Potential guanine nucleotide exchange factor (GEF). GEF proteins activate some small GTPases by exchanging bound GDP for free GTP. Its interaction with presenilin proteins as well as its ability to stimulate Tau/MAPT phosphorylation suggest that it may be involved in Alzheimer disease. Ectopic expression in nerve cells decreases the secretion of amyloid-beta APBA1 protein and lowers the rate of cell-substratum adhesion, suggesting that it may affect the function of some small GTPase involved in the regulation of actin cytoskeleton or cell adhesion receptors. Interacts with presenilin proteins PSEN1 and PSEN2. Interacts with CRK. Expressed in brain, spinal cord, pituitary gland, testis (PubMed:19129390). Not expressed in heart, liver, kidney, spleen and lung. In brain, it is highly expressed in the cerebral cortex and hippocampus, while it is absent in other tissues, except in spinal cord. In the cerebral cortex, it is found within the intermediate (III and IV) and deep (V and VI) layers, whereas it is weakly expressed in superficial layer I. It is also abundant in the piriform cortex. Within the hippocampus, it is expressed in the pyramidal neurons of the CA1, CA2, and CA3 regions and the dentate gyrus. The DOCKER domain may mediate some GEF activity. DOCK3 knockout mice show sensorimotor impairment and structural changes in several brain regions, including the spinal cord and cerebellum. Structural changes are consistent with central axonal dystrophy and include a disorganized cytoskeletons, and abnormal accumulation of autophagic vacuoles associated with impaired axonal transport. Common features of mutant mice are gait abnormalities, limb weakness, ataxia, and an impaired ability to swim. Belongs to the DOCK family.