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. 2014 Nov 19;5:361. doi: 10.3389/fgene.2014.00361

FIGURE 2.

FIGURE 2

Proposed mechanism for miR-155-mediated myeloid leukemogenesis. Overexpression of miR-155 leads to the activation of the PI3K-Akt pathway through negative regulation of Src Homology 2 domain-containing Inositol-5-Phosphatase (SHIP1). SHIP1 is a phosphatase that mediates the conversion of phosphatidylinositol triphosphate (PIP3) to phosphatidylinositol diphosphate (PIP2). PIP3 normally acts as a docking site for signaling molecules in the PI3K-Akt pathway and helps relay the signal. Upon miR-155 overexpression and thus, SHIP1 downregulation, PIP3 level is increased, which leads to the activation of the PI3K-Akt pathway. Green arrows indicate increased, and red arrows decreased activity upon miR-155 overexpression.