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简介：提炼伴随转变从的变化对在蝗虫的独居的阶段状态群居是那么激烈的很长时间，这些阶段被看作不同种类。是鲍里斯·乌瓦罗夫介绍了polyphenism的概念。研究的十年表明阶段转变在morphometry，表皮的颜色，行为和生理学的几个方面暗示变化。在最近的十年，特别地，相当很多分子的研究被承担了揭开阶段相关的差别。他们导致了新奇卓见进corazonin的角色，neuroparsins，一些朊酶禁止者，phenylacetonitrile等等。蝗虫的EST数据库的来临(例如坑等，2004)是在生理、行为的蝗虫研究的很令人鼓舞的新奇开发。然而，最吸引人的问题的答案，也就是是否有阶段转变的初发的分子的inducer，在不久的将来可能不在活动范围以内。

简介：Theuseofmolecularbiologyandgenomicstoolsinplantbiologyresearchhasgreatlyexpandedourunderstandingofthemolecularmechanismsthatunderlieplantdevelopmentandphysiology.Thesuccessfulestablishmentofresearchresourcessuchasmutantpopulationshasledtoprogressinavarietyoffields,includingplantreproductivedevelop-ment,signaltransduction,hormonefunctions,defenseresponsesandepigeneticcontrol.Inthefuturetheseadvanceswillpotentiallyfacilitatecropimprovementthroughmolecularbreeding.

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简介：Apoptosisisaformofgeneticallyprogrammedcelldeath,whichplaysakeyroleinregulationofcellularityinavarietyoftissueandcelltypesincludingthecardiovasculartissues.Underbothphysiologicalandpathophysiologicalconditions,variousbiophysiologicalandbiochemicalfactors,includingmechanicalforces,reactiveoxygenandnitrogenspecies,cytokines,growthfactors,oxidizedlipoproteins,etc.,mayinfluenceapoptosisofvascularcells.TheFas/Fasligand/caspasedeath-signalingpathway,Bcl-2proteinfamily/mitochondria,thetumorsuppressivegenep53,andtheproto-oncogenec-mycmaybeactivatedinatheroscleroticlesions,andmediatesvascularapoptosisduringthedevelopmentofatherosclerosis.Abnormalexpressionanddysfunctionoftheseapoptosis-regulatinggenesmayattenuateoracceleratevascularcellapoptosisandaffecttheintegrityandstabilityofatheroscleroticplaques.Clarificationofthemolecularmechanismthatregulatesapoptosismayhelpdesignanewstrategyfortreatmentofatherosclerosisanditsmajorcomplication,theacutevascularsyndromes.

简介：脯氨酸在调整synapticneurotransmission在起一个重要作用哺乳动物并且昆虫神经系统。编码脯氨酸transporter基因(CsProT)和它的其他的拼接的抄本(CsProT圣)的全身的互补DNA序列从有斑纹的茎borer(SSB)被克隆，Chilosuppressalis，在亚洲的最重要的米饭害虫之一。氨基酸序列的比较证明CsProT高度类似于从Manducasexta(MasProT)孤立的脯氨酸transporter。CsProT和CsProT圣基因的相对送信人RNA表示层次的发展变化在SSB被检验。CsProT圣的表示水平比在所有发展时期的CsProT的高得多，建议3结束拼接变体是主要抄本而不是CsProT。在蛹的阶段的两基因的最高的表达式水平意味着那脯氨酸可以从蛹在变形涉及一些不清楚的函数到成人生活。

简介：跟随基因组学革命，我们对应力位于防卫下面的分子的机制的知识极大地被扩展了。在强壮的选择压力下面，许多动物可以发展提高的应力忍耐。这能被改变蛋白质的结构完成(通过在基因的编码区域的变化)或由改变蛋白质的数量(通过在transcriptional的变化规定)。进化的后者类型能被替换在兴趣(cis规章的变化)或由改变transcriptional管理者蛋白质(trans规章的变化)的结构或数量的基因的倡导者完成。metallothionein系统是在重金属的上下文的最好学习的压力反应系统之一。Metallothionein表示被假定被金属抄写因素1调整(MTF-1)；然而，直到现在，MTF-1的参与仅仅为一些脊椎动物和果蝇被证明了。象线虫和蚯蚓那样的无脊椎动物上的数据建议metallothionein正式就职的另外的机制可能是在场的。Cd忍耐的详细研究为土壤生活跳虫的种被做，Orchesellacincta。种类是完了的这的metallothionein基因在暴露金属的领域人口表示了。metallothionein倡导者的分析表明了有功能的意义，出现在简历记者试金的广泛的多型性。在比较20张不同人口的研究，高快车的倡导者等位基因的频率断然在土壤与金属的集中被相关，特别Cd。跳虫学习证明涉及细胞的应力反应的基因的那个cis规章的变化可以贡献金属公差的进化。

简介：Stressinducedtheseriousdisorderofcardiacfunctionandcardiovasculardiseases.Apoptosisisthecellularbasisinstressinducedcardiacinjury.Inourpreviousstudywefoundthatmanystressorsresultedinmitochondrialdamage.Itiscertainthatmitochondriaisimportantmediatorintriggeringapoptoticcelldeath,butthemechanism,bywhichthestressinducedmitochondrialinjuryleadstocardiomyocyteapoptosis,remainsunclear.Wedesignedthepresentstudytoinvestigatethechangesofthemitochondriaincardiomyocytesundergoingstressanditsroleininducingapoptosis.Herewereportedthatstresschangedthemembranefluidityofmitochondriaandinducedthelipidperoxidationofmitochondrialmembranein

简介：Thispaperpresentsamechanicalmodelofjumpingrobotbasedonthebiologicalmechanismanalysisoffrog.Bybiologicalobservationandkinematicanalysisthefrogjumpisdividedintotake-offphase,aerialphaseandlandingphase.Wefindthesimilartrajectoriesofhindlimbjointsduringjump,theimportanteffectoffootduringtake-offandtheroleofforelimbinsupportingthebody.Basedontheobservation,thefrogjumpissimplifiedandamechanicalmodelisputforward.Therobotlegisrepresentedbya4-barspring/linkagemechanismmodel,whichhasthreeDegreesofFreedom(DOF)athipjointandoneDOF(passive)attarsometatarsaljointonthefoot.TheshoulderandelbowjointseachhasoneDOFforthebalancingfunctionofarm.Thegroundreactionforceofthemodelisanalyzedandcomparedwiththatoffrogduringtake-off.Theresultsshowthatthemodelhasthesameadvantagesoflowlikelihoodofprematurelift-offandhighefficiencyasthefrog.Analysisresultsandthemodelcanbeemployedtodevelopandcontrolarobotcapableofmimickingthejumpingbehavioroffrog.

简介：Themechanismofesterhydrolysishasbeenextensivelystudied;however,theprecisefunctionofactive-siteresiduesinpromotingcatalysisisunclear.WedescribeherethestructuralmodelsforthecomplexofacatalyticantibodyFvfragmentwithaphosphonatetransition-stateanalogue,constructedbyusinggenecloning,sequencingandmolecularmodeling,mainlybasedonaknownX-raystructureofacatalyticantibody.HydrophobicandelectrostaticanalysesoftheFv/analogandFv/substrateinteractionsuggestthehydrolysismechanism:TyrL91andTyrH97playimportantrolestostabilizetheβ-naphthylgroupofhaptenthroughπ-stack;HisH35donatesapairoffreeelectronsattheatomNE2toanactivewaterandletittobeapartialhydroxide,whichattacksthecarbonatomofthecarbonylgroupofthesubstrate.BothHisH35andArgL96canformhydrogenbondsandstabilizetheanionictetrahedralintermediateformedduringturnover.Thismechanismemphasizesthatanactivewaterbridgemaybeformedduringhydrolysisprocess.

简介：Ourpreviousstudiesshowedapredominanceofhighmolecularweightproteingroupintumornuclearmatrices.Contrarytonormalcells,proteinsofthisgrouparepreferentiallyphosphorylated.Phosphoproteinsofhepatomanuclearmatrixareselectivelysubjectedtorapidproteolysis.Byalkalitreatmentandamonoclonalantibodyagainstphosphotyrosylresiduethepresenceoftwohighmolecularweightbandsofphosphotyrosyl-containingproteinswasdetectedinnuclearmatricesoftumorbutnotofnormallivercells.Highmolecularweightproteingroupoftumornuclearmatricesrevealedalsoarapidturnoverandpreferentialincorporationoflabeledaminoacidsselectivelyinhibitedbychloramphenicol.

简介：组蛋白deacetylases(HDAC)并且嘘一乙酰转移ases(帽子)是其酶的活动控制蛋白质离氨酸残余的乙酰化状态的二抵抗酶家庭，尤其是在核心histones.Acetylation的N终端扩展包含的那些嘘通过它对染色质符合构造的影响影响基因表示。Inaddition，几non-histone蛋白质由特定的离氨酸残余的乙酰化状态在他们的稳定性或生物功能被调整。HDAC在大量的生物学过程干涉并且是部分一多每个成员在有它的专业化功能的蛋白质家庭。另外，HDAC活动紧通过指向的招募，protein-proteininteractions和translational以后修正被控制。房间周期前进，房间幸存和区别的控制在这些酶的最重要的角色之中。因为这些过程被恶意的转变影响，HDAC禁止者作为反被开发在癌症病人的肿瘤的药和areshowing鼓励功效。

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简介：Thetangentresistanceontheinterfaceofthesoil-moldboardisanimportantcomponentoftheresistancetomovingsoil.Wedevelopedsimplifiedmechanicalmodelstoanalyzethisresistance.Wefoundthatitiscomposedoftwocomponents,thefrictionalandadhesiveresistances.Thesetwocomponentsoriginatefromthesoilpore,whichinducedacapillarysuctioneffect,andthesoil-moldboardcontactareaproducedtangentadhesiveresistance.Thesetwocomponentsvarieddifferentlywithsoilmoisture.Thuswepredictedthatresistancereductionagainstsoilexertedonthenon-smoothbionicmoldboardismainlyduetotheeliminationofcapillarysuctionandthereductionofphysical-chemicaladsorptionofsoil.

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简介：Amolecularmodelofpancreaticzymogengranule（ZG）iscriticalforunderstandingitsfunctions.WehaveextensivelycharacterizedthecompositionandmembranetopologyofratZGproteins.Inthisstudy,wereportthedevelopmentoftargetedproteomicsapproachestoquantifyrepresentativemouseandhumanZGproteinsusingLC-SRMandheavyisotope-labeledsyntheticpeptides.TheabsolutequantitiesofmouseRab3DandVAMP8weredeterminedas1242±218and2039±151（mean±SEM）copiesperZG.ThesizedistributionandtheaverageddiameterofZGs750±23nm（mean±SEM）weredeterminedbyatomicforcemicroscopy.TheabsolutequantificationofRab3Dwasthenvalidatedusingsemi-quantitativeWesternblottingwithpurifiedGST-Rab3Dproteinsasaninternalstandard.Toextendourproteomicsanalysistohumanpancreas,ZGswerepurifiedusinghumanaciniobtainedfrompancreaticislettrans-plantationcenter.OnehundredandeightyhumanZGproteinswereidentifiedforthefirsttimeincludingboththemembraneandthecontentproteins.Furthermore,thecopynumberperZGofhumanRab3DandVAMP8weredeterminedtobe1182±45and485±15（mean±SEM）.ThecomprehensiveproteomicanalysesofmouseandhumanpancreaticZGshavethepotentialtoidentifyspecies-specificZGproteins.ThedeterminationofproteincopynumbersonpancreaticZGsrepresentsasignificantadvancetowardsbuildingaquantitativemolecularmodelofaprototypicalsecretoryvesicleusingtargetedproteomicsapproaches.TheidentificationofhumanZGproteinslaysafoundationforsubsequentstudiesofalteredZGcompositionsandsecretioninpancreaticdiseases.

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