Journal
FLY
Volume 1, Issue 6, Pages 330-332Publisher
LANDES BIOSCIENCE
DOI: 10.4161/fly.5399
Keywords
CYLD; NF-kappa B; JNK; ubiquitin; Drosophila
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Funding
- Biotechnology and Biological Sciences Research Council Funding Source: Medline
- Medical Research Council Funding Source: Medline
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The nuclear factor-kappaB (NF-kappa B) and c-Jun NH2-terminal kinase (JNK) signaling pathways regulate diverse biological processes, including the immune and inflammatory response, cell growth, apoptosis, and tumour formation. Not surprisingly therefore defects to either pathway contributes to the progression of numerous human disorders. Enhancing our understanding of the mechanisms that control signaling through these pathways is therefore significant as it may enable development of specific treatments. In this regard, CYLD was recently identified as a negative regulator of NF-kappa B and JNK signaling. CYLD has a C-terminal catalytic domain characteristic of deubiquitinating enzymes, and this is essential for CYLD to remove ubiquitin from certain proteins that positively mediate signaling through the NF-kappa B and JNK pathways. Recent studies have revealed a requirement for CYLD in many different processes and have provided some insight into the underlying mechanisms.
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