NDLI: Differential suppression by protease inhibitors and cytokines of apoptosis induced by wild-type p53 and cytotoxic agents.

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Differential suppression by protease inhibitors and cytokines of apoptosis induced by wild-type p53 and cytotoxic agents.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lotem, J. Sachs, L.
Description	Author Affiliation: Lotem J ( Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.);
Abstract	Apoptosis induced in myeloid leukemic cells by wild-type p53 was suppressed by different cleavage-site directed protease inhibitors, which inhibit interleukin-1 beta-converting enzyme-like, granzyme B and cathepsins B and L proteases. Apoptosis was also suppressed by the serine and cysteine protease inhibitor N-tosyl-L-phenylalanine chloromethylketone (TPCK) [corrected], but not by other serine or cysteine protease inhibitors including N alpha-p-tosyl-L-lysine chloromethylketone (TLCK), E64, pepstatin A, or chymostatin. Protease inhibitors suppressed induction of apoptosis by gamma-irradiation and cycloheximide but not by doxorubicin, vincristine, or withdrawal of interleukin 3 from interleukin 3-dependent 32D non-malignant myeloid cells. Induction of apoptosis in normal thymocytes by gamma-irradiation or dexamethasone was also suppressed by the cleavage-site directed protease inhibitors, but in contrast to the myeloid leukemic cells apoptosis in thymocytes was suppressed by TLCK but not by TPCK. The results indicate that (i) inhibitors of interleukin-1 beta-converting enzyme-like proteases and some other protease inhibitors suppressed induction of apoptosis by wild-type p53 and certain p53-independent pathways of apoptosis; (ii) the protease inhibitors together with the cytokines interleukin 6 and interferon-gamma or the antioxidant butylated hydroxyanisole gave a cooperative protection against apoptosis; (iii) these protease inhibitors did not suppress induction of apoptosis by some cytotoxic agents or by viability-factor withdrawal from 32D cells, whereas these pathways of apoptosis were suppressed by cytokines; (iv) there are cell type differences in the proteases involved in apoptosis; and (v) there are multiple pathways leading to apoptosis that can be selectively induced and suppressed by different agents.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	22
Volume Number	93
Language	English
Publisher	National Academy of Sciences
Publisher Date	1996-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Apoptosis Drug Effects Cytokines Pharmacology Endopeptidases Protease Inhibitors Tumor Suppressor Protein P53 Amino Acid Chloromethyl Ketones Butylated Hydroxyanisole Caspase 1 Cathepsin B Cathepsin L Cathepsins Cysteine Endopeptidases Metabolism Enzyme Precursors Granulocyte-Macrophage Colony-Stimulating Factor Granzymes Interferon-gamma Interleukin-6 Oligopeptides Pepstatins Serine Endopeptidases Tosyllysine Chloromethyl Ketone Tosylphenylalanyl Chloromethyl Ketone Tumor Cells, Cultured Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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