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. Author manuscript; available in PMC: 2010 Nov 15.

Published in final edited form as: J Cell Physiol. 2009 May;219(2):438–448. doi: 10.1002/jcp.21687

Fig. 4 — Mutant p57^KIP2 is defective in regulating in situ phosphorylation of p220^NPAT. (A–C) Immunofluorescence microscopy detecting the T1270 (A) or T1350 (B) epitopes (green) was performed as described in Fig. 1 using cells transfected with wild type mouse p57^KIP2 or three different mutants (i.e., p57^KIP2-T, -CC, or -CCT) (A,B) or human p57^KIP2 compared with a human p27^KIP1-p57^KIP2 chimera (C). Insets show merged images of p57^KIP2 and DAPI signals in transfected cells. The percentages on each panel indicate the number of cells with a microscopic phenotype.

Fig. 4 — Mutant p57^KIP2 is defective in regulating in situ phosphorylation of p220^NPAT. (A–C) Immunofluorescence microscopy detecting the T1270 (A) or T1350 (B) epitopes (green) was performed as described in Fig. 1 using cells transfected with wild type mouse p57^KIP2 or three different mutants (i.e., p57^KIP2-T, -CC, or -CCT) (A,B) or human p57^KIP2 compared with a human p27^KIP1-p57^KIP2 chimera (C). Insets show merged images of p57^KIP2 and DAPI signals in transfected cells. The percentages on each panel indicate the number of cells with a microscopic phenotype.