[Paradis S] No mutants known. Encodes AKT kinase, related to akt-1. Overexpression does not suppress age-1. akt-2::GFP is widely expressed. Inhibition of akt-2 by RNAi has no obvious phenotype, inhibition of both akt-2 and akt-1 leads to dauer-constitutive phenotype. Predicted gene F28H6.1
akt-2 encodes a homolog of the serine/threonine kinase Akt/PKB, AKT-2, that is required for progression through the dauer stage of development and for the negative regulation of adult lifespan; inactivation of akt-2 causes animals to arrest constitutively at the dauer stage, while having an increased life span; widely expressed, AKT-2 is activated by the phospholipid products of phosphoinositide 3-kinase AGE-1/PI3K and by PDK-1, a homolog of vertebrate 3-phosphoinositide-dependent kinase-1 (PDK-1) Normal akt-2 (and akt-1) activity is required for excess pdk-1 activity to suppress the dauer-arrest phenotype of age-1, indicating that the 3-phosphoinositide-dependent kinase-1 homolog PDK-1 transduces signals from AGE-1 to AKT-2 (and AKT-1); conversely, the akt-2 loss-of-function phenotype is suppressed by daf-16 null mutations, indicating that the Fork head transcription factor DAF-16 is downstream of AKT-2 (and AKT-1), and that AKT-1 and AKT-2 act primarily to antagonize DAF-16.
Enables phosphatidylinositol-3,4,5-trisphosphate binding activity and protein serine/threonine kinase activity. Involved in determination of adult lifespan; insulin receptor signaling pathway; and regulation of synaptic assembly at neuromuscular junction. Expressed in several structures, including excretory canal; neurons; pharynx; rectum; and vulva. Human ortholog(s) of this gene implicated in several diseases, including carcinoma (multiple); coronary artery disease (multiple); and glucose metabolism disease (multiple). Is an ortholog of human AKT1 (AKT serine/threonine kinase 1); AKT2 (AKT serine/threonine kinase 2); and AKT3 (AKT serine/threonine kinase 3).
Map position created from combination of previous interpolated map position (based on known location of sequence) and allele information. Therefore this is not a genetic map position based on recombination frequencies or genetic experiments. This was done on advice of the CGC.