IndraLab

Statements


| 7

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"Furthermore, A20 and CYLD are recognized for their tumor suppressing functions because deficiency or mutation of A20 or CYLD is associated with lymphoma and familiar cylindromatosis, respectively [ xref – xref ]."

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"These results suggest that ITCH modulates TRAF6 deubiquitylation by interacting with A20 and CYLD in cardiomyocytes."

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"This mechanism is plausible because in H. pylori infection, we detected the interaction of A20 with a complex composed of TRAF6, CYLD, TIFA and TAK1 (Fig.  xref ), likely via A20’s association with TIFA (Lim et al, xref ) because recombinant A20 and CYLD did not interact directly (Fig.  xref )."

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"Adding just another level of complexity to an already crowded CD137 signalosome, we have recently observed the functional association of K63-DUBs A20 and CYLD to the CD137 signalosome."

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"IP assay results indicated that the methylated TRAF2 weakened the interaction with A20 or CYLD."
| PMC

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"ITCH is a E3 ubiquitin ligase that has been shown to be part of the A20 and CYLD ubiquitin-editing complexes, aiming at the regulation/termination of NF-κB signaling ( xref )."

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"In protecting M1-linked chains from degradation, A20 suppresses TNF-induced cell death by stabilising complex I. Antagonising interactions between A20 and CYLD may provide a mechanism for regulating the interplay between complex I and complex II-mediated signalling pathways (Fig. xref )."