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We further assessed the expression level of miR-34a in LPS SV by qPCR.
Five days later, we assessed the expression level of native γ-COP using the mouse anti-γ-COP antibody (Figure S1).
We therefore assessed the expression level of the Pm3b transgene in the four GM lines by semi-quantitative RT-PCR using RNA isolated from leaves of seedlings grown in the glasshouse (Figure S1).
To identify the mechanism by which ECT2 blocks G1 progression, we assessed the expression level of cyclin-dependent kinase inhibitors (p16INK4A, p21cip1, p27kip1), cyclin D1, cyclin E, and CDK4 (Figure 6B).
We further assessed the expression level of miR-20b in a panel of breast cancer cell lines.
We assessed the expression level of these fusion proteins relative to their endogenous proteins by Western blotting.
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We also assessed the expression levels of VRK1 in spermatogonial populations using flow cytometry.
As an additional measure of adipocyte differentiation, we assessed the expression levels of the differentiation gene marker PPAR-gamma.
We next assessed the expression levels of Ptch and Gli1 in xenografts from HGC-27 by quantitative real-time PCR.
In order to characterize and investigate the cells grown in the HFB, we assessed the expression levels of various adhesion molecules and stem cell markers before and after culturing the cells in simulated hypogravity.
Since PTEN is a known target of miR-21, which has been reported to be up-regulated in PC [13] [15], we assessed the expression levels of miR-21 in tumor remnants as shown below.
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