PLK2

PLK2, also called SNK, contrasts with its mitotic paralog PLK1 by acting earlier in the cell cycle and in post-mitotic neurons. Transcriptionally induced in G1 and by serum stimulation, PLK2 supports centriole duplication together with PLK4 and restrains unscheduled proliferation, giving it tumor-suppressive traits in several contexts. In the brain, PLK2 homeostatically phosphorylates α-synuclein at Ser129, limiting its toxic aggregation, and it contributes to synaptic scaling and neuronal survival after stress. Reduced PLK2 activity has been linked to α-synucleinopathies and to some cancers. Recombinant PLK2 enables studies of centriole biology, α-synuclein regulation, and PLK-family redundancy.