| 175410 |
Q968Y9 |
INSR_CAEEL |
Insulin-like receptor (IR) (EC 2.7.10.1) (Abnormal dauer formation protein 2) [Cleaved into: Insulin-like receptor subunit alpha; Insulin-like receptor subunit beta] |
DISRUPTION PHENOTYPE |
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). {ECO:0000269|PubMed:11274053, ECO:0000269|PubMed:18245374, ECO:0000269|PubMed:18436204, ECO:0000269|PubMed:18782349, ECO:0000269|PubMed:22560223, ECO:0000269|PubMed:24332851, ECO:0000269|PubMed:24385923, ECO:0000269|PubMed:28853436, ECO:0000269|PubMed:9252323, ECO:0000269|PubMed:9790527}. |