Quantitative metabolomics services for biomarker discovery and validation.
Specializing in ready to use metabolomics kits.
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GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR-ABL1 Solute carrier family 22 member 1 Multidrug resistance protein 1 CRK PIK3R1 Imatinib Imatinib Imatinib 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 Cytoplasm JAK-STAT Pathway Drug Influx Drug Efflux Imatinib 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 . Imatinib is administered orally through tablets and capsules. 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. 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.
Nucleus GRB2 GAB2 SOS1 CRKL CBL STAT5A JAK2 SKP2 CDKN1B MTOR RPS6KB1 BAD BCL2L1 MDM2 TP53 MYC BCR-ABL1 SLC22A1 ABCB1 CRK PIK3R1 Imatinib Imatinib Imatinib 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 SLC22A1 ABCB1 CRK PIK3R1 Imt Imt Imt Ras Akt RAF MEK MAPK FOXO