Atypical kinesin that plays a key role in enteric neuron development. Acts by repressing a cell growth signaling pathway in the enteric nervous system development, possibly via its interaction with GRB2 that prevents GRB2-binding to SHC, thereby attenating the GDNF-Ret signaling. Binds to microtubules but lacks microtubule-based motility due to the absence of ATPase activity. Interacts with GRB2 (via SH2 domain). Expressed in several neuronal populations. Strong expression is detected in substantia nigra in brain and enteric nervous system in colon at P12. In colon sections at 12.5 dpc, 14.5 dpc, and P12, it is exclusively expressed in enteric nervous system (ENS). Also detected in dorsal root ganglion and spinal cord gray matter at 14.5 dpc. Mice exhibit growth retardation, become emaciated, and die within 5 weeks of birth. The median and mean life span is 15 and 16 days. Macroscopic dissection reveal that mice suffered from megacolon, with dilation from the distal small intestine to the proximal colon and display enteric nerve hyperplasia. Severe occlusion are observed in the distal colon, because the colon motility is not coordinated. Defects are due to abnormal enteric nervous system (ENS) proliferation. Belongs to the TRAFAC class myosin-kinesin ATPase superfamily. Kinesin family. KIF26 subfamily. In contrast to other kinesin-like proteins, residues required for ATPase activity are missing.