30 U87-MG MCF10A P-REX2a DHPH P-REX2a+ P-REX2a-N212A PTEN PTEN Dution Butler P-R

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30 U87-MG MCF10A P-REX2a DHPH P-REX2a+ P-REX2a-N212A PTEN PTEN Dution Butler P-REX2 AKT 05 Molar Ratio (P-REX2a/PTEN) 1.5 E MCF10A (reduced growth factors) 2contro P-REX2 1OHM 6077 5.076 50.01-71.54 ?2DeM 9.AS 4.R31 30.214L.Ga 60 0.5 40 Fig. 2. Inhibition of PTEN phosphatase activity by P-REX2a. (A) Full-length P-REX2a, or a deletion of the DHPH domain (ADHPH), or the DHPH domain alone were added in the indicated molar volumes to 40 nM PTEN, purified from HEK293 cells, and phosphatase activity of PTEN was assayed with 20 ?M oo di-Ga-PIP3. This is a representative experiment error bars indicate standard deviation in 3), "P

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Ans.

c. PTEN is expressed as an activated mutant of N212A which encodes the p110 subunit of P13Kalpha. PREX2a and GEF inhibits PTEN lipid phosphatase activity and stimulates the p13k pathway in the presence of PTEN.

d. MCF10A cells undergo anoikis process (Epithelial cells undergo the apoptosis and lose contact with the extracellular matrix and bind to an inappropriate integrin).Expression of p473Akt suppresses the cleavage of caspase-3 and PARP in MCF10A cells and Co-overexpression of P-REX2a with T308Akt, suppresses anoikis. And thus, Akt and PREX2 enhance survival through pathways that are at least partially independent, in the apoptotic cascade.

e. Proliferation of MCF10A cells is significantly reduced by knockdown of PREX2a and DHPH and proliferation of PREX2 is increased compared with the control cells. This suggests that PREX2 a serves as an oncogenic role in the regulation of cell proliferation.

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