Serine/threonine-protein kinase that acts as a key regulator of NRAS signaling by mediating phosphorylation of NRAS at 'Ser-89', thereby enhancing NRAS-binding to its downstream effectors. ATP + L-seryl-[protein] = ADP + H(+) + O-phospho-L-seryl-[protein] ATP + L-threonyl-[protein] = ADP + H(+) + O-phospho-L-threonyl-[protein] Divalent metal cations. Has a preference for Mn(2+). Specifically inhibited by ZT-12-037-01 (1a) (N2-cyclopropyl-N4-(1-isopropylpiperidin-4-yl)- 6,7-dimethoxyquinazoline-2,4-diamine) (PubMed:30712867). Inhibition by ZT-12-037-01 (1a) blocks oncogenic NRAS-driven melanocyte malignant transformation and melanoma growth (PubMed:30712867). Interacts (via N-terminus) with BAG1. Monocytes, hepatocytes, epithelial cells, T- and B-lymphocytes. Gain-of-function variants in STK19 are involved in NRAS-driven melanomagenesis (PubMed:30712867). Melanoma are malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites (PubMed:30712867). Conditional knockin mice overexpressing Asn-89 variant exhibit hyperpigmentation of the skin, ears, and tail, and the melanin content in skin was significantly increased after tamoxifen induction (PubMed:30712867). Moreover, knockin mice overexpressing Asn-89 variant promote NRAS 'Arg-61'-driven melanomagenesis (PubMed:30712867). Belongs to the STK19 family.