Signalling through growth factor receptors can activate the PI3K/Akt/mTOR pathway and the JAK3/STAT5 pathway

Signalling through growth factor receptors can activate the PI3K/Akt/mTOR pathway and the JAK3/STAT5 pathway. (A) Growth factor receptors first stimulate PI 3 kinase, and through inositol phosphates activate AKT which then phosphorylates mTOR. The phosphorylation of p70S6K and 4EBP by mTOR and the phosphorylation downstream of RPS6 and EIF-4B stimulate translational initiation and contribute to cell growth. The activity of the mTOR pathway is controlled by PTEN a phosphoinositol 3,4,5-triphosphatase that catalyzes the reverse reaction of PI3K. Rapamycin (RAPA) inhibits mTOR kinase activity and has immunosuppressant activity on cells that use the mTOR pathway in the absence of PTEN inhibition. (B) Engagement of Growth factor receptors leads to activation of JAK3 which induces phospharylation and nuclear translocation of STAT5. The Foxp3 promotor has several STAT5B consensus sequences that can be bound and lead to promotor activity. Abbreviations: PI3K, phosphatidylinositol 3-kinase; Akt, protein kinase B; PTEN, phosphatase and tensin homolog deleted on chromosome 10; RAPA, rapamycin; mTOR, mammalian target of rapamycin; p, phosphorylation; JAK, Janus kinase; STAT, signal transducer and activator of transcription; Foxp3, forkhead box P3.

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Interleukin-2 receptor downstream events in regulatory T cells. () Robert Zeiser, et al. Cell Cycle. ;7(4):458-462. Figure: F1. All organisms Homo sapiens Mus musculus Drosophila melanogaster

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