ALS2

ALS2 contains functional domains, including RhoGAP and VPS9 domains, which contribute to its GTPase activity, protein interactions, or membrane association.

ALS2 plays a role in regulating axonal growth, neurite outgrowth, or cytoskeletal organization, potentially influencing neuronal development and connectivity.

ALS2 exhibits a predominantly cytoplasmic localization, with possible associations with endosomes, the Golgi apparatus, or cytoskeletal structures.

Dysregulation or mutations in ALS2 can contribute to motor neuron degeneration in ALS, a progressive neurodegenerative disorder characterized by the selective loss of motor neurons in the brain and spinal cord.

ALS2 expression levels can vary among different tissues and cell types, and they are regulated by factors such as developmental cues, cellular stress, or specific signaling pathways.

Genetic variations or mutations in ALS2 have been associated with juvenile forms of ALS and hereditary spastic paraplegia, suggesting their impact on ALS2 function and disease pathogenesis.

ALS2 interacts with various proteins involved in vesicle trafficking, cytoskeletal dynamics, or signaling cascades, forming complexes critical for its functional roles.

Post-translational modifications, such as phosphorylation or acetylation, can regulate ALS2 function, stability, or interactions with other proteins.

Targeting ALS2 or its associated pathways may offer potential therapeutic strategies for ALS and related motor neuron disorders, aiming to restore neuronal connectivity, enhance vesicle trafficking, or alleviate cellular stress in affected motor neurons.

ALS2 modulates signaling pathways, such as the Rho GTPase signaling pathway, which are involved in cytoskeletal dynamics, vesicle transport, or cellular responses to extracellular signals.