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At the cellular level, early OA subchondral bone remodeling is driven by an imbalance between bone-resorbing osteoclasts and bone-forming osteoblasts
F., Inglehearn C
Weinstain R, Slanina T, Kand D, Klan P
It inhibits NOTCH1 signaling by using its GCT activity to cleave a -glutamyl-cysteine bond at glutamate 1669 of the immature NOTCH receptor, thereby preventing the essential S1 cleavage and subsequent activation ( FIGURE 6 The physiological importance of this mechanism is underscored by severe developmental phenotypes upon its disruption
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