CYLD in Ubiquitin Signaling and Tumor Pathogenesis

Fumiyo Ikeda; Ivan Dikic

doi:10.1016/j.cell.2006.05.003

CYLD in Ubiquitin Signaling and Tumor Pathogenesis

Fumiyo Ikeda, Ivan Dikic

Department of Molecular and Cellular Biology

Research output: Contribution to journal › Short survey

23 Citations (Scopus)

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-κB and activates transcription of proliferation genes in response to growth signals.

Original language	English
Pages (from-to)	643-645
Number of pages	3
Journal	Cell
Volume	125
Issue number	4
DOIs	https://doi.org/10.1016/j.cell.2006.05.003
Publication status	Published - May 19 2006

All Science Journal Classification (ASJC) codes

Biochemistry, Genetics and Molecular Biology(all)

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10.1016/j.cell.2006.05.003

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Ikeda, F., & Dikic, I. (2006). CYLD in Ubiquitin Signaling and Tumor Pathogenesis. Cell, 125(4), 643-645. https://doi.org/10.1016/j.cell.2006.05.003

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title = "CYLD in Ubiquitin Signaling and Tumor Pathogenesis",

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-κB and activates transcription of proliferation genes in response to growth signals.",

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