Inhibits the interaction of APBA2 with amyloid-beta precursor protein (APP), and hence allows formation of amyloid-beta. May enhance the activity of HIF1A and thus promote glycolysis under normoxic conditions; the function requires its ABM domain and may implicate the stabilization of the interaction between HIF1AN and APBA3. Interacts with the N-terminal domain of APBA2. Interacts with NEK2. Interacts with APBA3; APBA3 seems to mediate the interaction between NECAB3 and HIF1AN. Additional isoforms seem to exist. Experimental confirmation may be lacking for some isoforms. Strongly expressed in heart and skeletal muscle, moderately in brain and pancreas. Phosphorylated by NEK2. May result from the retention of an intron in the cDNA.