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Dithiothreitol is a strong reducing agent.It can restore the protein disulfide bond and cause the accumulation of misfolded proteins and induce endoplasmic ER Stress.In response to ER stress,cells activate a set of tightly controlled regulatory programs to restore the normal function of the ER.If the protective mechanisms are not sufficient to restore normal ER function,apoptosis will occur to remove the stressed cells.A variety of anticancer therapies have been linked to the induction of ER stress in cancer cells,suggesting that strategies devised to stimulate its prodeath function or block its prosurvival function,could
Dithiothreitol is a strong reducing agent. It can restore the protein disulfide bond and cause the accumulation of misfolded proteins and induce endoplasmic ER Stress. In response to ER stress, cells activate a set of tightly controlled regulatory programs to restore the normal function of the ER .If the protective mechanisms are not sufficient to restore normal stressed ER function, apoptosis will occur to remove the stressed cells. A variety of anticancer therapies have been linked to the induction of ER stress in cancer cells, suggesting that strategies devised to stimulate its prodeath function or block its prosurvival function, could