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Plasma and tissue GSH levels decline with age, while markers of oxidative damage increase, creating a "redox imbalance" implicated in the pathogenesis of age-related diseases [2][3][10][11]
The making of bispecific antibodies
For PTH1R 37 and GCGR 38 (whose crystal structures were determined with PGS domain fusion in ICL3 and T4L fusion at ICL2, respectively), agonist binding failed to promote the outward movement of the intracellular half of TM6 as seen in the inactive state, probably due to the fusion
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