Differential effect of β1C and β1A integrin cytoplasmic variants on FAK, AKT, and MAP kinase pathways. The schematic drawings illustrate the β1C effect on intracellular signaling pathways in response to exogenous and endogenous integrin engagement by fibronectin (Fn; A) or in response to either exogenous β1C (B) or exogenous β1A (C) ligation by TS2/16. The inhibitory effect of β1C on Ras/ERK2, but not on FAK and AKT pathways, is shown in A. The failure of β1C to induce ERK2 activation is shown in B. A previously described activation of the MAP kinase pathway by PI 3-kinase, downstream of Ras (King et al., 1997), is blocked in our model (A). It is also shown that AKT is activated in response to fibronectin (A), β1C (B), or β1A (C) engagement.