This order-to-disorder or disorder-to-order transition can influence the conformational equilibrium between the bent and extended states of PLN monomers. Specifically, phosphorylation can shift the conformational equilibrium towards the extended state via a cooperative effect. Furthermore, the phosphorylation at Ser16 can also inactive the SERCA-PLN complex, independent of it bding in either the transition state or in the active state, by disrupting the interactions between SERCA and PLN. According to the experimental and theoretical studies, a crucial hydrogen bond formed by PLN and SERCA maybe lost. In this case, the activity of Ca2+ pump is recovered. Interestingly, the dephosphorylation of Ser16 may drive PLN to the original equilibrium again so as to make the regulation cycle move on. Using the allosteric model, our findings show for the first time how the two different conformations of PLN monomer are produced. The results of this study also reveal the mechanism of SERCA Ca2+ pump’s regulation by PLN. Left ventricular dyssynchrony has been shown to correlate with the time delay needed for electrical activation from the septum to the free wall of the left ventricle. The magnitude of improvement in synchrony after cardiac resynchronisation therapy correlates with the electrical delay measured at the implanted coronary sinus lead during sinus rhythm. In addition, the response to CRT correlates with the electrical delay measured between the implanted coronary sinus lead and the right ventricular lead, the interlead delay. As a consequence, implanting the Compound-K electrode at the site of latest electrical activation of the individual patient seems reasonable. Although the area of latest electrical activation during SR has been mapped endocardially, it may not correspond to epicardial activation times within the CS. In addition, the limited number and locations of CS branches accessible for positioning the CS lead further restricts applicability of preimplant mapping results. Finally, during CRT, the region with latest activation during SR might not correspond to the region with the greatest electrical separation during RV pacing. In other words, simultaneous RV pacing from the implant lead might not match with preimplant mapping results during SR. The purpose of this study was to predict electrical activation within different CS branches during CRT implantation using a three dimensional imaging system and compare SR and RV pacing in different types of conduction block. Given the high interindividual variability of CS branch morphology, the lead positions during mapping are reported by segments. We have refined this concept by Ginsenoside-F5 proposing a coordinate system with gradation of the mitral ring to predict the site of latest electrical activation to guide CS lead implantation. For the first time electrical delays within the CS branch system during SR and RV apical pacing are compared with aid of 3D mapping systems. The main findings of this study are that electrical delays within the CS during SR in patients with or without LBBB are highly variable and unpredictable. Of note the electrical activation in the posterior wall does not start from the apical segment, as shown also with 3D mapping. Secondly, RV pacing homogenizes electrical delays into a predictable parabolic distribution with greatest delays observed at 162u on the mitral ring reaching around 75% of QRS duration near the base of the heart. The considerable differences between SR and RV apical pacing with respect to regions of latest activation and electrical separation of RV and LV electrodes may have an influence on the choice for LV lead implantation. Individual mapping of CS activation in each patient is time consuming.