ADP-Ribosylation Factor-Like 8B (ARL8B) ELISA Kits

Human ADP-Ribosylation Factor-Like 8B (ARL8B) interaction partners

1. These findings suggest that membrane repair mediated by Arl8b may be an important mechanism distinguishing avirulent from virulent M. tuberculosis-induced necrotic cell death

2. Authors present evidence that Arl8b facilitates lipid hydrolysis to maintain efficient metabolism for a proliferative capacity in low nutrient environments, suggesting a likely explanation for the complete inability of Arl8b-depleted tumor cells to grow in vivo.

3. LAMTOR1 is a negative regulator of Arl8b- and BORC-dependent late endosomal positioning.

4. Data indicate that E3 ubiquitin-protein ligase RNF167 ubiquitinates Arl8B at the lysine residue K141 and reduces the level of the ADP-ribosylation factor-like 8B Arl8B protein.

5. Arl8b regulates the association of the human HOPS complex with lysosomal membranes.

6. a small GTP-binding protein, ADP-ribosylation factor-like 8b (Arl8b), is identified as a critical factor required for NK cell-mediated cytotoxicity.

7. The authors find that Arl8B is required for kinesin-1 recruitment to Salmonella-containing vacuoles, migration of the vacuoles to the cell periphery 24 h after infection and for cell-to-cell transfer of bacteria to neighbouring cells.

8. a critical regulator of cargo delivery to lysosomes

9. Results suggest that the novel GTPases Gie1 and Gie2 associate with microtubules, and might be involved in chromosome segregation.

10. Arl8b is involved in trafficking processes for lysosomes.

11. Data show that with MAK3 knockdown, p53 is stabilized and phosphorylated and there is a significant transcriptional activation of proapoptotic genes downstream of p53, and that localization of Arl8b is altered, suggesting that Arl8b is a Mak3 substrate.

Mouse (Murine) ADP-Ribosylation Factor-Like 8B (ARL8B) interaction partners

1. Arl8b mediates lysosomal degradation of maternal proteins in the visceral yolk sac endoderm, thereby contributing to mouse embryonic development.

2. MHC class II presentation is controlled by the lysosomal Arl8b.

3. Arl8B is required for LPS-stimulated lysosome tubulation in macrophages.

4. Arl8B plays an important role of Arl8B in neurite formation.