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Definition: How does the activation of receptor tyrosine kinases affect cellular signaling?

The activation of RTKs occurs when a ligand, such as a growth factor or hormone, binds to the extracellular domain of the receptor. This binding induces a conformational change in the receptor, leading to the activation of its intracellular tyrosine kinase domain.

Once activated, the tyrosine kinase domain of the RTK phosphorylates specific tyrosine residues on the receptor itself (autophosphorylation) and on downstream signaling molecules. This phosphorylation serves as a molecular switch, recruiting and activating various signaling proteins, such as adaptor proteins and enzymes, to propagate the signal.

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The activated RTKs can initiate multiple signaling pathways, including the mitogen-activated protein kinase (MAPK) pathway, phosphoinositide 3-kinase (PI3K)/Akt pathway, and Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. These pathways regulate gene expression, protein synthesis, cell cycle progression, and cell survival.

The activation of RTKs also leads to the recruitment and activation of downstream effector proteins, such as Ras and Raf, which further amplify the signaling cascade. This amplification allows for precise regulation and coordination of cellular responses to extracellular signals.

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Overall, the activation of receptor tyrosine kinases plays a critical role in cellular signaling by transmitting extracellular signals into intracellular responses. Dysregulation of RTK signaling has been implicated in various diseases, including cancer, making them attractive targets for therapeutic interventions.

Keywords: signaling, activation, receptor, tyrosine, cellular, kinase, activated, kinases, various