Responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating downstream targets (PubMed:11703092). Involved in axon regeneration after injury, probably downstream of dlk-1 and mkk-4 and upstream of mak-2 (PubMed:21670305, PubMed:19737525). May phosphorylate mak-2 (PubMed:19737525). Plays a role in cilium length regulation, possibly by reducing rab-5 mediated endocytosis (PubMed:26657059). Plays a role in the formation of muscle connections, also called muscle arm extensions, between the body wall and the motor axons in the dorsal and ventral cord (PubMed:27123983). ATP + L-seryl-[protein] = ADP + H(+) + O-phospho-L-seryl-[protein] ATP + L-threonyl-[protein] = ADP + H(+) + O-phospho-L-threonyl-[protein] Activated by phosphorylation on threonine and tyrosine. Interacts with mak-2 (PubMed:19737525). May interact with vhp-1 (PubMed:21670305). May interact with uev-3 (PubMed:20592265). Expressed throughout the intestine. The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases. Dually phosphorylated on Thr-285 and Tyr-287, which activates the enzyme. Weak defect in the extension of body wall muscle connections or arms towards the ventral nerve cord. Double knockout with madd-3 suppresses the muscle arm extension defects, eva-1 and rab-7 expression defects and restores the defect in the recruitment of madd-4 to the muscle membrane in the madd-3 single knockout. Triple knockout with madd-3 and unc-54 results in paralysis (as in the unc-54 single knockout), and suppresses the lethality phenotype in the double madd-3 and unc-54 mutant. Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily.