| Receptors such as FLT3 and KIT play an essential role in the production of blood cells. However, mutations in FLT3 and KIT receptors contribute to abnormal blood cell production, leading to blood disorders like acute myeloid leukemia (AML). One of the hallmarks of AML is the activated and phosphorylated form of Stat5 in the nucleus. The Kapur lab has shown Focal adhesion kinase (FAK) to be hyperactive in AML cells. In the present study, we have targeted FAK in order to inhibit the activation and nuclear translocation of Rac-1 and Stat5. To further these studies, we investigated PAK-1 and PAK-2. We hypothesize PAKs to play an important role in the translocation of Rac-1 and Stat5 in the nucleus. This study aims to highlight the importance of analyzing signaling molecules downstream of mutated receptors that are involved in AML, and target them as an alternative treatment strategy. |
