Functional inactivation of UV irradiation resistance associated gene (UVRAG) is implicated in common human cancers. It was originally accepted that UVRAG functions as a promoter of the autophagy pathway by forming a stable complex with Beclin 1. However, recent studies have highlighted novel non-autophagic roles of UVRAG, and these reports indicate that UVRAG is much more versatile than we originally expected. In addition to regulating catabolic autophagy, UVRAG is involved in regulating endosomal membrane trafficking, repairing DNA lesions, patrolling the centrosome, and preventing apoptosis. These studies are beginning to shed light on the complexity and cross-talk between the signaling networks involving UVRAG, which normally control diverse cellular processes, and how disruption of these networks leads to tumor formation.
Functional inactivation of UV irradiation resistance associated gene (UVRAG) is implicated in common human cancers. It was originally accepted that UVRAG functions as a promoter of the autophagy pathway by forming a stable complex with Beclin 1. However, recent studies have highlighted novel non-autophagic roles of UVRAG, and these reports indicate that UVRAG is much more versatile than we originally expected. In addition to regulating catabolic autophagy, UVRAG is involved in regulating endosomal membrane trafficking, repairing DNA lesions, patrolling the centrosome, and preventing apoptosis. These studies are beginning to shed light on the complexity and cross-talk between the signaling networks involving UVRAG, which normally control diverse cellular processes, and how disruption of these networks leads to tumor formation.
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