交替的聚嘌呤序列影响劳氏肉瘤病毒在体内的整合。
Alternate polypurine tracts affect rous sarcoma virus integration in vivo.
作者信息
Oh Jangsuk, Chang Kevin W, Alvord W Gregory, Hughes Stephen H
机构信息
HIV Drug Resistance Program, National Cancer Institute at Frederick, Frederick, MD 21702-1201, USA.
出版信息
J Virol. 2006 Oct;80(20):10281-4. doi: 10.1128/JVI.00361-06.
Abstract
When the endogenous polypurine tract (PPT) of the Rous sarcoma virus (RSV)-derived vector RSVP(A)Z was replaced with alternate retroviral PPTs, the fraction of unintegrated viral DNA with the normal consensus ends significantly decreased and the retention of part of the PPT significantly increased. If the terminus of the U3 long terminal repeat (LTR) is aberrant, RSV integrase can correctly process and integrate the normal U5 LTR into the host genome. However, the canonical CA is not involved in joining the aberrant U3 LTR to the host DNA, generating either large duplications or deletions of the host sequences instead of the normal 5- or 6-bp duplication.
摘要
当源自劳氏肉瘤病毒（RSV）的载体RSVP(A)Z的内源性多嘌呤序列（PPT）被其他逆转录病毒PPT取代时，具有正常共有末端的未整合病毒DNA的比例显著降低，而PPT部分的保留显著增加。如果U3长末端重复序列（LTR）的末端异常，RSV整合酶可以正确处理正常的U5 LTR并将其整合到宿主基因组中。然而，典型的CA不参与将异常的U3 LTR连接到宿主DNA，而是产生宿主序列的大片段重复或缺失，而不是正常的5或6个碱基对的重复。
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本文引用的文献
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2
Alternate polypurine tracts (PPTs) affect the rous sarcoma virus RNase H cleavage specificity and reveal a preferential cleavage following a GA dinucleotide sequence at the PPT-U3 junction.交替的聚嘌呤序列（PPTs）影响劳氏肉瘤病毒核糖核酸酶H的切割特异性，并揭示了在PPT-U3连接处的GA二核苷酸序列之后的优先切割。
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