Transmembrane protein that regulates gamma-aminobutyric acid type A receptor (GABA(A)R) trafficking, channel deactivation kinetics and pharmacology, necessary for fast inhibitory transmission in the brain. Enhances the action of benzodiazepine, a primary GABA(A)Rs target drug, in the brain. May affect channel kinetics of AMPA-type glutamate receptors (AMPAR), the brain's main excitatory neurotransmitter, necessary for synaptic hippocampal plasticity, and memory recall. May regulate the induction and maintenance of long-term potentiation at Schaffer collaterals/CA3-CA1 excitatory synapses. Interacts with GABA(A)R (GABA type A receptor) subunits GABRA1, GABRA2 and GABRG2; the interaction is direct. Does not interact with GABRB2 and GABRB3 subunits. May interact with AMPAR subunits GRIA1, GRIA2 and GRIA3 and AMPAR auxiliary proteins SHISA6 and SHISA7. May interact (via PDZ-binding motif) with DLG4/PSD-95 (via PDZ domain); the interaction is direct. Localizes at GABAergic inhibitory synapses and colocalizes with gephyrin in hippocampal neurons. The PDZ-binding motif interacts with PDZ-domain of scaffolding protein DLG4. The GRID (GABA(A)R-interacting domain) is critical for its subcellular localization and interaction with GABA(A)R. Belongs to the shisa family. SHISA7 has been reported to interact with AMPAR subunit GRIA1 in heterologous conditions and in the brain (By similarity). However, it was later demonstrated that SHISA7 does not colocalize neither interact with AMPAR, but with GABA(A)R (By similarity). Therefore additional experiments are needed to understand the discrepancy for SHISA7 function.