Small GTPases Rab involved in autophagy (PubMed:27103069). The small GTPases Rab are key regulators of intracellular membrane trafficking, from the formation of transport vesicles to their fusion with membranes. Rabs cycle between an inactive GDP-bound form and an active GTP-bound form that is able to recruit to membranes different sets of downstream effectors directly responsible for vesicle formation, movement, tethering and fusion (PubMed:27103069). May regulate the homeostasis of SNCA/alpha-synuclein. Together with PICK1 proposed to ensure selectively GRIA2 exit from the endoplasmic reticulum to the Golgi and to regulate AMPAR compostion at the post-synapses and thus synaptic transmission (By similarity). Interacts (in GTP-bound form) with PICK1 (via PDZ domain); a PICK1 homodimer may allow simultaneous association of RAB39B and GRIA2 to PICK1 which is involved in GRIA2 trafficking. Interacts with isoform c of RASSF1; the interaction is strong (By similarity). Interacts with isoform a of RASSF1; the interaction is weak (By similarity). Interacts with the DLG4/PSD-95 (By similarity). Partial colocalization with markers that cycle from the cell surface to the trans-Golgi network. Highly expressed in the brain. The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry. Its association with Parkinson disease is however unclear (PubMed:26739247, PubMed:27459931). According to a number of studies, variations affecting this gene are not a frequent cause of Parkinson disease, suggesting that RAB39B does not play a major role in Parkinson disease etiology (PubMed:26739247, PubMed:27459931). Belongs to the small GTPase superfamily. Rab family.