Component of the AP2-containing clathrin coat that may regulate clathrin-dependent trafficking at plasma membrane, TGN and endosomal system. A possible serine/threonine-protein kinase toward the beta2-subunit of the plasma membrane adapter complex AP2 and other proteins in presence of poly-L-lysine has not been confirmed (By similarity). By regulating the expression of excitatory receptors at synapses, plays an essential role in neuronal function and signaling and in brain development (PubMed:26203146). Interacts with clathrin and AP2B1; the interaction mediates the association with the AP-2 complex. Colocalizes to the trans-Golgi network (TGN) and to endosomal membranes with clathrin, transferrin and plasma membrane adapter AP1 and AP3 complexes. Ubiquitously expressed. Could autophosphorylate in presence of poly-L-lysine. Disruption of the gene results in perinatal lethality due to impaired neuronal functions. Mutant animals that survive to adulthood show growth retardation and severe sensorimotor deficits. The neurologic deficits in these mice is associated with the degeneration of several neuronal populations, most notably CA3 pyramidal neurons of the hippocampus, resulting from excitotoxicity. This is associated with excessive expression and activation of calcium-permeable glutamate receptors at the synapse. A wide variety of clathrin-mediated functions and lysosomal pathways are however preserved in mutant mice. Belongs to the protein kinase superfamily.