Impaired B and T Cell Antigen Receptor Signaling in p110δ PI 3-Kinase Mutant Mice

By K. Okkenhaug, A. Bilancio, Géraldine Farjot, H. Priddle, S. Sancho, E. Peskett, Wayne Pearce, Stephen Meek, A. Salpekar, M. Waterfield and 2 more. Science, 2002

1,030 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/5809bd10bbb62696481b5269884cf03424375a06

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Citations in the corpus

Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, background): “In contrast, mice without functional PI3Kδ or expressing a catalytically inactive version of PI3Kδ (“knockin”) [76–78] or PI3Kγ [79–81] are viable and fertile, and show attenuated function of immune cells.”
The PI3K/AKT Pathway as a Target for Cancer Treatment. (2016, background): “Loss of p110δ results in functional defects in lymphocytes, neutrophils, and mast cells (8), whereas loss of p110γ impairs thymocyte development, T cell activation, and neutrophil migration (9).”
The p110δ Isoform of Phosphoinositide 3-Kinase Controls Clonal Expansion and Differentiation of Th Cells1 (2006, methodology): “Therefore, while anti-CD28 can deliver a sufficiently strong signal in vitro to rescue the proliferative defect (19), the provision of physiological costimulation in vivo is insufficient to rescue the proliferative response in p110 D910A/D910A T cells.”
T cell receptor signaling controls Foxp3 expression via PI3K, Akt, and mTOR (2008, neutral): “These data identify p110 as a dominant isoenzyme and the hierarchy of p110 / may set Foxp3 regulation apart from lymphocyte activation, where p110 appears dominant (25, 26).”