信息來源:新華網(wǎng)
抑制艾滋病病毒增殖新進(jìn)展
人體細(xì)胞中一種名為“APOBEC”的蛋白質(zhì)能阻礙艾滋病病毒增殖,但它通常會(huì)被艾滋病病毒合成的一種蛋白質(zhì)分解。日本京都大學(xué)研究人員利用一種酶提高了“APOBEC”蛋白質(zhì)抑制艾滋病病毒增殖的能力。
據(jù)日本共同社6日報(bào)道,日本京都大學(xué)講師高折晃史等人利用人體細(xì)胞研究發(fā)現(xiàn),“APOBEC”蛋白質(zhì)擁有促使艾滋病病毒基因變異,進(jìn)而阻礙其增殖的功能,不過通常它會(huì)被后者合成的一種蛋白質(zhì)分解,從而不能充分發(fā)揮抵御該病毒的能力。
研究人員為感染艾滋病病毒的細(xì)胞注入一種名為“A激酶”的酶,在這種酶的作用下,“APOBEC”蛋白質(zhì)變得不容易被分解,從而使其更好地抑制了艾滋病病毒的增殖。
在各國艾滋病防治工作中,艾滋病病毒耐藥性的增強(qiáng)是一個(gè)重要威脅,高折晃史希望上述研究成果能成為開發(fā)新型****的線索。這一研究成果發(fā)表在英國《自然結(jié)構(gòu)和分子生物學(xué)》雜志電子版上。(創(chuàng)賽新聞中canspecsci.com)
創(chuàng)賽推薦抑制艾滋病病毒增殖新進(jìn)展原始出處:
NatureStructural&MolecularBiologyPublishedonline: 05October2008; | doi:10.1038/nsmb.1497
Phosphorylationof APOBEC3G by protein kinase A regulates its interaction withHIV-1 Vif
KotaroShirakawa,AkifumiTakaori-Kondo,MasaruYokoyama, Taisuke Izumi,MasashiMatsui,Katsuhiro Io,Toshihiro Sato,Hironori Sato&TakashiUchiyama
ApolipoproteinBmRNA-editingenzymecatalyticpolypeptide–like 3G (APOBEC3G,referredto here asA3G) is apotentantiretroviral host factoragainsthumanimmunodeficiency virustype 1(HIV-1). HIV-1viralinfectivityfactor (Vif) counteracts A3Gbypromotingitsdegradation via theubiquitin-proteasomepathway.Recentstudiesdemonstrated thatprotein kinaseA(PKA)phosphorylatesactivation-induced deaminase(AID),anothermember ofthe APOBEC3family. A3G has twoputativePKAphosphorylationresidues. Here weshow that PKA bindsandspecificallyphosphorylatesA3G at Thr32 invitro and in vivo.Thisphosphorylationevent reducesthe bindingof A3G to Vif anditssubsequentubiquitination anddegradation,and thus promotesA3Gantiviralactivity.Computer-assistedstructural modelingandmutagenesisstudies suggestthat theinteraction between A3GThr32and Arg24 iscrucial forinteractionwith Vif. These dataimplythatPKA-mediatedphosphorylation of A3Gcan regulatetheinteractionbetween A3G andVif.