Cell receptor complexes phosphorylation rates

Thus, for effective gene transcription, programmed and targeted by the shape and phosphorylation status of ER and coactivators, a dynamic and cyclic process of transcription complex assembly [255] and destruction of transcription complexes by the proteasome is required. Estrogen- and SERM-receptor complexes have differing accumulation patterns in the target cell nucleus [151, 256] primarily because the relative rates of destruction of the complexes are different [251]. 

Endogenous norepinephrine stimulates cardiac beta receptors. Receptor-linked cAMP-dependent protein kinases phosphorylate calcium channels to increase intracellular calcium. Elevated intracellular calcium increases conduction velocity (phase 0) and decreases the threshold potential in normal SA and AV node cells (see Figure 12.13). Beta blockers slow spontaneous conduction velocity in the SA node by approximately 10-20 percent. In addition, beta blockers can slow conduction velocity while increasing the refractory period of the AV node. These effects control the ventricular rate in atrial fibrillation or flutter and terminate paroxysmal supraventricular tachycardias. They are also safer, although somewhat less effective, than other drugs for suppression of premature ventricular complexes (PVCs). Drugs in this class approved by the FDA for treatment of various arrhythmias include propranolol, acebutolol, and esmolol. Problems with the beta blockers include drowsiness, fatigue, impotence, and depressed ventricular performance. 

---