Ultraviolet radiation (UVR) is the most common external mutagen which cells are exposed to. UVR directly causes a diverse range of DNA damage, which consists of modified bases, various strand breaks and protein-DNA adducts. The generation of reactive oxygen species (ROS) following UVR also indirectly contributes to single-strand DNA base lesions and oxidative lesions in the DNA. Persistent DNA damage consequently leads to genomic instability and promotes melanoma and non-melanoma development. In melanocytes, a G-protein coupled receptor called melanocortin-1-receptor (MC1R) has been directly linked to melanogenesis, enhanced cytoprotection and augmented DNA repair processes in response to UVR exposure. We have previously identified the rapid and transient induction of the NR4A family of orphan nuclear receptors upon MC1R signalling activation in melanocytes. Using immunofluorescence imaging, we revealed that upon exposure to UVR, all members of the NR4A nuclear receptors are recruited to distinct nuclear foci. While the NR4A2 foci appear to represent sites of active nucleotide excision repair and double-strand break repair, emerging evidence suggests that NR4A3 is recruited to entirely different nuclear compartment. Using mutational analysis, we show that the recruitment of NR4A3 maybe directed by the Histidine-repeat harboured in the N-terminal domain of NR4A3. Furthermore, the co-localisations of NR4A3 foci with SC35 and Ape1 proteins further provide insights into the involvement of NR4A3 in RNA processing and base excision repair. Based on current data, we propose that NR4A nuclear receptors may represent different repair components contributing to genomic maintenance and cyto-protection following UVR-induced carcinogenesis.