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. Author manuscript; available in PMC: 2023 Jan 6.
Published in final edited form as: Mol Cell. 2021 Dec 22;82(1):90–105.e13. doi: 10.1016/j.molcel.2021.11.031

Figure 6: APC7 operates in the context of Cdh1-APC to drive Ki-67 degradation in neurons.

Figure 6:

A. Electron tomography of P8 cerebellum.

B. Calbindin IF in sagittal sections of P12 cerebellum. An expanded region from the Cdc20f/f,Math1-cre is shown (PCL, Purkinje cell layer).

C. In vitro ubiquitination of full-length Ki-67 by recombinant Cdh1-APC and Cdc20-APC. Ki-67 was immunoprecipitated from wild-type P7 cerebellum and detected by Ki-67 IB.

D. In vitro ubiquitination of human Ki-67 amino acids 1–300 (left) and 765–1000 (right) by Cdh1-APC and Cdc20-APC.

E. Ki-67 IB in P12 cerebellum.

F. Densitometry quantitation of Ki-67 IB. Mutants were normalized and compared to littermates. Error bars SEM (N = 4, p-value by two-tailed unpaired t-test).

G. IF of Ki-67 in primary cerebellar granule neuron cultures.

H. Quantitation of Ki-67 IF normalized to nuclear area in cultured neurons on the indicated DIV. Error bars interquartile range (p-values by Kruskal-Wallis test for non-parametric data followed by Dunn test).