Journal
CELL DEATH AND DIFFERENTIATION
Volume 21, Issue 3, Pages 407-415Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2013.154
Keywords
bendless; cell death; cell migration; JNK; TNF
Categories
Funding
- National Basic Research Program of China (973 Program) [2010CB944901, 2011CB943903]
- National Natural Science Foundation of China [31071294, 31171413, 31371490]
- PhD Programs Foundation of Ministry of Education of China [20120072120030, 20120072110023]
- Shanghai Committee of Science and Technology [09DZ2260100]
- National Institutes of Health
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The TNF-JNK pathway is a highly conserved signaling pathway that regulates a wide spectrum of biological processes including cell death and migration. To further delineate this pathway, we carried out a genetic screen for dominant modifiers of the cell death phenotype triggered by ectopic expression of Eiger (Egr), the Drosophila TNF ortholog. Here we show that Bendless (Ben), an E2 ubiquitin-conjugating enzyme, modulates Egr-induced JNK activation and cell death through dTRAF2. Furthermore, Ben physically interacts with dTRAF2 and regulates Egr-induced dTRAF2 polyubiquitination. Finally, Ben is required for JNKdependent tumor progression, cell migration, oxidative stress resistance and longevity. Our results indicate that Ben constitutes an essential component of the evolutionarily conserved TNF-JNK pathway that modulates cell death and invasion, tumor progression, stress response and lifespan in metazoans.
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