This study investigates the metabolic consequences of a phosphomimetic mutation at serine 82 (S82D) in 4E-BP1, a key regulator of cap-dependent translation. Mice harboring this mutation exhibit glucose intolerance, suggesting that constitutive phosphorylation at this site disrupts normal glucose homeostasis.
The S82D phosphomimetic mutation in 4E-BP1 leads to impaired glucose tolerance in mice, highlighting the critical role of dynamic phosphorylation at this site in maintaining metabolic homeostasis.
4E-BP1(S82D) Knockin mouse model developed by genOway, featuring a serine-to-aspartic acid substitution at position 82 to mimic constitutive phosphorylation. The model was generated via homologous recombination in embryonic stem cells, followed by Cre-mediated excision of a selection cassette.
Glucose metabolism, Insulin resistance, Phosphorylation, Translational control, Metabolic disorders
Point mutation Knockin model, Homologous recombination, Cre-loxP system, Phosphomimetic mutation, Glucose tolerance testing
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
