The malfunctional PSIIRC undergoes repair that involves its partial disassembly
Removal and proteolysis of the D1 protein subunit, generation of a new D1 protein, and refolding of the repaired PSIIRC to a functional complex. Under physiological light and temperatures, the rates of impairment and repair are balanced, and the steady-state concentration of the PSIIRC maintains continuous photosynthetic activity and growth. Failure to balance the two processes eventually results in cell death. The activity Fingolimod Src-bcr-Abl inhibitorof PSIIRC is highly sensitive to the ambient temperature. Short-term temperature elevation was found to enhance the rate of light-induced oxygen evolution. This phenomenon is reflected by a higher flux of electrons that traverse the PSIIRC complex. The increased flux is probably enabled by the enhanced rate of the QB/QBH2 turnover because of the increased membrane fluidity under short exposure to elevated temperatures and before membrane lipids saturation takes place. The increased ICI 182780 Estrogen Receptor inhibitor flux has a dual effect: it enhances the probability of localized reactive oxygen species generation by PSIIRC and the subsequent impairment and degradation of the D1 subunit; the increased supply of electrons to PSI and thereby to the carbon fixation domain results in an increased probability of ROS generation at that site that can lead to the inhibition of protein synthesis and the consequent decrease of the D1 repair activity.
The malfunctional PSIIRC undergoes repair that involves its partial disassembly Removal and proteolysis of the D1 protei
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