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GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR-ABL1 CRK PIK3R1 Nilotinib Ras Akt RAF MEK MAPK FOXO Transcription Proliferation and Survival Survival Proliferation 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. Nucleus Outer Membrane Nucleus Inner Membrane Protein Synthesis PI3K/Akt Pathway MAPK/ERK Pathway Cytosol JAK-STAT Pathway As Nilotinib 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. Nilotinib 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. Decreased signalling of the JAK-STAT pathway decreases the cell's likelihood for proliferation and survival. 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.
Nucleus GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR-ABL1 CRK PIK3R1 Nilotinib Ras Akt RAF MEK MAPK FOXO
GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR- ABL1 CRK PIK3R1 Nilot Ras Akt RAF MEK MAPK FOXO Transcription Proliferation and Survival Survival Proliferation 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. Nucleus Outer Membrane Nucleus Inner Membrane Protein Synthesis PI3K/Akt Pathway MAPK/ERK Pathway Cytosol JAK-STAT Pathway As Nilotinib 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. Nilotinib 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. Decreased signalling of the JAK-STAT pathway decreases the cell's likelihood for proliferation and survival. 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.
Nucleus GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR- ABL1 CRK PIK3R1 Nilot Ras Akt RAF MEK MAPK FOXO