Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 89 (1), 89-93

The Defect Seen in the Phosphatidylinositol Hydrolysis Pathway in HIV-infected Lymphocytes and Lymphoblastoid Cells Is Due to Inhibition of the Inositol 1,4,5-trisphosphate 1,3,4,5-tetrakisphosphate 5-phosphomonoesterase

Affiliations

The Defect Seen in the Phosphatidylinositol Hydrolysis Pathway in HIV-infected Lymphocytes and Lymphoblastoid Cells Is Due to Inhibition of the Inositol 1,4,5-trisphosphate 1,3,4,5-tetrakisphosphate 5-phosphomonoesterase

K E Nye et al. Clin Exp Immunol.

Erratum in

  • Clin Exp Immunol 1992 Oct;90(1):160

Abstract

Lymphocytes infected in vivo with HIV or lymphoblastoid cells exposed in vitro to either HIV or its envelope glycoprotein (gp120) show a defect in inositol polyphosphate-mediated signal transduction together with an associated abnormality in intracellular calcium regulation. The defect in patients reverses after treatment with the anti-retroviral agent zidovudine (AZT). We present evidence that the defect is at the level of the Ins (1,3,4,5)P4 5-phosphomonoesterase (PME) in these cells and that, though elevation of the intracellular ATP level partially down-regulates the activity of this enzyme, such changes alone are unable to account for the complete inhibition seen in HIV-infected cells.

Similar articles

See all similar articles

Cited by 3 PubMed Central articles

References

    1. Curr Opin Immunol. 1991 Aug;3(4):537-42 - PubMed
    1. Annu Rev Biochem. 1987;56:159-93 - PubMed
    1. Adv Immunol. 1990;48:227-360 - PubMed
    1. AIDS. 1990 Jan;4(1):41-5 - PubMed
    1. J Biol Chem. 1991 Jun 15;266(17):11176-83 - PubMed

Publication types

MeSH terms

Feedback