Cyclin-Q (CCNQ)

Cyclin-Q (CCNQ), also known as Cyclin M or FAM58A, is a member of the cyclin family that functions primarily as the activating regulatory subunit for cyclin-dependent kinase 10 (CDK10)[3][6]. The CCNQ gene encodes a protein that forms a stoichiometric complex with CDK10 to confer kinase activity. This complex has important roles in cell cycle progression, particularly during transitions associated with the G2/M and M phases, and in transcriptional regulation by phosphorylating substrates such as retinoblastoma protein (Rb1), c-MYC, and the C-terminal domain of RNA polymerase II[3][5]. Cyclin Q/CDK10 also participates in repressing cilium assembly and maintaining actin cytoskeleton integrity through the phosphorylation of regulators like PKN2, impacting RhoA signaling[2]. Mutations in the FAM58A gene lead to developmental syndromes (notably STAR syndrome), and emerging evidence suggests involvement in cancer progression via cell proliferation control[2][5][6]. There are no known selective inhibitors or clinically targeted drugs for Cyclin Q; pan-CDK inhibitors exhibit only limited activity against this target[5]. Safety concerns in therapeutic targeting stem from its widespread roles in cell division, neurodevelopment, and organogenesis.

Other names

Cyclin-QCCNQCyclin MCycMFAM58ACyclin-related protein FAM58ACDK10-activating cyclinFamily with sequence similarity 58 member Acyclin Mcyclin-Q

Inhibition of Cyclin Q/CDK10 complex would impair phosphorylation of cell cycle and transcriptional regulators (such as Rb1, c-MYC, RNA polymerase II), likely leading to altered proliferation and gene expression\nPossible impairment of cilia regulation and actin cytoskeleton architecture