The ultraviolet (UV) reaponee of mammalian cells is charactarlxed by a rapid and eelectlve Increaee In gene expreeelon medlated by AP-1 and NF-KB. The effect on AP-1 tmnecriptional activity reeuite, in part, from enhanced phoephorylatlon of the cJun NHrterminal activation domain. Here, we deacrlbe the molecular cloning and chamcterixation of JNKl, a dletant relative of the MAP kinaae group that is activated by dual phoephorylation at Thr and Tyr during the UV reeponee. Significantly, Ha-Raa partially actlvatee JNKl and potentiatea the activation caueed by UV. JNKl binds to the c&n traneactlvation domaln and phoephorylatea It on Ser-63 and Ser-73. Thus, JNKl la a component of a novel signal tmnaduction pathway that la activated by oncoprotelna and UV irradiation. These properties indicate that JNKl activation may play an important role in tumor promotion.