Probable pseudokinase that acts as an adapter protein (PubMed:12015115, PubMed:23283987). Component of an integrin containing attachment complex, which is required for muscle development and maintenance (PubMed:22253611). Involved in the assembly of dense bodies and M lines during body wall muscle development by recruiting several of their components including integrin pat-3, cpna-1, unc-89 and unc-112 to integrin-mediated attachment sites (PubMed:12015115, PubMed:23283987). Plays a role in distal tip cell (DTC) migration and in oocyte development probably by regulating the actin cytoskeleton (PubMed:16476426). During the formation of neuromuscular junctions at the larval stage, negatively regulates membrane protrusion from body wall muscles (PubMed:16495308). May be involved in thermotolerance and lifespan (PubMed:24314125). Interacts (via protein kinase domain) with unc-112 (via N-terminus) (PubMed:12015115, PubMed:24692564). Interacts (via ANK repeats) with unc-97 (via first LIM domain) (PubMed:12015115, PubMed:17662976). Interacts (via protein kinase domain) with pat-6 (via C-terminus CH domain) (PubMed:12781130). May form a complex with unc-112, unc-97 and pat-6 (PubMed:12781130, PubMed:17662976, PubMed:24692564). Does not interact with integrin pat-3 (PubMed:12015115). Component of an integrin containing attachment complex, composed of at least pat-2, pat-3, pat-4, pat-6, unc-52, unc-97 and unc-112 (PubMed:22253611). Colocalizes in dense bodies and M lines with integrin pat-3. Localization to muscle attachment sites is regulated by pat-2, unc-52 and unc-112 (PubMed:12015115). Co-localizes with pat-3 and pat-6 at body wall muscle attachment sites (PubMed:12781130, PubMed:17662976). Expressed in body wall muscle. Expression starts in body wall muscles at the 1.5-fold embryonic stage. The protein kinase domain is predicted to be catalytically inactive. Embryonic lethality due to 1.5 fold stage-onset paralysis. Mutant embryos have defects in maintaining polarization of several components involved in the assembly of dense bodies and M lines, such as integrin pat-3, unc-89 and unc-112 to muscle attachment sites (PubMed:12015115). RNAi-mediated knockdown causes sterility resulting from oocyte accumulation in the proximal gonad and distal tip cell (DTC) migration defects (33 percent of animals). Actin cytoskeleton in the proximal gonad appears disorganized (PubMed:16476426). RNAi-mediated knockdown results in impaired mobility, mitochondrial fragmentation and disrupted integrin attachment complexes in muscle (PubMed:22253611). This leads to degradation of muscle proteins in the cytosol, myofibrillar defects and disruption of sarcomere organization (PubMed:22253611). RNAi-mediated knockdown in hatched embryos but not in adults causes adult-onset paralysis characterized by the collapse of myosin filaments in body wall muscles and a decrease in pharyngeal pumping (PubMed:24314125). In L1 larval stage, results in the formation of large myosin aggregates in body wall muscle cells (PubMed:22761445). In L4 larval stage, causes ectopic membrane extensions from body wall muscles (PubMed:16495308). In adults, causes an increase in lifespan, resistance to heat stress and increased expression of stress response factors hsf-1, sod-3, hsp-16.2 and gst-4 (PubMed:24314125). Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family.