Adapter protein that negatively regulates different signaling pathways to coordinate cell differentiation, proliferation, migration and growth (PubMed:10837248, PubMed:10850493, PubMed:10850494, PubMed:10949024, PubMed:23305818, PubMed:25329475). Functions by binding to key regulatory proteins and either blocks their activity or regulates their turnover by the proteasome (PubMed:10837248, PubMed:10850493, PubMed:10850494, PubMed:10949024, PubMed:23305818, PubMed:25329475). In various developing tissues functions as a cell cycle regulator that mediates cell proliferation according to the requirements of the developmental program (PubMed:10850493, PubMed:10850494, PubMed:10837248, PubMed:15581871). Acts by inducing the proteasomal degradation of the CD25 mitotic activators stg and twe at critical stages of development to delay entry into mitosis and thus mediate cell proliferation (PubMed:10850493, PubMed:10850494, PubMed:10837248, PubMed:15581871, PubMed:23290551, PubMed:29025897). During gastrulation, negatively regulates stg to delay mitosis in the ventral region of the embryonic mesoderm thus allowing invagination to be completed before cell division takes place (PubMed:10837248, PubMed:10850493, PubMed:10850494). Delaying stg-dependent mitosis during bristle development and in migrating germline pole cells also arrests their cell divisions, whereas in cystocytes it promotes their cell divisions (PubMed:10837248, PubMed:10850493, PubMed:15581871). Involved in the regulation of the mid-blastula transition; promotes the destruction of twe resulting in the cell cycle arrest in G2 of cycle 14 which delays mitosis and thus reduces cell proliferation allowing cell fate specification and morphogenesis to take place (PubMed:23290551). In germline cells, blocks border cell migration during oogenesis by binding to slbo/C/EBP and promoting its ubiquitination and degradation by the proteasome (PubMed:23305818, PubMed:10949024, PubMed:29025897). May function in a negative feedback loop with slbo to coordinate proper border cell migration (PubMed:23305818). During tissue growth negatively regulates insulin signaling by binding to Akt1 and blocking its phosphorylation-dependent activation (PubMed:25329475, PubMed:29025897). However it may also function downstream in the insulin signaling pathway, acting with Akt1 to direct foxo degradation (PubMed:25329475). Essential for the proper formation of operant place and aversive olfactory memories (PubMed:18430923, PubMed:28669782). Interacts with slbo (PubMed:10949024). Interacts with Akt1 (PubMed:29025897, PubMed:25329475). Weakly cytoplasmic (PubMed:29025897). In the main body follicle cells, strong nuclear accumulation at stage 10 that decreases to low levels in the cytoplasm by stage 12 (PubMed:23305818). In border cells, high levels of expression detected prior to border cell (BC) delamination (from stages 7 to 8) (PubMed:23305818). At stage 9, expression levels remains high in BC as their migration begins but decreases throughout migration. By stage 10 levels are low in BC nuclei when they arrive at the nurse cell/oocyte boundary (PubMed:23305818). Expressed throughout the brain with highest levels of expression detected in the cell body rind and lower levels of expression detected in the neurophil (at protein level). Zygotic expression first occurs in the prospective embryonic mesoderm, and later in the ectoderm as well (PubMed:10837248). Expression decreases over embryogenesis (PubMed:10837248). High levels of expression in embryos at the beginning of cycle 14 (PubMed:10850494). During cellularization, expression declines but persists throughout gastrulation and until late embryogenesis (PubMed:10850494). In stage 5 embryos, ubiquitously expressed with increased expression in the ventral region (PubMed:10850493). During gastrulation, highest levels of expression are in the ventral cells (PubMed:10850494). The protein kinase domain is predicted to be catalytically inactive. Low viability with only 14% of mutants survive to adulthood (PubMed:10850493). The egg chambers of surviving females often have only eight germline cysts half of which have an oocyte and the other half do not (PubMed:10850493). Early stage 9 to stage 10 embryos, display increased levels of slbo (PubMed:10949024). RNAi-mediated knockdown in embryos produces premature mitosis in part or all of the ventral region, resulting in many mutants displaying defects in gastrulation including partial invagination of the mesoderm (PubMed:10837248). RNAi-mediated knockdown results in an increase in phosphorylated Akt1 but has no effect on total Akt1 levels (PubMed:25329475, PubMed:29025897). RNAi-mediated knockdown in the fat body increases lipid accumulation, larval weight, fat body cell size and the size of fat body nuclei (PubMed:25329475). The increase in larval weight results in delayed pupariation (PubMed:25329475). Flies also display an increase in triglyceride levels which is consistent with the increase in the number and size of lipid bodies (PubMed:25329475). RNAi-mediated knockdown in the fat body does not result in a significant change in triglyceride levels but flies display an increase in glycogen levels and an increase in lipid droplet size (PubMed:29025897). No effect on glucose or trehalose levels in the hemolymph (PubMed:25329475, PubMed:29025897). RNAi-mediated knockdown in late stage border cells, partially reduced border cell migration (PubMed:23305818). 'tribbles' is named after fictional small round organisms from the Star Trek universe that proliferate uncontrollably. Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. Tribbles subfamily.