In the present study, we have demonstrated in vitro the capacity of Lrrk2, and truncated constructs which included the KKK domain, to carry out the phosphorylation of Asyn at serine 129. This is the reaction that may underlie the pathology of PD. Furthermore, we have shown that the disease causing G2019S GDC0068 enhances that kinase activity. This suggests a contributing mechanism to PD pathogenesis and indicates that Lrrk2 may be a target for future therapeutic intervention [9] and [10].
Acknowledgments
This research was supported by a grant from The Pacific Alzheimer Research Foundation and The National Natural Science Foundation of China (30670645).
Keywords
Protein splicing; Intein; Extein; Pyrococcus abyssi; Ribonucleotide reductase; Homing endonuclease
Introduction
Protein splicing is evaporation the process by which an intervening polypeptide, called an intein, facilitates its excision from flanking sequences, the exteins, concomitant with the ligation of the exteins. This converts the precursor fusion protein (NIC) to linked exteins (NC) and excised intein (I).
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Distribution patterns Although both species are considered
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