Probable dual specificity kinase acting on both serine/threonine and tyrosine-containing substrates. Negatively regulates p38 MAPK signaling to allow for the plasma membrane of body wall muscle cells to form projections, also called muscle arms, that extend and connect the body wall muscles to target motor neurons. Negative regulation of p38 MAPK signaling may in turn modulate the trafficking of the muscle specific receptor eva-1 to the lysosome, to ensure proper display of the eva-1 receptor on the plasma membrane of muscle cells and allow for muscle arm extension towards guidance cues. Enriched in the cytoplasm. Expressed in body wall, vulval and anal depressor muscles. Expressed from embryogenesis to adulthood. Viable, but sterile. Defective extension of body wall muscle connections or arms towards the ventral nerve cord. Reduced expression of the late endosome marker rab-7, and the eva-1 and unc-40 receptors, which are expressed in muscles, and impaired recruitment of madd-4 to the muscle membrane. Double knockout with cup-5 results in increased expression of the eva-1 receptor and rab-7 positive endosomes. Double knockout with eva-1, gex-2, madd-2, madd-4, mkk-4, unc-15, unc-60, unc-93 or unc-98 results in severe muscle arm extension defects as compared to the single knockouts. Double knockout with proteins involved in the p38 MAPK signaling pathway including cebp-1, mak-2, pmk-3 or sek-3 suppress the muscle arm extension defects and eva-1 expression defects in the madd-3 single knockout. Double knockout with dlk-1 also suppresses the eva-1 expression defect, but does not suppress the muscle arm extension defects in the madd-3 single knockout. Double knockout with cebp-1, mak-2 or pmk-3 restores the defect in the recruitment of madd-4 to the muscle membrane in the madd-3 single knockout. Furthermore, double knockout with pmk-3 restores the reduced rab-7 expression level defect in the madd-3 single knockout. Double knockout with unc-54 results in lethality. Triple knockout with unc-54, and either cebp-1, dlk-1, mak-2, pmk-3 or sek-3 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. Lammer subfamily.