The tumour suppressor CYLD negatively regulates NF-κB signalling by deubiquitination

By A. Kovalenko, Christine Chable‐Bessia, G. Cantarella, A. Israël, D. Wallach, G. Courtois. Nature, 2003

1,103 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e773ade791d69313173667cba6ab541a4977f216

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Citations in the corpus

Frequent engagement of the classical and alternative NF-kappaB pathways by diverse genetic abnormalities in multiple myeloma. (2007, background): “…is a deubiquitinating enzyme that removes ubiquitin moieties from activated TRAF2, TRAF6, IKKg, and BCL3, thereby interfering with NF-kB signaling at multiple regulatory levels (Brummelkamp et al., 2003; Kovalenko et al., 2003; Massoumi et al., 2006; Regamey et al., 2003; Trompouki et al., 2003).”
Ubiquitin signalling in the NF-κB pathway (2005, background): “One of these DUBs is the cylindromatosis tumour suppressor protein CYLD, which inhibits IKK activation by cleaving Lys 63-linked polyubiquitin chains on several proteins, including TRAF2, TRAF6 and NEM”
A genomic and functional inventory of deubiquitinating enzymes. (2005, background): “One such example is the protein product of the Cylindromatosis tumor-suppressor gene (CYLD), a DUB involved in inhibiting NF-κB signaling (Brummelkamp et al., 2003; Kovalenko et al., 2003; Trompouki et al., 2003).”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “Thus, molecular signaling mechanisms within the TRIF-dependent pathway illustrate how selective binding of different molecules, i.e., either TRAF3 or TRAF6, results in recruitment and downstream activation of TBK1-IRF versus TAK1-IKK-NF- B, respectively (Fig.”
To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis (2003, background): “…CYLD was recently shown to interact directly with TRAF2 and IKKg/NEMO and to function as a TRAF2 deubiquitinating enzyme to negatively regulate IKKmediated activation of NF-kB downstream of CD40, XEDAR and EDAR (Brummelkamp et al., 2003; Kovalenko et al., 2003; Trompouki et al., 2003).”
Regulation and Cellular Roles of Ubiquitin-specific Deubiquitinating Enzymes (2009, background): “CYLD interacts directly with TRAF2, an adaptor molecule involved in signaling by members of the family of TNF/nerve growth factor receptors (188, 189).”
Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks (2004, background): “The tumor suppressor CYLD has been shown to regulate negatively NF-kB signaling by deubiquitination (Kovalenko et al., 2003).”