Lembo D, Angeretti A, Gaboli M, Cavallo R, Landolfo S
Institute of Microbiology of Novara, Institute of Microbiology of Turin, University of Turin, Italy.
New Microbiol. 1995 Apr;18(2):111-6.
Cotransfection of NIH 3T3 cells with a mammalian expression vector containing a v-Ha-ras gene, together with a plasmid carrying the human immunodeficiency virus (HIV) long terminal repeat (LTR) linked to the chloramphenicol acetyl transferase (CAT) reporter gene, significantly stimulated CAT activity. High HIV LTR activation was also observed in cell lines carrying stably transfected ras oncogenes, activated by point mutation or amplification. By contrast an inactivated form of ras (Ha-ras Asn-17) did not stimulate the HIV-LTR but strongly inhibited its basal activity. Activation of the p21ras protein may thus be one of the signals that regulate LTR driven transcription during HIV infection.
将含有v-Ha-ras基因的哺乳动物表达载体与携带与氯霉素乙酰转移酶（CAT）报告基因相连的人类免疫缺陷病毒（HIV）长末端重复序列（LTR）的质粒共转染NIH 3T3细胞，可显著刺激CAT活性。在通过点突变或扩增激活的稳定转染ras癌基因的细胞系中也观察到高HIV LTR激活。相比之下，ras的失活形式（Ha-ras Asn-17）不刺激HIV-LTR，但强烈抑制其基础活性。因此，p21ras蛋白的激活可能是HIV感染期间调节LTR驱动转录的信号之一。
