RNF11, a new piece in the A20 puzzle

The ubiquitin-editing protein A20 limits the duration of NF-kB activation and is essential to control inflammatory responses. Recent experiments have established that A20 mediates its inhibitory function in a complex with two other proteins, TAX1BP1 and the E3 ligase Itch. In a paper published in this issue, it is shown that RNF11 is also a critical component of the A20 ubiquitin-editing complex. NF-kB transcription factors regulate the expression of numerous genes involved in inflammation and immunity (Li and Verma, 2002). Activation of NF-kB is normally transient, and persistent NF-kB activation is associated with several autoimmune diseases and cancer. The duration of NF-kB activation is controlled by a number of inhibitory proteins, including A20, which functions in a negative feedback loop to limit NF-kB activation. A20 is essential