Figure 2.

Pim-dependent inactivation of the negative regulator SOCS. (a) In v-Abl as well as in (b) PMT-mediated signaling, activation of the JAK-STAT pathway leads to the constitutive expression of the otherwise short-lived serine/threonine kinase Pim. Phosphorylation of its downstream target, the suppressor of cytokine signaling (SOCS) inhibits the ability of SOCS to act as an ubiquitin ligase. Thus JAK molecules accumulate in the cell leading to the hyperactivation of STAT3 signaling, increased cell survival and anchorage-independent growth.