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. 2006 Aug 28;174(5):625–630. doi: 10.1083/jcb.200606051

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Copyright © 2006, The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 2. — Depletion of PCM-1 leads to cell cycle arrest in G1 or G0 phase. (A) Immunoblots of MRC-5 cells treated with control RNA or siRNA against PCM-1, pRb, or both PCM-1 and pRb simultaneously. Blots were probed with antibodies against PCM-1, cyclin A, the licensing factor MCM3, the DNA replication factor PCNA, pRb, and α-tubulin. (B) Immunoblots of cells treated with control RNA or siRNAs against PCM-1, pericentrin, or both simultaneously. Blots were probed with antibodies against MCM3, pRb, and α-tubulin. Arrowheads in A and B indicate migration positions of hyper- and hypophosphorylated pRb. (C) MRC-5 cells treated with control RNA, siRNA against PCM-1, or siRNA against PCM-1 and pRb simultaneously. The percentages of cells staining positively for the proliferation marker Ki-67 or for incorporated BrdU are shown. Experimental conditions were similar to Fig. 1 B. Error bars indicate SD. (D) Flow-cytometric analysis of MRC-5 cells treated with control RNA or siRNA against PCM-1. (E) Immunoblots of MRC-5 cells treated with control RNA or siRNA against PCM-1 for 48 or 120 h or with siRNA against pericentrin for 72 h. Blots were probed with antibodies against p53, α-tubulin, or p21.