Figure 1.
Genetic aberrations causing primary immunodeficiencies and hyperactivated PI3K-δ signaling in B lymphocytes. The indicated gene products cause primary immunodeficiencies and hyperactivated PI3K-δ signaling in B lymphocytes as a result of GOF mutations (red) or loss-of-function mutations (green). Drug treatments intended to diminish activated PI3K-δ signaling are also shown. FOXO1, forkhead box protein O1; mTORC1, mammalian target of rapamycin complex 1; mTORC2, mTOR complex 2; PtdIns(4,5)P2, phosphatidylinositol 4,5-bisphosphate; PtdIns(3,4,5)P3, phosphatidylinositol (3,4,5)-trisphosphate; PTEN, phosphatase and tensin homolog; RPS6, ribosomal protein S6.

Genetic aberrations causing primary immunodeficiencies and hyperactivated PI3K-δ signaling in B lymphocytes. The indicated gene products cause primary immunodeficiencies and hyperactivated PI3K-δ signaling in B lymphocytes as a result of GOF mutations (red) or loss-of-function mutations (green). Drug treatments intended to diminish activated PI3K-δ signaling are also shown. FOXO1, forkhead box protein O1; mTORC1, mammalian target of rapamycin complex 1; mTORC2, mTOR complex 2; PtdIns(4,5)P2, phosphatidylinositol 4,5-bisphosphate; PtdIns(3,4,5)P3, phosphatidylinositol (3,4,5)-trisphosphate; PTEN, phosphatase and tensin homolog; RPS6, ribosomal protein S6.

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