Mediates microtubule-dependent, anterograde transport connecting the Golgi network, endosomes, autophagosomes, lysosomes and plasma membrane, and participates in several cellular processes such as regulation of lysosomal pH, lysosome protein degradation, receptor-mediated endocytosis, autophagy, transport of proteins and lipids from the TGN, apoptosis and synaptic transmission (PubMed:10191118, PubMed:24227717, PubMed:15588329, PubMed:29780879, PubMed:26450516, PubMed:16714284, PubMed:25878248, PubMed:17855597). Facilitates the proteins transport from trans-Golgi network (TGN)-to other membrane compartments such as transport of microdomain-associated proteins to the plasma membrane, IGF2R transport to the lysosome where it regulates the CTSD release leading to regulation of CTSD maturation and thereby APP intracellular processing (PubMed:24227717). Moreover regulates CTSD activity in response to osmotic stress (By similarity). Also binds galactosylceramide and transports it from the trans Golgi to the rafts, which may have immediate and downstream effects on cell survival by modulating ceramide synthesis (PubMed:10191118). At the plasma membrane, regulates actin-dependent events including filopodia formation, cell migration, and pinocytosis through ARF1-CDC42 pathway and also the cytoskeleton organization through interaction with MYH10 and fodrin leading to the regulation of the plasma membrane association of Na+, K+ ATPase complex (PubMed:18621045, PubMed:24792215). Regulates synaptic transmission in the amygdala, hippocampus, and cerebellum through regulation of synaptic vesicles density and their proximity to active zones leading to modulation of short-term plasticity and age-dependent anxious behavior, learning and memory (PubMed:29135436, PubMed:29780879). Regulates autophagic vacuoles (AVs) maturation by modulating the trafficking between endocytic and autophagolysosomal/lysosomal compartments, which involves vesicle fusion leading to regulation of degradation process (PubMed:16714284, PubMed:25878248, PubMed:26450516). Participates also in cellular homeostasis of compounds such as, water, ions, amino acids, proteins and lipids in several tissue namely in brain and kidney through regulation of their transport and synthesis (PubMed:19284480, PubMed:20219947, PubMed:25878248). Homooligomer (PubMed:11590129). Interacts with DCTN1, KIF3A, RAB7A and RILP (By similarity). Interacts with CLN5 (PubMed:19941651). Interacts with KCNIP3 (PubMed:17189291). Excluded from the synaptic vesicles. Expressed throughout the brain, such as, in the cerebral cortex, hippocampus, cerebellum and several different cerebral nuclei (at protein level). In the cerebral cortex, expressed in all cortical layers. In the hippocampus, expressed in the granule cells in the dentate gyrus and the pyramidal cells of the hippocampus proper. In the cerebellum expressed in the granular and molecular layers, and in the Purkinje cell layer. Expression is osmoregulated in renal medullary cells. Highly glycosylated. Farnesylation is important for trafficking to lysosomes. Embryos are viable and fertile and by 12 months of age do not exhibit obvious clinical signs but have significantly shortened life spans (PubMed:10527801, PubMed:17962032). Mice show elevation of lysosomal enzymes in brain and accumulation of autofluorescent storage material in neurons, retina and other cell types that increases with age (PubMed:10527801, PubMed:10440905, PubMed:17962032, PubMed:17855597). They also show neuropathological abnormalities with loss of certain cortical interneurons and hypertrophy of many interneuron populations in the hippocampus (PubMed:10527801). Moreover display progressive neurological deficits, including impaired motor function, decreased overall activity, acquisition of resting tremors, and increased susceptibility to pentilentetrazole-induced seizures (PubMed:17855597). Mice exhibit progressively impaired inner retinal function, altered pupillary light reflexes, losses of inner retinal neurons, and reduced brain mass. Mice show behavioral changes including reduced spontaneous activity levels and impaired learning and memory (PubMed:17962032). Cln3 hypomorphic mutant mice, harboring the ~1 kb common juvenile neuronal ceroid lipofuscinosis (JNCL) mutation, express multiple Cln3 mRNA splice variants and mutant battenin protein. Homozygous Cln3 mice exhibit a progressive JNCL-like disease, with perinatal onset of subunit c of ATP synthasedeposition in many cell types and later onset of neuronal dysfunction and behavioral deficits (PubMed:12374761). Can serve as an animal model for studying neuronal ceroid lipofuscinosis 3/Batten disease (PubMed:10527801, PubMed:10440905, PubMed:17962032, PubMed:12374761). Belongs to the battenin family.