简介：Thereareabout17chromosomesinyeastSaccharomycescerevisiae.Amiddlesizedchromosome,chromosomeV,waschoseninthisworkforstudyingandconstructingthephysi-calmaps.ChromosomeVfromstrainA364awasisolatedbypulsed-fieldgradientgelelectrophoresis(PFGE).GelslicescontainingchromosomeVDNAweredigestedwithtworarecuttingenzymes,NotⅠandSfiⅠ,andthree6-Ntrecognizingenzymes,SmaⅠ,SstⅡandApaⅠ.Severalstrategies-partialorcompletedigestions,digestionwithdifferentsetsoftwoenzymes,andhybrid-izationwithclonedgeneticallymappedprobes(CAN1,URA3,CEN5,PRO3,CHO1,SUP19,RAD51,RAD3)——wereusedtoaligntherestrictionfragments.Thereare9,9,15,17,and20sitesforNotⅠ,SfiⅠ,SmaⅠ,SstⅡandApaⅠrespectivelyinthemapoftheA364achromosomeV.Itstotallengthwascalculatedtobe620Kb(Kilo-bases).Thedistributionsofthecuttingsitesforthesefiveenzymesthroughthewholechromosomearenotuniform.Acomp-arisonbetweenthephysicalmapandthegeneticmapwasalsomade.

简介：LRP16以前在乳癌房间作为导致雌激素的基因被识别。到在子宫内膜的癌症(EC)的雌激素和它的功能的效果的LRP16的应答的海角房间仍然是不清楚的。这里，我们证明LRP16基因的信使rna水平和倡导者活动被17beta-estradiol(E2)显著地在雌激素受体高山增加哈(嗯高山哈)-positiveIshikawa人EC房间。尽管Ishikawa细胞的生长率没被LRP16的宫外的表示显然影响，Transwell试金的结果显示出LRP16-overexpressing细胞的侵略能力的近似one-thirdincrease。由于分子的屏蔽，我们观察到E-cadherin的表示，与肿瘤转移联系的一个必要粘附分子，被LRP16镇压。进一步的倡导者分析以一种剂量依赖者方式表明了那LRP16inhibitedE-cadherintransactivation。然而，抑制被雌激素剥夺废除，显示由LRP16requires的E-cadherin抄写的down规定嗯高山哈调停。染色质免疫降水分析表明到E-cadherin倡导者的ERalpha的绑定被LRP16反对，建议那LRP16能防碍嗯调停alpha的抄写。这些结果建议起来由雌激素的LRP16的规定能被在人的EC调整E-cadherin的down涉及侵略生长。

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