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RAS like proto-oncogene B (RALB) encodes a small GTPase in the Ras superfamily that cycles between GTP-bound active and GDP-bound inactive states to regulate diverse cellular processes. It functions in gene expression, cell migration, proliferation, oncogenic transformation, membrane trafficking, exocytosis of dense core vesicles, suppression of apoptosis, and cytokinesis by recruiting the exocyst complex to the midbody and leading edges of cells. RALB interacts with downstream effectors and participates in ligand-dependent endocytosis of receptors like EGF and insulin receptors. As a proto-oncogene, its dysregulation promotes cancer, with associations to leukemia and pancreatic cancer through pathways like ERK signaling and NTRK signaling. Despite its role in oncogenesis, no approved drugs directly target RALB, presenting opportunities and challenges in selective inhibition due to homology with other Ras family members like RALA.
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