Extended Data Fig. 3: Phosphorylation of IRF3 after treatment with PI3K isoform inhibitors or knock down of PI3K isoform subunits under STING agonist treatment. | Nature Cancer

Extended Data Fig. 3: Phosphorylation of IRF3 after treatment with PI3K isoform inhibitors or knock down of PI3K isoform subunits under STING agonist treatment.

From: Dual targeting of PI3Kγ and STING overcomes regulatory B cell- and myeloid cell-driven immune suppression in pancreatic cancer

Extended Data Fig. 3: Phosphorylation of IRF3 after treatment with PI3K isoform inhibitors or knock down of PI3K isoform subunits under STING agonist treatment.The alternative text for this image may have been generated using AI.

(a) Phosphorylation of IRF3 at B cells from KPC transgenic mice after treatments with MSA-2 (5 µM) or combination of MSA-2 (5 µM) with IPI-549 (20 nM – 500 nM). (b) Phosphorylation of IRF3 at Human CD4+ T cells, Human CD8+ T cells and Human NK cells after treatments with MSA-2 (5 µg/mL) or combination of MSA-2 (10 µg/mL) with IPI-549 (10 μM) or SH-273 (10 μM). (c, d) Phosphorylation of IRF3 at B cells from KPC transgenic mice after treatments with MSA-2 (5 µM) or combination of MSA-2 (5 µM) with SH-344 (100 nM – 500 nM, c), or combination of MSA-2 (5 µM) with TGR-1202 (50 nM – 500 nM, d). (e, f) Western blot of B cells from KPC transgenic mice after knocking down of p110γ (e), p101 (e) or p110δ (f) by shRNA. The data represents two independent experiments (a-f).

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