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GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR-ABL1 CRK PIK3R1 Bafetinib Ras Akt RAF MEK MAPK FOXO Transcription Proliferation and Survival Survival Proliferation Nucleus Outer Membrane Nucleus Inner Membrane Protein Synthesis PI3K/Akt Pathway MAPK/ERK Pathway Cytosol JAK-STAT Pathway Decreased signalling of the JAK-STAT pathway decreases the cell's likelihood for proliferation and survival. Both the JAK-STAT pathway and the MAPK/ERK pathway influence the cell's transcription. Inhibiting these pathways decreases transcription so the cell will eventually die. The PI3K/AKT pathway is responsible for many regulatory functions of the cell and it's inhibition would affect downstream processes of protein synthesis and cellular proliferation. With decreased protein synthesis, less cellular functions will be able to proceed eventually killing the cell. As Bafetinib is still under clinical trials there is no defined way in literature of routes administration. It is most likely administered intravenously into the blood so it can travel to the bone marrow. Bafetinib specifically binds and inhibits the BCR/ABL1 fusion protein tyrosine kinase. The BCR-ABL1 is an abnormal enzyme created by the Philadelphia chromosomal translocation. This chromosomal translocation is associated with chronic myeloid leukemia . Inhibition of BCR/ABL1 inhibits the JAK-STAT, MAPK/ERK, and PI3K/Akt pathways cascade effects.
Nucleus GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR-ABL1 CRK PIK3R1 Bafetinib Ras Akt RAF MEK MAPK FOXO
Nucleus GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR- ABL1 CRK PIK3R1 Bafeti Ras Akt RAF MEK MAPK FOXO