This study investigates the role of 4E-BP1 serine 82 phosphorylation in regulating cell proliferation and tumor suppression. Mice with a serine-to-alanine substitution at position 82 (S82A) in 4E-BP1 exhibit increased susceptibility to polycystic kidney and liver disease, as well as T-cell lymphomas upon sublethal irradiation, indicating the importance of this phosphorylation site in maintaining tissue homeostasis.
Loss of 4E-BP1 serine 82 phosphorylation leads to proliferative polycystic disease and increased lymphoma incidence in aged or irradiated mice, highlighting the critical role of this modification in controlling cell proliferation and preventing tumorigenesis.
4E-BP1 (S82A) Knockin mouse model developed by genOway, featuring a serine-to-alanine substitution at position 82 to prevent phosphorylation at this site. The model was generated via homologous recombination in embryonic stem cells, followed by Cre-mediated excision of a selection cassette.
Cancer biology, Cell cycle regulation, Phosphorylation, Tumor suppression, Translational control
Point mutation Knockin model, Homologous recombination, Cre-loxP system, Phosphorylation site mutation, Functional protein analysis
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
