Bacterial toxin RelE induces apoptosis in human cells

The bacterial protein RelE severely restricts prokaryotic cell growth, probably by acting as a global inhibitor of translation. It is ubiquitous in prokaryotes as part of the RelE–RelB toxin–antitoxin system, and may be activated by nutritional stress. When the relE gene from Escherichia coli was ex...

Full description

Saved in:
Bibliographic Details
Published in:FEBS letters 2002-05, Vol.519 (1), p.191-194
Main Authors: Yamamoto, T.-A.M, Gerdes, K, Tunnacliffe, A
Format: Article
Language:English
Subjects:
Anti-Bacterial Agents - pharmacology
Apoptosis - drug effects
Bacterial Proteins - antagonists & inhibitors
Bacterial Proteins - genetics
Bacterial Proteins - toxicity
Cell Division - drug effects
Cell Survival - drug effects
Clone Cells - drug effects
Clone Cells - metabolism
DNA Fragmentation
DNA, Antisense - genetics
DNA, Antisense - pharmacology
DNA, Bacterial - genetics
Gene Expression - drug effects
Gene Transfer, Horizontal
Growth inhibition
Human cell
Humans
Mammalian cell
Osteosarcoma - metabolism
RelB
RelE
Tetracyclines
Toxin–antitoxin
Transcription, Genetic - drug effects
Tumor Cells, Cultured
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The bacterial protein RelE severely restricts prokaryotic cell growth, probably by acting as a global inhibitor of translation. It is ubiquitous in prokaryotes as part of the RelE–RelB toxin–antitoxin system, and may be activated by nutritional stress. When the relE gene from Escherichia coli was expressed inducibly in a human osteosarcoma cell line, it was shown to retard growth and to lead to cell death by apoptosis. RelE is therefore unusual among bacterial toxins in possessing broad activity against both prokaryotes and eukaryotes, perhaps by acting on evolutionarily conserved components of the translation machinery.
ISSN:0014-5793
1873-3468
DOI:10.1016/S0014-5793(02)02764-3