Abstract
Absence of CYLD, which encodes a deubiquitinating enzyme, causes an inherited disease characterized by benign skin tumors. In this issue of Cell, Massoumi et al. (2006) show that CYLD deubiquitinates the coactivator Bcl-3, thereby preventing its translocation into the nucleus, where it normally interacts with NF-kappaB and activates transcription of proliferation genes in response to growth signals.
MeSH terms
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B-Cell Lymphoma 3 Protein
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Deubiquitinating Enzyme CYLD
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Genes, Tumor Suppressor
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Humans
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NF-kappa B / metabolism
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Neoplasms / metabolism*
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Neoplasms / pathology
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Proto-Oncogene Proteins / metabolism
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Signal Transduction / physiology*
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Transcription Factors
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism*
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Ubiquitin / metabolism*
Substances
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B-Cell Lymphoma 3 Protein
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BCL3 protein, human
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NF-kappa B
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Proto-Oncogene Proteins
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Transcription Factors
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Tumor Suppressor Proteins
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Ubiquitin
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CYLD protein, human
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Deubiquitinating Enzyme CYLD