ARL8

There is limited information regarding the role of ARL8 in cancer. However, some studies suggest that ARL8 may contribute to cancer progression and metastasis through its involvement in processes like cell migration and invasion. Further research is needed to fully understand its significance in cancer biology.

ARL8 regulates the movement of late endosomes along microtubules by interacting with molecular motors, such as dynein and kinesin, which facilitate their transport towards the cell periphery or the microtubule-organizing center (MTOC).

Yes, studies have shown that ARL8 can regulate cell migration and invasion. It is involved in the organization and dynamics of the actin cytoskeleton, which play critical roles in these cellular processes.

ARL8 plays a role in regulating phagosome maturation by mediating the fusion of phagosomes with late endosomes/lysosomes. It interacts with proteins such as SKIP and VARP, which are involved in tethering and docking of phagosomes to lysosomes. This allows for the delivery of lysosomal enzymes and acidification of the phagosome, leading to the degradation of engulfed pathogens.

Although not extensively studied, some reports suggest that dysregulation of ARL8 may contribute to certain pathological conditions, including lysosomal storage disorders and cancer.

Investigating ARL8 can provide valuable insights into the mechanisms underlying endosomal trafficking, lysosomal function, and autophagy. Furthermore, understanding its involvement in diseases may offer opportunities for therapeutic interventions targeting these pathways.

Yes, ARL8 has been reported to undergo post-translational modifications, including geranylgeranylation, which is important for its proper localization and function.

ARL8 plays a role in lysosome positioning by mediating the interaction between lysosomes and the microtubule cytoskeleton. It associates with the dynein motor complex and helps transport lysosomes along microtubules to different regions within the cell.

Yes, ARL8 has been found to play a crucial role in neurite outgrowth, axonal transport, and synaptic vesicle recycling in neuronal cells, indicating its importance in neuronal development and function.

Currently, there are no well-established animal models specifically for ARL8 deficiency. However, researchers have used genetic manipulation techniques, such as knockout or knockdown experiments, in animal models to study the consequences of ARL8 loss-of-function.

Yes, certain studies have implicated dysregulation of ARL8 in cancer progression, including tumor growth, invasion, and metastasis. However, more research is needed to fully understand its exact role in different types of cancer.

While the direct role of ARL8 in cellular metabolism is not well-characterized, some studies suggest its involvement in metabolic processes such as lipid metabolism and mitochondrial dynamics. Further research is needed to fully understand the extent of its impact on cellular metabolism.

Yes, ARL8 has been found to interact with various proteins, including FYCO1, SKIP, WDR91, VARP, and BART. These interactions are involved in regulating different cellular processes such as autophagy, lysosome positioning, and endocytosis.

Since ARL8 has been implicated in neurodegenerative diseases, it could be a potential therapeutic target. However, further research is needed to fully understand its role and develop specific interventions.

Yes, ARL8 can influence cellular signaling pathways by regulating the intracellular trafficking and localization of signaling molecules. It can modulate the activation and signaling of some proteins, thereby impacting various cellular processes and responses.

ARL8's involvement in lysosomal biogenesis and function make it a potential therapeutic target for lysosomal storage disorders. However, further investigations are needed to explore this possibility and develop targeted interventions.

Yes, ARL8 is involved in membrane trafficking pathways such as endocytosis and recycling. It regulates the trafficking of vesicles and transport intermediates to specific cellular compartments, contributing to membrane remodeling and organelle homeostasis.

Yes, ARL8 can undergo post-translational modifications like phosphorylation and ubiquitination. These modifications can affect its activity, stability, and interaction with other proteins, thereby modulating its cellular functions.

Yes, ARL8 has been implicated in immune system function. It is involved in regulating phagosome maturation, antigen presentation, and lysosomal degradation of pathogens in immune cells such as macrophages.

As of now, there is limited information available regarding genetic mutations or polymorphisms in the ARL8 gene. Further studies are required to explore potential associations between ARL8 gene variations and disease susceptibility.

Yes, ARL8 has been implicated in endocytic trafficking. It is involved in regulating the recycling of internalized receptors and trafficking of endosomes to specific cellular compartments.

Yes, ARL8 can interact with other GTPases, such as Rab proteins, to coordinate and regulate various cellular processes like vesicle trafficking and organelle dynamics.

Given the significance of ARL8 in various cellular processes, it has the potential to be targeted for therapeutic interventions. However, specific inhibitors or modulators of ARL8 are still under development and require further research.

Yes, ARL8 interacts with various proteins to carry out its functions. For example, it interacts with SKIP and Hook proteins for endosomal trafficking, and with HOPS complex members for autophagy regulation.

Yes, ARL8 is involved in autophagy, which is a process of cellular self-degradation and recycling. It regulates autophagosome biogenesis and maturation by interacting with proteins such as FYCO1 and SKIP.

While the direct association between ARL8 dysfunction and specific diseases is not well-established, there is emerging evidence suggesting its involvement in certain disorders. For example, ARL8 dysregulation has been implicated in neurodegenerative diseases like Alzheimer's and Parkinson's disease.