Kif16b, a member of the kinesin-3 family, has a characteristic PhoX homology (PX) domain. It binds to membranes containing phosphatidylinositol-3-phosphate (PI(3)P) and moves along microtubule filaments to the plus end, regulated by coiled coils in the stalk region. Its physiological function involves transporting intracellular cargo, forming endosomal tubules, and is crucial for membrane transport-related pathways [1].

Kif16b knockout (KO) mouse embryos failed to develop epiblast and primitive endoderm lineages and died at the peri-implantation stage, similar to FGFR2 knockout embryos. This indicates that the KIF16B/Rab14 complex is critical for the biosynthetic Golgi-to-endosome traffic of the fibroblast growth factor receptor (FGFR) during early embryonic development [2]. In neurons, loss of KIF16B induced the aggregation of early endosomes and perturbed the trafficking and functioning of receptors like the AMPA and NGF receptors, suggesting its importance in the correct localization of early endosomes in mouse hippocampal neurons [3].

In conclusion, Kif16b is essential for intracellular cargo transport, endosomal tubule formation, and early embryonic development as well as neuronal receptor trafficking. The study of Kif16b KO mouse models has provided insights into its role in early embryonic development and neuronal function, highlighting its significance in understanding the mechanisms of these biological processes and potentially related diseases.