tyrosine kinase
Summary
Enzymes that phosphorylate tyrosine residues on target proteins, transducing signals from growth factor receptors. Dysregulation drives many cancers; common drug target ('-tinib' family).
Detail
Tyrosine kinases (TKs) catalyze ATP-dependent transfer of phosphate to tyrosine residues, activating downstream signaling cascades (RAS-MAPK, PI3K-AKT, JAK-STAT) that control proliferation, survival, and differentiation. Receptor TKs include EGFR, HER2, PDGFR, VEGFR, FGFR, and insulin receptor; non-receptor TKs include ABL, SRC, and JAK. Gain-of-function mutations or fusions drive cancer: BCR-ABL (CML, t(9;22) Philadelphia chromosome → imatinib), HER2 amplification (breast cancer → trastuzumab), EGFR mutations (NSCLC → erlotinib/gefitinib), KIT (GIST → imatinib). TK inhibitors end in '-tinib'; monoclonal antibodies to receptor TKs end in '-mab'. Key boards: Philadelphia chromosome + imatinib mechanism.
Sources
- First Aid for USMLE Step 1 2024
- Pathoma
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