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Human immunodeficiency virus, cytoplasmic

Abrahamyan LG, Mkrtchyan SR, Binley J, Lu M, Melikyan GB, Cohen FS. The cytoplasmic tail slows the folding of human immunodeficiency virus type 1 Env from a late prebundle configuration into the six-helix bundle. J Virol 2005 79(1) 106-115. [Pg.277]

Edwards TG, Wyss S, Reeves JD, et al. Truncation of the cytoplasmic domain induces exposure of conserved regions in the ectodomain of human immunodeficiency virus type 1 envelope protein. J Virol 2002 76(6) 2683-2691. [Pg.281]

Wyss S, Dimitrov AS, Baribaud F, Edwards TG, Blumenthal R, Hoxie JA. Regulation of human immunodeficiency virus type 1 envelope glycoprotein fusion by a membrane-interactive domain in the gp41 cytoplasmic tail. J Virol 2005 79(19) 12231-12241. [Pg.282]

Bedinger P, Moriarty A, II RCvB, Donovan NJ, Steimer KS, Littman DR. Internalization of the human immunodeficiency virus does not require the cytoplasmic domain of CD4. Nature 1988 334 162-165. [Pg.287]

Roth ), Dobbelstein M, Freedman DA, Shenk T, Levine AJ (1998) Nucleo-cytoplasmic shuttling of the hdm2 oncoprotein regulates the levels of the p53 protein via a pathway used by the human immunodeficiency virus rev protein. EMBO J 17 554-564... [Pg.156]

Wolff, B., Sanglier, J. J., Wang, Y. (1997). Leptomycin B is an inhibitor of nuclear export inhibition of nucleo-cytoplasmic translocation of the human immunodeficiency virus type 1 (HIV-1) Rev protein and Rev-dependent mRNA. Chem. Biol., 4, 139-147. [Pg.237]

Rather uniquely, ICAM-1 is also subverted as receptor by human pathogens in at least three different ways. Major group rhinoviruses and A-type coxsackieviruses use ICAM-1 to release their RNA into the host cell cytoplasm. Erythrocytes infected by the malarial parasite Plasmodium falciparum, are able to bind ICAM-1 in the surface of endothelial cells (Berendt et al., 1992 Ockenhouse et al., 1992), and use this cytoadherence to sequester themselves in deep vascular beds, including the brain, minimizing exposure of the parasite to immune surveillance. Finally, human immunodeficiency virus-1 (HIV-1), uses ICAM-1 as a coreceptor (Bastiani et al., 1997 Fortin et al., 1997 Rizzuto and Sodroski, 1997). HIV-1 acquires several host cell membrane proteins when it buds from infected cells, making it possible for ICAM-1 to be incorporated into the envelope of the virions. This results in an increase of subsequent virus-cell interactions, enhancement of virus infectivity, and extension of the host cell range. [Pg.224]

DNA and RNA decoys are smaU oUgonucleotide fragments that mimic the start sequences of potentiaUy harmful genes. By doing so, the decoys can effectively trap the transcriptional and translational machinery, thereby causing a sharp decrease in mRNA or protein production. There has been success with this approach in human immunodeficiency virus (HIV) research. DNA and RNA decoys have been used to halt the function of REV proteins, which are responsible for making late transcripts of RNA and exporting them to the cytoplasm [5], and the TAT protein, which binds and activates the natural promoter for HIV-1 [6]. [Pg.684]

Spumavirus (the foamy viruses) Lentivirus (human, feline, simian, and bovine immunodeficiency viruses). Enveloped, spherical, negative-sense, and ssRNA (two identical strands). Synthesis occurs in the host cell cytoplasm maturation involves budding through the host cell plasma membrane. These viruses contain the enzyme reverse transcriptase. The retroviruses (except the Spumavirus and Lentivirus genera) represent the RNA tiunor viruses, causing leukemias, carcinomas, and sarcomas. [Pg.1216]


See other pages where Human immunodeficiency virus, cytoplasmic is mentioned: [Pg.174]    [Pg.389]    [Pg.146]    [Pg.231]    [Pg.512]    [Pg.182]    [Pg.445]    [Pg.36]    [Pg.57]    [Pg.218]    [Pg.330]    [Pg.107]   


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