RNA Interference (RNAi) effectors have been used to inhibit rogue RNAs in mammalian cells.
More than 60 putative EHEC type III effectors have been proposed using the proteomic approach [39] and bioinformatic studies [40].
Small GTPases and their downstream effectors have been implicated in steroid action in vitro and in vivo [4], [5], [14], [15], [29], [30], [37].
Several effectors have been shown to interact with the GTP-bound form of ARL-1 [18], [18], 27, particularly the GRIP domain of several golgins/tethering factors.
Many hypersensitive response and pathogenicity (Hrp) outer proteins (Hops) and effectors have been discovered in biotrophic phytopathogens, including P. syringae [5], [25], [35] [38].
It is remarkable that at least nine different Avr genes corresponding to RXLR effectors have been described in three species of oomycete plant pathogens in the last five years [6], [7], [8], [9], [16], [17], [18], [21].
The Yop effectors have been shown to interfere with several signal transduction pathways within eukaryotic cells [21], paralyzing phagocytosis, cell migration, NF-κB activation and other functions that are required for innate and adaptive immune responses [22].
Previous studies have shown how the primary sequences of RXLR effectors have been shaped by positive selection, and how the genes themselves undergo accelerated birth and death evolution [21], [24].
Three of the effectors have been cloned and fully characterized.
Three effectors have been implicated; AexT/AexU, Act2 and Hcp.
In C. gigas, several antimicrobial effectors have been recently characterized.
