Final answer:
Receptor Tyrosine Kinases (RTKs) are a type of enzyme-linked receptor crucial in cellular signaling. They respond to ligand binding by dimerizing and autophosphorylating, thus initiating a cascade of cellular responses involving cell proliferation and differentiation. Disorders such as cancer can occur if RTKs are mutated or overactive.
Step-by-step explanation:
Receptor Tyrosine Kinase Systems (RTKs)
Receptor Tyrosine Kinases (RTKs) are critical components of cellular signaling pathways. They are enzyme-linked receptors that span the plasma membrane, with both extracellular and intracellular domains. The extracellular domain binds signaling molecules, like insulin or growth factors. Upon ligand binding, the receptors dimerize, activating the intracellular kinase domain, which then transfers phosphate groups from ATP to tyrosine residues on the receptor itself, a process known as autophosphorylation.
Following autophosphorylation, the phosphorylated tyrosines provide active docking sites for other signaling proteins, leading to a cascade of cellular responses. Important cellular functions controlled by RTK signaling include cell proliferation, differentiation, and survival. In some cases, mutations or overactivity of RTKs can lead to diseases such as cancer and neuromuscular disorders. To terminate the signal, a protein called a phosphatase removes the phosphates from the phosphotyrosine residues, effectively shutting down the signaling pathway.
An example of an RTK is the epidermal growth factor receptor (EGFR), which when activated, stimulates cell proliferation. The equilibrium constant, k, affects the likelihood of the receptor being bound or unbound to the ligand, influencing signal strength. The characteristic response to signals like EGF is typically cell proliferation, but in the case of mutations, it can result in uncontrolled growth as seen in cancer.