Cyclin-dependent kinase that phosphorylates the transcription factor ETS2 (in vitro) and positively controls its proteasomal degradation (in cells). Involved in the regulation of actin cytoskeleton organization through the phosphorylation of actin dynamics regulators such as PKN2. Is a negative regulator of ciliogenesis through phosphorylation of PKN2 and promotion of RhoA signaling. ATP + L-seryl-[protein] = ADP + H(+) + O-phospho-L-seryl-[protein] ATP + L-threonyl-[protein] = ADP + H(+) + O-phospho-L-threonyl-[protein] Heterodimer with CCNQ, the interaction is required for kinase activity. Interacts with ETS2. Interacts with PRK2. CDK10 knockout results in partial prenatal lethality. Surviving mice display severe growth retardation, a reduced volume of mineralized matrix in the head, femur, tibia and fibula, bifidity or clefting of C1 (atlas) or C2 (axis), and absence of the dens. Additional defects are present in the kidney, lung, heart, spleen, liver, and muscle. At cellular level, CDK10 knockout does not affect cell proliferation. However, knocked-out mouse embryonic fibroblasts (MEFs) develop longer cilia. Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. CDC2/CDKX subfamily.