Gabarapl2, also known as GABA type A receptor-associated protein-like 2, was initially linked to protein transport and membrane fusion, but has since become well-known for its role in autophagy. It is part of the GABARAP subfamily along with GABARAP and GABARAPL1. Although there is functional redundancy among subfamily members, Gabarapl2 is involved in a complex network of molecular interactions, physiological processes, and pathologies, with functions ranging from cellular differentiation to intracellular degradation [1].

In the context of autophagy, it has been shown that ammonia can increase autophagy and mitophagy, as measured by an increase in autophagy markers including Gabarapl2. SIRT5, a mitochondrial sirtuin, regulates ammonia-induced autophagy by controlling glutamine metabolism, and Gabarapl2 is one of the markers affected in this process [2]. Additionally, in HeLa cells treated with gamma interferon, Gabarapl2 plays a critical role in the growth restriction of Toxoplasma gondii. It is recruited to the membrane structures surrounding parasitophorous vacuoles, and autophagy adaptors are necessary for its proper localization and function in this IFN-γ-induced immune response [3]. In gastric carcinoma, integrated analysis of single-cell and bulk-RNA sequencing data identified Gabarapl2 as a potential prognostic biomarker and candidate therapeutic target, with different immune infiltration states associated with it [4].

In conclusion, Gabarapl2 has multifaceted functions mainly centered around autophagy-related processes, which are crucial in various physiological and pathological conditions. Its role in immune responses against Toxoplasma gondii infection and as a biomarker in gastric carcinoma, as revealed through model-based research, highlights its significance in understanding disease mechanisms and developing potential therapies.