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DBZ is an inhibitor of γ-secretase aspartyl protease that improves efficiency of iPSC generation and production of iPSCs from mouse and human keratinocytes without KLF4 and CMYC.
DBZ is an inhibitor of γ-secretase aspartyl protease. DBZ blocks amyloid precursor protein-like (APPL) and Notch cleavage. By inhibiting Notch and the Notch pathway, DBZ improves efficiency of iPSC generation and production of iPSCs from mouse and human keratinocytes without KLF4 and CMYC. In an animal model of Alzheimer's disease, DBZ inhibits the cleavage of amyloid precursor protein into Aβ40. DBZ promotes cochlear supporting cell proliferation and hair cell mitotic regeneration in neonatal mice. DBZ in combination with iDOT1L enables maintenance of human naïve-state pluripotency in non-hypoxic conditions.
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