ALS2 C-terminal like protein (ALS2CL)

ALS2 C-terminal like protein (ALS2CL) is a cytosolic adaptor and regulatory protein highly homologous to the carboxy-terminal region of alsin (ALS2). ALS2CL is characterized by MORN (membrane occupation and recognition nexus) motifs and flanking pleckstrin homology (PH) and VPS9 domains[1][2]. It acts as a weak guanine nucleotide exchange factor (GEF) and a strong binding partner for the small GTPase Rab5. ALS2CL modulates Rab5-dependent endosome dynamics, resulting in altered endosomal compartment morphology, and is predicted to be involved in endosomal/vesicular transport, particularly within the cytosolic and vesicular compartments of cells[1][2][3]. It is not a receptor, classical enzyme, nor a transporter, but an effector and regulator of endosomal machinery. While ALS2CL itself is not directly implicated as a causative gene for amyotrophic lateral sclerosis (ALS), it is functionally related to ALS2/alsin and may play a minor or modifying role in neurodegeneration or trafficking abnormalities[1][2][3]. No specific drugs, clinical biomarkers, or safety liabilities have been defined for this protein.

Other names

ALS2CLALS2CR6-like proteinALS2 C-terminal like