Description: Alternative splicing removes the TRAF2-binding motif of Ubiquitin carboxyl-terminal hydrolase CYLD (Cyld), abrogating binding to TNF receptor-associated factor 2 (Traf2). Mice expressing solely the alternatively spliced Isoform 3 of Ubiquitin carboxyl-terminal hydrolase CYLD (Cyld) (sCYLD) show an altered B-cell expansion profile and have more stable NF-kB proteins.
Participants: (1) Ubiquitin carboxyl-terminal hydrolase CYLD (Cyld) (2) TNF receptor-associated factor 2 (Traf2)
(1) Regulation of B cell homeostasis and activation by the tumor suppressor gene CYLD.Hövelmeyer et al. J. Exp. Med. (2007) (2) Alternative splicing in the NF-kappaB signaling pathway.Leeman et al. Gene (2008) (3) The tumour suppressor CYLD negatively regulates NF-kappaB signalling by deubiquitination.Kovalenko et al. Nature (2003)
Other switches involving interfacesMATH domain - 1 more (view)
