Insulin receptor-like tyrosine kinase which regulates metabolism, controls longevity and prevents developmental arrest at the dauer stage (PubMed:9252323, PubMed:9790527, PubMed:11743719, PubMed:24332851, PubMed:28853436, PubMed:21334311, PubMed:29500338, PubMed:24385923). Binding of INS family members may either stimulate, or antagonize, association of the receptor with downstream mediators such as pdk-1 and age-1 (PubMed:11274053). Required for germline progenitor proliferation during larval development (PubMed:22278922). Required for the response to environmental stimuli such as light, food, pheromone, and temperature (PubMed:24332851, PubMed:29500338). Negatively regulates resistance to UV and oxidative stress (PubMed:24332851). In a daf-16/FOXO-dependent manner, plays a role in regulating the response to white light (PubMed:29500338). Role in immune function and pathogen resistance (PubMed:18782349). Negatively regulates autophagy (PubMed:22560223). Regulates daf-18/PTEN protein levels (PubMed:23995781). Plays a role in controlling seam cell development during the larval stages (PubMed:21471153). ATP + L-tyrosyl-[protein] = ADP + H(+) + O-phospho-L-tyrosyl-[protein] Autophosphorylation activates the kinase activity (By similarity). Interaction with shc-1 may inhibit its activity (PubMed:18832074). Tetramer of 2 alpha and 2 beta chains linked by disulfide bonds. The alpha chains contribute to the formation of the ligand-binding domain, while the beta chains carry the kinase domain (By similarity). Interacts (via cytoplasmic domain) with shc-1 (PID domain) (PubMed:18832074). Interacts (via kinase domain) with daf-18 (via C-terminus) (PubMed:23995781). Accumulation of fat, pigmented intestine, increased lifespan, increased dauer formation and increased resistance to pathogens. Severe loss of function mutants display recessive early embryonic lethality (PubMed:9252323, PubMed:9790527, PubMed:11274053, PubMed:18782349, PubMed:18245374). RNAi-mediated knockdown in germline, hypodermis, intestine or in muscles causes increased lifespan (PubMed:24332851, PubMed:28853436). RNAi-mediated knockdown in a ncl-1 mutant (e1942) background reduces the increased longevity of the daf-2 single mutant, and reduces the increased ribosomal protein synthesis in the ncl-1 single mutant (e1942) (PubMed:28853436). RNAi-mediated knockdown in adults causes an increase in lgg-1 positive autophagic vesicles (PubMed:22560223). RNAi-mediated knockdown results in an increase in the number of muscle arm extensions (PubMed:18436204). RNAi-mediated knockdown together with tatn-1 RNAi extends the lifespan of the single daf-2 RNAi mutant (PubMed:24385923). Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily.