It's interesting to note that once the DCM-producing mutation K36Q in cTnI was introduced within the existence of Ca2+, the simulation confirmed that Ser 22 and 23 no longer interacted closely with cTnC, in accord with our speculation that the Ca2+-cTnC-cTnI N terminus interaction is exclusive which is destabilized immediately by phosphorylation an
5c–d). CX-5461-mediated S33 phosphorylation of RPA was independent of your mobile cycle stage and was not restricted towards the nucleoli in HR-deficient cells. So, the development of ssDNA constructions in CX-5461 treated cells can lead to replication fork stalling and ATR activation with HRD exacerbating CX-5461-mediated replication stress wh
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