Kinesin family binding protein (KIFBP (KBP also widely used))

Kinesin family binding protein is a tetratricopeptide repeat-containing, α-solenoid scaffold protein that modulates the activity of a subset of kinesin family motor proteins—most notably by binding their motor domains and sterically inhibiting their ability to associate with microtubules[1]. This regulatory role is essential for intracellular transport, correct mitotic spindle assembly, and polarization of cells, with critical involvement in neuronal development and maintenance[3][2]. Mutations in KIFBP cause Goldberg-Shprintzen syndrome, a rare congenital neurodevelopmental disorder with complex symptoms[3][2]. There is emerging interest in targeting the KBP—kinesin interaction as a therapeutic strategy for cancers in which KIF15 is upregulated[2]. KBP does not itself serve as a receptor, enzyme, transporter, or ion channel, but rather functions through *protein-protein interactions*, most commonly with several kinesin family members (including KIF1B and KIF15)[1][3][5]. No clinically approved drugs currently target KBP, and risks of such interventions include impaired neural development and mitotic errors[1][3][2].

Other names

KIF-binding proteinKBPKIAA1279DKFZP586B0923TTC20KIF1 binding proteinKIF1BPMutant KIF1 binding protein

For hypothetical or research drugs: disruption of KBP—kinesin interactions, which would block kinesin-mediated microtubule transport and mitotic progression