Key regulator of cytokinesis that cross-links antiparrallel microtubules at an average distance of 35 nM. Essential for controlling the spatiotemporal formation of the midzone and successful cytokinesis. Required for KIF14 localization to the central spindle and midbody. Required to recruit PLK1 to the spindle. Stimulates PLK1 phosphorylation of RACGAP1 to allow recruitment of ECT2 to the central spindle. Acts as an oncogene for promoting bladder cancer cells proliferation, apoptosis inhibition and carcinogenic progression. Homodimer. Interacts with the C-terminal Rho-GAP domain and the basic region of RACGAP1. The interaction with RACGAP1 inhibits its GAP activity towards CDC42 in vitro, which may be required for maintaining normal spindle morphology. Interacts (via N-terminus) with the C-terminus of CENPE (via C-terminus); the interaction occurs during late mitosis. Interacts (via N-terminus) with KIF4A (via C-terminus); the interaction is required for the progression of mitosis. Interacts (via N-terminus) with KIF23 (via C-terminus); the interaction occurs during late mitosis. Interacts with KIF14 and KIF20A. Interacts with PLK1. Interacts with KIF20B. Colocalized with KIF20B in the nucleus of bladder carcinoma cells at the interphase. Colocalized with KIF20B in bladder carcinoma cells at prophase, metaphase, early anaphase, at the midzone in late anaphase and at the contractile ring in telophase. Predominantly localized to the nucleus of interphase cells. During mitosis becomes associated with the mitotic spindle poles, and localizes with the cell midbody during cytokinesis. Co-localizes with PRC1 in early mitosis and at the spindle midzone from anaphase B to telophase. During the stages 11.5-13.5 dpc it is expressed in most embryonic tissues. Within the telencephalon, it is predominantly expressed inside the ventricular zone where expression reaches its peak at 15.5 dpc and starts to decrease by 18.5 dpc. Expression is also observed in mitotically active cells outside the telencephalon, but not in adult brain. Microtubule binding occurs via a basic patch in the central spectrin-like domain and requires also the unstructured C-terminal domain. Phosphorylation by CDK1 in early mitosis holds PRC1 in an inactive monomeric state, during the metaphase to anaphase transition, PRC1 is dephosphorylated, promoting interaction with KIF4A, which then translocates PRC1 along mitotic spindles to the plus ends of antiparallel interdigitating microtubules. Dephosphorylation also promotes MT-bundling activity by allowing dimerization. Phosphorylation by CDK1 prevents PLK1-binding: upon degradation of CDK1 at anaphase and dephosphorylation, it is then phosphorylated by PLK1, leading to cytokinesis (By similarity). Belongs to the MAP65/ASE1 family. Probable intron retention.