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. 2015 Dec 3;44(1):67–74. doi: 10.1177/0300060515600188

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© The Author(s) 2015

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page(https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — Knockdown of structural maintenance of chromosomes (SMC) 1A mRNA by lentivirus-mediated small interfering RNA (siRNA) in HT-29 cells. (a) Microscopic images of control siRNA lentivirus-infected HT-29 cells (Control) and SMC1A siRNA lentivirus-infected HT-29 cells (SMC1A-KD): a, Control cells under a fluorescence microscope; b, Control cells under a light microscope; c, SMC1A-KD cells under a fluorescence microscope; d, SMC1A-KD cells under a light microscope. Scale bar: 50 µm. (b) Real-time polymerase chain reaction analysis of the SMC1A mRNA levels in Control and SMC1A-KD cells. Data presented as mean ± SD (n = 3). *P < 0.05, Student’s t-test. (c) Western blot analysis of SMC1A protein levels in Control and SMC1A-KD cells; Representative blot from three independent experiments that had similar results. β-actin was the loading control. The colour version of this figure is available at: http://imr.sagepub.com.