Direct activation of protein phosphatase-2A 0 by HIV-1 encoded protein complex NCp7:vpr

• Published in: FEBS letters Vol. 401; no. 2; pp. 197 - 201
• Main Authors: Tung, H.Y.Lim, De Rocquigny, Hughes, Zhao, Ling-Jun, Cayla, Xavier, Roques, Bernard P, Ozon, René
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 20.01.1997
• Subjects: HIV-1; NCp7; Protein phosphatase-2A; vpr; HIV-1; NCp7; vpr; Protein phosphatase-2A
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/S0014-5793(96)01470-6

The effects of HIV-1 encoded proteins NCp7, vpr and NCp7:vpr complex on the activity of protein phosphatase-2A 0 have been tested. We report that NCp7 is an activator of protein phosphatase-2A 0 and that vpr activated protein phosphatase-2A 0 only slightly. We also report that NCp7 and vpr form a tight complex which becomes a more potent activator of protein phosphatase-2A 0 than NCp7 alone. The ability of NCp7 to activate protein phosphatase-2A 0 is regulated by vpr. The C-terminal portion of vpr prevents NCp7 from activating protein phosphatase-2A 0 while the N-terminal portion of vpr potentiates the effect of NCp7 on the activity of protein phosphatase-2A 0. Our findings indicate that vpr may be acting as a targeting subunit which directs NCp7 to activate protein phosphatase-2A 0. In view of the fact that protein phosphatase-2A functions as an inhibitor of G 2 to M transition of the cell cycle and is involved in other key cellular processes such as the control of RNA transcription, the results presented in this report may explain how HIV-1 causes cell cycle arrest which may lead to CD 4+ T cell depletion and also how it disturbs normal cellular processes of its host cell.