Postnatal KIF2A is a key regulator for axon/dendrite determination of developing dentate granule cells, and its loss developed apical axons in dentate molecular layer, broke hippocampal wiring, and induced temporal lobe epilepsy.

Structural, functional, and genetic analyses reveal how kinesin-4 motor KLP-12 precisely modulates the curvature of the microtubule plus-end to inhibit the microtubule dynamics for achieving the proper length control of axons.

KIF2C plays an important role in synaptic plasticity and cognition behaviors in mice by regulating activity-dependent microtubule dynamic.

Kinesin Kif2C is recruited to DNA damage sites, modulates the mobility and dynamics of DNA damage foci, and promotes DNA double strand break repair.

Structural analysis of the kinesin-13 MCAK bound to its C-terminal tail reveals the molecular basis for the conformation of kinesin-13 in solution and the mechanism that triggers long-range conformational changes upon microtubule binding.

Pathogenic mutations in KIF22, which dominantly cause bone dysplasia, improperly activate the motor during anaphase in dividing cells leading to chromosome recongression.

An interaction between two proteins enables the spindle—the structure that segregates chromosome pairs during mitosis—to change size as cells divide.

Eliminating eukaryotic initiation factor 2 (eIF2) from wild-type budding yeast had little impact on translation of individual mRNAs, including those with regulatory upstream open-reading frames, even when canonical initiation factor eIF2 activity was impaired.

Geometrical features of microtubule arrays regulate the collective activity of motor and non-motor proteins.