Sentence examples for repression cells from inspiring English sources

For setting up the repression, cells were peletted down in mid-log phase and shifted to pre- warmed 0.15X YEP medium without any carbon source and incubated for 4 hours [ 22].

For mTOR repression, cells were incubated with pp242 (1 μM) or rapamycin (1 μM or 200 nM for GH3 cells) for different time periods (6 h for Fao, 12 h for MEFs, 24 h for 3T3-L1 and GH3).

Paradoxical results on Tcf-4-regulated OPN expression in MCF10AT (activation) and Rama37 (repression) cells were shown to be a result of differential Wnt signalling competency in MCF10AT and Rama37 cells.

As shown in Figure 8, depending on the levels of c-MYC repression, cells with ~50% c-MYC knock-down (sh1) displayed significant reversal in target gene expression such as LAMC2 and VAV3, but cells with ~25% c-MYC knock-down (sh2) only showed relatively minor change.

We discuss the potential applications of the engineered repressor strategy that relate to target gene analysis, mechanisms of repression, cell regulation, and possible anti-viral and cancer therapy.

Together, this suggests that the information driving the quantitative effects of Hox proteins on Wnt repression, cell ingression, and elongation is built in the structure of the proteins themselves rather than reflecting the actual amounts of Hox proteins present.

This indicates a strong repression of cell wall synthesis, cell wall modification, pectin degradation, cell expansion and cell wall turnover.

A negative feedback loop involving Nrm1p and Yox1p bound to MBF leads to transcriptional repression as cells exit G1 phase.

This effect is possibly mediated through binding sites for NF-κB/Rel proteins in a regulatory module of the scute gene required for maintenance of scute expression in precursors as well as repression in cells surrounding precursors.

MicroRNAs (miRNAs) are a class of 18- to 24-nt, small, noncoding RNAs, which bind the 3' UTR of target mRNAs to mediate translational repression in cells [ 11- 13].

Ago2 is the effector component of the miRNA-induced silencing complex (miRISC) that directly binds miRNAs and mediates messenger RNA repression in cells [ 14, 15].