Improved tyrosine phosphatase activation in high density cells is proposed as the process of contact inhibition of growth. The next data will show that the power of EGFR to signal to their substrates has not been affected, while our data are in line with the very fact that EGFR activation in high-density cells is restricted, probably, from the increased tyrosine phosphatase activation in these cells. Also, the information to be introduced will argue for inhibition of a stage other than the EGFR as the important point of contact inhibition of EGF dependent growth. If withdrawal of the EGFR in high-density cells has any affect downstream EGF dependent pathways egf dependent natural compound library Akt activation was evaluated to determine. The phosphorylation specific Akt antibody, phosphoserine 473, was used to determine Akt activation. In contrast to the reduced EGFR service observed at all-time points in the high density cells, EGF similarly triggered Akt at 10 min and 5 min in both high and low density cells. After 10 min, contrary to the low density cells, Akt activation substantially decreased by 60?70% within the cells. Akt initial remained fairly constant throughout the 30 minute time course in-the low density cells. The size of Akt was similar under both density conditions, and h catenin showed no huge difference under the low and high density conditions. These results suggest that Akt activation Meristem together with EGFR activation in high density cells was diminished, however the time span of withdrawal of Akt and EGFR actions change. At this point within our studies, it was unclear if the suppressed EGF dependent Akt activation in the high density cells was merely a direct reflection of the reduced EGFR activation in these cells or if high density immediately suppresses EGF dependent Akt activation. The rest of our studies will demonstrate a fresh paradigm for contact inhibition of growth, that immediate elimination of Akt activation rather than the Doxorubicin Adriamycin suppressed EGFR activation is liable for contact inhibition of EGF dependent growth of these cells. EGFR activation is suppressed in high density cells relative to low density cells, it’d be predicted that most EGF dependent signals downstream of the EGFR should be inhibited relative to the low density cells. EGF dependent Erk1 2 activation was evaluated, to try this hypothesis. As seen in Fig. 4A, Erk1 was activated in the high density cells even though the EGFR in these cells were less activated, and Erk1 was activated to similar extents in the highand low density cells. Equally, EGF dependent Erk2 activation within the high density cells was like the lowdensity cells. Erk1 2 masses were similar at both densities.