Hi everyone,
so i have treated a cell line (that had KRAS ontogenically activated) with a drug that was thought to inhibit AKT phosphorylation. Indeed, Akt phosphorylation for the treated cells upon immunoblotting showed to having decreased bands compared to that control. However when I immunoblotted with p-ERK, the treated cells showed increased levels of p-ERK compared to the control.
my question is, how is the AKT decreased while p-ERK increased?! any ideas?
is the KRAS oncogene plays a role in keeping p-ERK at high levels while the effect of the drug only targeted the AKT phosphorylation?can this happen even its downstream KRAS
these results are suppose to happen its not a technical issue. My question is more to theoretical side
Thank you in advance
Hi Delilah,
this is a well established fact: There is corsstalk between the pathways. Inhibiting pAKT will give a feedback towards the Ras/Ras/MAPK pathway. This can be abbrogated by adding a MEK inhibitor.
Hope that helps.
@ Thomas , Thank you so much for your input.
But isn't the cross talk supposed to also decrease p-ERK if the p-AKT is already decreased?
Hi,
which cell line are you using? The isoforms of Ras might have redundant roles on Erk phosphorylation. It is well known that activation of Ras triggers the activation of MAP kinase cascade in Ras-Erk pathway finally resulting in the phosphorylation of Erk. Because the Ras isoform which you are using is a constitutively activated k-Ras, it is possible that it can increase the phosphorylation of Erk in your cell line independent of PI3K-mTOR pathway.
How is the pErk looks like in your mutant cell line compared to control when not treated with Akt inhibitor?
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