简介：Genestellcellswhattodo,forexample,whentorepairDNAmistakesorwhentodie,andcanbeturnedonorofflikealightswitch.Knowingwhichgenesareswitchedon,orexpressed,isimportantforthetreatmentandmonitoringofdisease.Now,forthefirsttime,Researchersinthelaboratoryof

简介：Objective:Toinvestigatetherelationshipbetweengenemutationandpathologicaltypeoflungcancer,inspectandverifytheconsistencybetweenhomologousgenesmutationinvariouspathologictype.Methods:CombinedwiththeCOSMICandUniProtdatabase,weobtainedthereportedoverallbig-samplemutationdataoflungcancerandtheproteinsequencesofthetop20mutatedgenes,respectively.Analyzethedataandclustertheproteinsequencesandthendeducethehomologousgene.Ultimately,analyzethemutationsofdifferentpathologicaltypesofhomologousgenes.Results:TP53(32.32%)hasthehighestmutationrateinlungcancer,followedbyEGFR(29.12%).Thecopynumbervariability(CNV)ofgenes:KRAS,LRP1B,CDKN2A,KMT2C,FAT1,PIK3CA,RB1,ERBB4,GRIN2AandKDRbetweeneachpathologicaltypeisstaticallysignificant(P<0.05).ThegenedifferentialexpressionratebetweenadenocarcinomaandsquamouscarcinomaofgeneTP53,KRAS,LRP1B,CDKN2A,STK11,FAT4,KMT2D,NFE2L2,KEAP1,PIK3CA,RB1,ERBB4,SMARCA4andKDRarestatisticallysignificant(P<0.05).ThesimilarityoftheproteinsequenceofEGFRandERBB4canreach93%,andFAT4andFAT1are81%.Forsmallcellcarcinoma,there’snodifferenceinCNVbetweenthetwogroupsofhomologousgenes,andnodifferencebetweenFAT4andFAT1inadenocarcinoma.Conclusion:TheCNVandgeneexpressionoflungcancer-associatedgenesarerelevanttopathologictypes.GFRandERBB4arehomologous,FAT4andFAT1arealsoamongthetop20mutationgenes.Additionally,there’snodifferenceinCNVbetweenthetwogroupsofsmallcellcarcinoma,whichisthesamebetweenFAT4andFAT1inadenocarcinoma.

简介：Tworecentstudieshavediscoveredasurprisinglinkbetweenthreeseeminglydifferentclinicaldiseases:onethatdestroysbonemarrow,anotherthatpreventssundamagefrombeingrepaired,andathirdwhichcauseschildrentoshowsignsofagingextremelyearly.Ithasbeenfoundthatallthreediseasesarecausedbymutationsinthesamegene.Mutationscomeinanumberofdifferentflavors,

简介：客观：击倒链球菌mutans(S.mutans)的全部勒克司基因经由相应再结合和构造的UA159紧张S的删除勒克司的变异的紧张。Mutans。学习S的酸抵抗之间的差别。MutansIngbrittC国际标准紧张和勒克司变异的紧张的酸抵抗。方法：二DNA碎裂定位在勒克司上面、下游基因被放大，在他们之间的PJT10的抗生素的一种抵抗基因被设计进PUC19为构造再结合的plasmidplasmidpUCluxKO。S.mutans房间与的ElectrotransformationpUCluxKO变异导致了抗生素的一种的隔离抵抗S。Mutanstransformants，它被聚合酶链反应，V.harveyiBB170光生物鉴定和定序的分析识别。S的答案。有一样的密度的Mutans标准紧张和勒克司变异的紧张被做并且在pH有教养为一样的period.Terminal生长状况的3.5～7.0BHI液体compared.Firstly在pH被酸化5.5BHI液体，二紧张在pH是有教养的3.0BHI液体。二紧张的酸忍耐回答是compared.Results:限制endonuclease分析证明那pUCluxKO变异的向量成功地被重新结合。S.mutans异种的删除勒克司的地位被PCR与为勒克司和抗生素的一种抵抗的基因特定的教材证实。S.mutans异种不能导致生物体之发光，indiating异种成功地被重新结合。在文化的二十代以后，构造中国S.mutans异种被证实稳定。aciduricity的重要差别在S.mutans标准紧张和标准紧张的抵抗是的勒克司变异的strain.The酸之间被观察比二紧张两个都显示了的勒克司变异的strain.The的强壮酸忍耐回答的能力。结论:S.mutans基因突变而产生之遗传的交换plasmid校正地被构造并且一S.mutans的勒克司否定的异种被构造，它能帮助推进在S.mutans的致病学习勒克司的角色。勒克司变异的紧张对酸忍耐回答的酸inactivation，而是能力更敏感仍然存在。

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