RNase H-mediated cleavage of the template strand

Stable Identifier
R-HSA-164528
Type
Reaction [transition]
Species
Homo sapiens
Related Species
Human immunodeficiency virus 1
Compartment
ReviewStatus
5/5
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As the reverse transcriptase activity of the HIV-1 RT heterodimer catalyzes the extension of the minus-strand DNA, the RNaseH activity catalyzes the degradation of the complementary viral genomic RNA sequences. Telesnitsky and Goff (1993) observed that two defective forms of reverse transcriptase can complement to restore retroviral infectivity. The RNase H active site is positioned within the HIV-1 RT heterodimer so as to attack the RNA strand of the RNA:DNA duplex at a point 18 bases behind the site of reverse transcription (Furfine and Reardon 1991; Ghosh et al. 1995; Gopalakrishnan et al. 1992; Wohrl and Moelling 1990). The rate of RNase H cleavage is substantially lower than the rate of DNA synthesis and the level of its activity in vivo is unclear, however (Kati et al. 1992). The product of these combined DNA synthesis and RNA degradation events is a DNA strand still duplexed with extended viral genomic RNA fragments.
Literature References
PubMed ID Title Journal Year
15542682 Effects of mutations in the G tract of the human immunodeficiency virus type 1 polypurine tract on virus replication and RNase H cleavage

Sarafianos, SG, Alvord, WG, Julias, JG, Hughes, SH, McWilliams, MJ, Arnold, E

J Virol 2004
10723025 The HIV-1 reverse transcription (RT) process as target for RT inhibitors

De Clercq, E, Anne, J, Jonckheere, H

Med Res Rev 2000
7681062 The sequence features important for plus strand priming by human immunodeficiency virus type 1 reverse transcriptase

Pullen, KA, Champoux, JJ, Rattray, AJ

J Biol Chem 1993
  Retroviruses

Varmus, HE, Hughes, SH, Coffin, JM

  1997
Participants
Participates
Catalyst Activity

RNA-DNA hybrid ribonuclease activity of RTC with minus strand DNA synthesis initiated from 3'-end [cytosol]

Disease
Name Identifier Synonyms
Human immunodeficiency virus infectious disease DOID:526 HIV infection
Authored
Reviewed
Created
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