ALS2CL, the novel protein highly homologous to the carboxy-terminal half of ALS2, binds to Rab5 and modulates endosome dynamics.
ALS2, the causative gene product for juvenile recessive amyotrophic lateral sclerosis (ALS2), is a guanine-nucleotide exchange factor for the small GTPase Rab5. Here, we report a novel ALS2 homologous gene, ALS2 C-terminal like (ALS2CL), which encodes a 108-kD ALS2CL protein. ALS2CL exhibited a specific but a relatively weak Rab5-GEF activity ... with accompanying rather strong Rab5-binding properties. In HeLa cells, co-expression of ALS2CL and Rab5A resulted in a unique tubulation phenotype of endosome compartments with significant colocalization of ALS2CL and Rab5A. These results suggest that ALS2CL is a novel factor modulating the Rab5-mediated endosome dynamics in the cells.
Mesh Terms:
Adaptor Proteins, Signal Transducing, Alternative Splicing, Amino Acid Sequence, Amyotrophic Lateral Sclerosis, Animals, Carrier Proteins, Endosomes, Guanine Nucleotide Exchange Factors, Hela Cells, Humans, Mice, Molecular Sequence Data, Protein Binding, Protein Structure, Tertiary, Sequence Alignment, Subcellular Fractions, Tissue Distribution, rab5 GTP-Binding Proteins
Adaptor Proteins, Signal Transducing, Alternative Splicing, Amino Acid Sequence, Amyotrophic Lateral Sclerosis, Animals, Carrier Proteins, Endosomes, Guanine Nucleotide Exchange Factors, Hela Cells, Humans, Mice, Molecular Sequence Data, Protein Binding, Protein Structure, Tertiary, Sequence Alignment, Subcellular Fractions, Tissue Distribution, rab5 GTP-Binding Proteins
FEBS Lett.
Date: Sep. 24, 2004
PubMed ID: 15388334
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