilyofthelargeaggregatingchondroitinsulfateproteoglycanslocatedprimarilywithintheextracellularmatrix(ECM).Versican,likeothermembersofitsfamily,hasuniqueN-andC-terminalglobularregions,eachwithmultiplemotifs.Alargeglycosaminoglycan-bindingregionliesbetweenthem.Thisreviewwillbeginbyoutliningthesestructures,inthecontextofECMproteoglycans.Thediversebindingpartnersaffordedtoversicanbyvirtueofitsmodulardesignwillthenbeexamined.TheseincludeECMcomponents,suchashyaluronan,typeⅠcollagen,tenascin-R,fibulin-1,and-2,fibrillin-1,fibronectin,P-andL-selectins,andchemokines.VersicanalsobindstothecellsurfaceproteinsCD44,integrinβ1,epidermalgrowthfactorreceptor,andP-selectinglycoproteinligand-1.Thesemultipleinteractorsplayimportantrolesincellbehaviour,andtherolesofversicaninmodulatingsuchprocessesarediscussed.

简介：补充系统对普通病原体在天生的防卫起一个关键作用。补充的激活导致柔韧、有效的解朊的串联，它通过有势力proinflammatory分子的生产在病原体以及在古典煽动性的反应的产生的opsonization和细胞溶解终止。然而，更最近，在有免疫力的反应的补充的角色由于连接补充激活到适应有免疫力的回答的观察被扩展了。补充是在允许综合主人防卫到病原的挑战的天生、适应的有免疫力的回答之间的一座功能的桥，这现在被欣赏。因此，它的函数的研究象主机免疫者反应的组织和组织一样允许卓见进主人病原体相互作用的分子的underpinnings。这评论试图总结在主人防卫上在天生、适应的有免疫力的回答和这些相互作用的后果补充戏的角色。

简介：InteractionbetweencytotoxicTlymphocyte-associatedantigen-4(CTLA4,CD152)andB7molecules(B7-1andB7-2)isofimportanceinthecellulareventsoflymphocyte,includingantigen-specificT-cellactivationandinductionofautoreactiveT-cell.WedescribehaerethefirstintroductionofamurinesolubleCTLA4gene,CTLA4Ig,toMm1cells,amacrophagiccellline.CTLA4IgwassuccessfullyexpressedonMm1cellsandtheexpressedCTLA4IgwasfoundtobefunctionallyactiveintheirbindingtoB7moleculesbyflowcytometryandimmunofluorescencestudies.ThebiologicalactivityofCTLA4IgfromthetransfectedMm1cellswasstudiedandshowedinhibitoryactivityonmixedlymphocyteculture.AhighCTLA4Igproducingmacrophagiccelllinewasobtained.AsMm1cellswereregardedasdifficultforgenetransfectionandtherehassofarbeennoreportonexpressionofCTLA4IggeneonMm1cells,theseresultssuggestedthattheCELA4IgexpressingMm1cellscouldbeusefulforanalysisofCTLA4andB8moleculeinteractioninbothmacrophageandT-cell.

简介：MIF受体的最近的克隆在我们分子的生物学的理解和MIF的免疫学充满重要差距。MIF受体象MIF一样，不掉进蛋白质调停人的任何确定的家庭，提供为MIF信号transduction的结构、功能的分析的新挑战和机会。

简介：MembersofBcl-2familyofproteinsareregulatorsofcelldeaththatcanbegroupedintosubfamiliesofprosurvivalandproapoptoticmolecules.Theyarecharacterizedbythepresenceofseveralconservedmotifs,knownastheBcl-2homology(BH)domains,designatedBH1,BH2,BH3andBH4.MutagenesisandstructuralstudiesrevealedthattheBHdomainsareimportantfunctionaldomainsthatarealsorequiredfordimerizationfunction.Recently,asubfamilyofproapoptoticmoleculesonlycontainsBH3motifhasbeenidentifiedsuggestingBH3domainalonemaybesufficientformediatingproapoptoticfunctionamong

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简介：<正>Usingsubtractioncloning,weidentifiedthehumanN-MycDownstream-RegulatedGene-2(hNDRG2),locatedat14q11.2,asacandidatetumorsuppressorgene.Semi-quantitativeRT-PCRshowedthattheexpressionofhNDRG2in15of27(56%)humanGBMtissuesandall6humanglioblastomacelllineswassignificantlylowerthanthatinthenormalbrain.TheexpressionofhNDRG2alsowasevaluatedin60lung-carcinomapatients.17of26casesofsquamouscarcinomaand4of11casesofsmallcelllungcancerdisplayed

简介：在Saccharomycescerevisiae，必要基因CDC13编码telomeric遗传上并且身体上与Stn1p和Ten1p交往的搁浅单人赛的DNA有约束力的蛋白质，并且为telomere结束保护和telomere长度控制被要求。Ten1由参予telomere长度规定和染色体结束保护的分子的机制留下逃犯。在这个工作，我们用净化的recombinantCdc13p和Ten1p在胶化过滤分析观察了Cdc13p和Ten1p的一个弱相互作用。Ten1p本身展出一项弱DNA有约束力的活动，但是提高telomericTG1鈥吗？Cdc13p的DNA有约束力的能力。Cdc13p是有Ten1p的co-immunoprecipitated。在变异的ten1-55或ten1-66房间，在Ten1p和Cdc13p之间的损害相互作用与telomericDNA导致长得多的telomeres，以及Cdc13p的一个减少的协会。一致地，Ten1-55和Ten1-66异种蛋白质没能刺激telomeric在vitro的Cdc13p的DNA有约束力的活动。这些结果建议Ten1p提高telomericCdc13p到的DNA有约束力的活动否定地调整telomere长度。

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简介：OverexpressionandactivationofHER-2/neu(alsoknownasc-erbB-2),aproto-oncogene,wasfoundinabout30%ofhumanbreastcancers,promotingcancergrowthandmakingcancercellsresistanttochemo-andradio-therapy.Wild-typep53iscrucialinregulatingcellgrowthandapoptosisandisfoundtobemutatedordeletedin60-70%ofhumancancers.Andsomecancerswithawild-typep53donothavenormalp53function,suggestingthatitisimplicatedinacomplexprocessregulatedbymanyfactors.Inthepresentstudy,weshowedthattheoverexpressionofHER-2/neucoulddecreasetheamountofwild-typep53proteinviaactivatingPI3Kpathway,aswellasinducingMDM2nucleartranslocationinMCF7humanbreastcancercells.BlockageofPI3KpathwaywithitsspecificinhibitorLY294002causedG1-Sphasearrest,decreasedcellgrowthrateandincreasedchemo-andradio-therapeuticsensitivityinMCF7cellsexpressingwild-typep53.However,itdidnotincreasethesensitivitytoadriamycininMDA-MB-453breastcancercellscontainingmutantp53.OurstudyindicatesthatblockingPI3KpathwayactivationmediatedbyHER-2/neuoverexpressionmaybeusefulinthetreatmentofbreasttumorswithHER-2/neuoverexpressionandwild-typep53.