Akt in the presence of EGF was born act Myr moderate Erh Increase the capacitance T Erh Zelllebensf and non proliferation. These results k Can eventually found Lich that can act to phosphorylate RPS6 M Myr in serum-free medium. FBS unaffected in the presence of 10, however, the treatment of cells erlotinib act Myr Akt abundance of p, wp RPS6 W While reduced fortune Gen. In the F Ability of erlotinib F block both the capacity t Lebensf and proliferation was not affected by BX-795 Akt Myr. The data in Fig. Schl gt before That p RPS6 mTOR and p are robust biomarkers for the antiproliferative effects of EGFR inhibitors in glioma cells. W Although the data in Figures 2 and 3 that it is not legally required to these effects. Identification of critical intermediates for the signaling between EGFR and mTOR, we treated glioma and PTENwt PTENmt erlotinib and analyzed phosphorylation of EGFR and different proteins After EGFR signal RTS. H and P p ufigkeiten EGFR PLC ? all been for a Hnlichen fa erlotinib independent-Dependent Ngig affected was influenced by the level of PTEN, w W While abundance of different PKC isozymes p. R is not the fullness of RPS6 p by treatment with the MAPK kinase inhibitor PD98059, au He between EGFR and MAPK mTOR affected. These data are consistent with the results of the image. 1B shows that the concentration of erlotinib block MAPK not sufficiently reduced the entire p RPS6 U373 glioma PTENmt: EGFR cells.
In contrast to the treatment with erlotinib PTENwt LN229: EGFR cells inhibited the phosphorylation of ERK and RPS6. Can block ERK phosphorylation Aloe-emodin Sun erlotinib a fa PTENindependent, w is W While inhibiting the phosphorylation of PTEN RPS6 available. We found After all, that EGFR Ngig mTOR independent Ngig of MAPK. The wealth of the entire p-PKC in B Forth lines established relative to PTENwt PTENmt. Zus tzlich immunoblot PTENmt lines, unlike PTENwt lines with a K Body recogn t he old phosphorylated forms of seven PKC isoforms showed constitutive expression of a broad band, probably a doublet, even if we do the sen two different bands. EGF treatment resulted in the appearance of some cells migrate slowly PKC isozyme was PTENwt p blocked by erlotinib. Serum EGFR cells of 10: a small upper band was observed in LN229. This group was reduced or absent in LN229 cells and parental wild-type or prim verst RKT cultures Ren wild-type EGFR and PTEN. We believe that a candidate p is the last isoenzyme PKC isozyme that links EGFR activation of mTOR signaling in glioma. In order to show that the differences between PKC phosphorylation and cell PTENwt PTENmt PTEN function, we have a number of isogenic cell lines, only the t-t activity PTEN generates distinction. Although the treatment of cells with an inhibitor of PTEN bisperoxovanadium PTENwt had no effect on T abundance or mobility t one PKC isoform bpv att