Evidences a(CHEBI:lactacystin) to p(HGNC:MAPT)

In SH-SY5Y neuroblastoma cells, treatment with lactacystin, a selective inhibitor of the 20S catalytic core, maintained levels of transfected wild-type full-length tau (4R0N) after cycloheximide treatment halted protein synthesis (65).

Additionally, incubation of rat brain extract (containing endogenous tau and proteasomal enzymes) with the proteasome activators Mg2+ and ATP resulted in lower total tau levels with an increase in smaller forms, compared to extract not supplemented with Mg2+ and ATP (73). The loss of tau was blocked by lactacystin giving further evidence that the proteasome was degrading tau (73).

Related to these data, reversible and irreversible proteasome inhibitors including lactacystin, leupeptin, and epoxomicin delay the degradation of endogenous and/or transiently overexpressed tau (Cardozo and Michaud, 2002; David et al., 2002; Zhang et al., 2005).

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