Figure 6. C-terminally truncated LBR mutants associated with Pelger-Huët anomaly and Greenberg skeletal dysplasia are rapidly degraded via the proteasome.
(A), (B) LBR KO cells expressing either WT LBR or the disease-associate LBR mutants were metabolically labeled with 35S and then chased with an excess of unlabeled cysteine/methionine. LBR was then retrieved at the indicated time points via immunoprecipitation, resolved by SDS-PAGE and imaged via autoradiography. (C), (D) Turnover of LBR 1402TΔ and LBR 1600* was measured on a shorter time scale in the absence or the presence of MG132.