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ARL8A
ARL8A Full Name
ADP-ribosylation factor-like 8A
ARL8A Introduction
ARL8A (ADP-ribosylation factor-like protein 8A) is a small GTPase belonging to the Arf-like (ARL) family and is primarily localized on lysosomal membranes, where it acts as an important regulator of lysosome positioning, trafficking, and functional organization. Although ARL8A shares functional redundancy with its paralog ARL8B, ARL8A itself remains less extensively characterized, creating challenges in fully understanding how lysosomal dynamics contribute to human disease. Current evidence indicates that active GTP-bound ARL8A serves as a molecular switch that recruits specific effector proteins to lysosomes, coordinating interactions between lysosomes and the cytoskeleton. Through association with the BLOC-one-related complex (BORC), ARL8A is recruited to lysosomal membranes and participates in microtubule-dependent lysosome movement. This regulatory mechanism is essential for maintaining proper lysosome distribution, intracellular cargo trafficking, and cellular adaptation to metabolic and environmental changes.
A growing body of research has revealed that ARL8A is a key component of the bidirectional lysosomal transport network rather than simply a regulator of outward lysosome movement. ARL8A and ARL8B can interact with effector proteins such as SKIP (PLEKHM2) to connect lysosomes with kinesin motors, promoting lysosome movement toward the cell periphery. Recent studies further identified RUFY3 and RUFY4 as ARL8 effectors that link ARL8-positive endolysosomes with the dynein-dynactin complex, enabling retrograde transport toward the perinuclear region. These discoveries have reshaped the understanding of ARL8A function, suggesting that ARL8A contributes to maintaining a dynamic balance between anterograde and retrograde lysosomal trafficking. By controlling lysosome localization, ARL8A may influence critical cellular processes including autophagy, endosomal maturation, nutrient sensing, membrane repair, and cellular migration.
Abnormal lysosomal trafficking has increasingly been recognized as a hallmark of cancer progression and other human disorders, making ARL8A a potential target of interest for disease research. Studies of breast cancer and other malignancies have reported increased expression of ARL8 family members, including ARL8A, in tumor cell models, suggesting that altered ARL8A-mediated lysosome positioning may contribute to cancer cell invasion, migration, and adaptation to stressful microenvironments. Because peripheral redistribution of lysosomes can enhance extracellular matrix remodeling and invasive behavior, dysregulated ARL8A pathways may participate in tumor progression through changes in lysosomal function rather than direct effects on cell proliferation. Beyond cancer, ARL8A-related lysosomal transport mechanisms are also relevant to broader areas of research involving neurodegeneration, lysosomal storage disorders, and cellular homeostasis. Understanding ARL8A regulation and its interaction networks may therefore provide valuable insights into lysosome-associated disease mechanisms and support the development of future therapeutic strategies targeting intracellular trafficking pathways.
Alternate Names for ARL8A
ARL8A; ADP-ribosylation factor-like 8A; ADP ribosylation factor like 10B , ARL10B; ADP-ribosylation factor-like protein 8A; FLJ45195; Gie2; ADP ribosylation factor like 10B; ADP ribosylation factor like 8A; ADP ribosylation factor like protein 10B; ADP ri
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