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Insulin Signaling, Lipoproteins and Atherosclerosis

胰岛素信号传导、脂蛋白和动脉粥样硬化

基本信息

批准号：
7329715
负责人：
ALAN richard TALL
金额：
$ 55.25万
依托单位：
COLUMBIA UNIVERSITY HEALTH SCIENCES
依托单位国家：
美国
项目类别：
财政年份：
2007
资助国家：
美国
起止时间：
2007-07-01 至 2012-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7329715
关键词：
Apolipoproteins B Apoptosis Apoptotic Area Atherosclerosis CD36 gene Caenorhabditis elegans Caloric Restriction Cells Cholesterol Collaborations Data Diabetes Mellitus Enzymes Exclusion Failure Foam Cells Genetic Glucose Hepatic Hepatocyte Histones Hyperinsulinism Induction of Apoptosis Insulin Insulin Receptor Insulin Resistance Insulin Signaling Pathway Knock-out LDL Cholesterol Lipoproteins Laboratories Leptin Lesion Ligation Link Lipoproteins Liver Longevity Low-Density Lipoproteins Mammalian Cell Mediating Metabolic Metabolism Modeling Modification Molecular Target Mus Necrosis Nuclear Numbers Orthologous Gene Peripheral Phosphorylation Plasma Predisposition Protein Overexpression Proteins Reagent Regulation Role Serum Signal Pathway Signal Transduction Sirtuins Stimulus Stress TLR4 gene Testing Transgenes Very low density lipoprotein Week Work base biological adaptation to stress deprivation feeding in vivo insulin signaling interest knock-down lipid biosynthesis macrophage oxidized low density lipoprotein research study response scavenger receptor transcription factor uptake

项目摘要

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IAmtehcehroasncislemrostiacrevapsocourlayrudnisdearsteooisd.aImnsaujloinr creasuisetaonfcme oartbthideitycealnludladrelaevthelincaduiasbeestemsa,nbyuttfhteheucnodmerplylicnagtions 糖尿病。在最近与 Tabas 和 Accili 实验室的合作研究中，我们表明 Itmrancsrcorpiogneasl feroxmpreinssuiolin oref cCeDp3to6r a(InRd) SderfAic,ieinct rmeaicsedisupltaykedeofemctoivdefieindsulliDnLsiagndalincgr,esceredaseudscpeopstitb-ility FC负载和其他刺激诱导的细胞凋亡。细胞凋亡易感性与诱导失败有关 IAinktot aLcDtiLvRity-/-dumrinceg trheesuEltRs istrfeosrmsaretisopnoonfsea.dvAacnccoerdinlegslyio,nbsoncoenmtaainrrinogw itnracrnesapslaendtantuiommnbferorsmofIRapdoepfictoietinct 小鼠 Idminecacrcerreaoaspsehedadgseaigsthneanrliondsgclalterhgroeosruigsnh.eTcprhoretiscuencrvoderedrslyh.ineIngpahtiycpoInRtvhse， rswsisemoftoduiesnl,dpLrtDojLehRcat-v/i-semtlhoiacweteinrwsVituhLliDnpLer/reLipsDhisLetarlaenlvceIRlswdaoenrfsidceinescy 和 Ifautrhtheerorsecvlearlousaiste, macetnhganbiostmhsatlinthkeinlgevinesl uolfinthresviesstasneclewainll,mancdroaplshoaginetfhoeamlivecre.llTshteo parhopeorossacllwerilolsies,ekantod 也肝脏中胰岛素信号传导与脂蛋白代谢变化之间的关系。目标1我们 Iwitllhcdoellafebcotrivaeteintosuilninvesigtingaltiengt.heInmpeacrthicaunliasrmwseawndill cdoentesremqiunencifedseocrfeinacsredasIRedsiagpnoaplintogsiasnidn lmowaecroApkhtaagcetsivity 导致核 FoxO1/3 活性增加、ER 应激/CHOP 诱导和细胞凋亡增加。目标 2 Iwleesiownilallemxtaecnrdopohuarginesvivinocrsetuadsmanadcrfouprthaegreaxpoloprteosthiseahnydpoathesriosmthaactodmepfelecxtivye。中的研究项目 1 和 3 将测试 SRA 和 FoxO 在调节这些影响中的作用。在目标 3 中，我们将确定是否 Idinecgreradsaetdionhewpiathtiicninthseulisnecsrigentoarlyinpgaltehawdasyt.oTdhecsreeaxspeedrhimepeantisc cFomxOpl1emacetnivtityhoasnedothf uPsroinjecrte3asex damapinoinBg the Iipmropvaidcteonfehwepmatoiclec FuolxaOr i1nsoivgehrtsexipntroestshieoncaounsheespoaftidcialibpeidticanddyslipipoidperomteiainamndetiatsbovlaismcu.laTricsopmropjleicattimonasy。