Journal
FEBS LETTERS
Volume 508, Issue 2, Pages 226-230Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/S0014-5793(01)03057-5
Keywords
acivicin; apoptosis; differentiation; ectoprotease; proliferation; signaling
Funding
- NIAID NIH HHS [R01 AI42772] Funding Source: Medline
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The inhibitor of gamma -glutamyl transpeptidase (gamma -GT) acivicin modulates cellular responses including growth, myeloid maturation and apoptosis. Whether these effects result from the inhibition of gamma -GT enzyme activity remains unclear. We compared the cellular effects of acivicin against a more potent and specific inhibitor of gamma -GT (L-2-amino-4-boronobutanoic acid (L-ABBA)) in gamma -GT-negative (B lymphoblastoid Ramos) and gamma -GT-positive (myelomonocytie HL-60, y-GT-transfected Ramos) cell lines. Under non-oxidative stress conditions, acivicin-induced cell growth arrest, apoptosis and macrophage maturation occurred independent of gamma -GT While L-ABBA did not influence any of these processes. Acivicin triggered tyrosine phosphorylation and increased nuclear factor kappaB activity. Further insight into the role of gamma -GT in cellular processes is needed. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
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