Sentence examples for con cells from inspiring English sources

Exact(22)

At low trypsin concentrations, CON cells were resistant to detachment from the culture plate whereas KINE cells detached in significantly greater numbers than CON cells.

The increase was comparable in both PD (+25%) and CON cells (+21%) suggesting a similar intrinsic ability to respond to exogenous T administration.

Finally, PD myoblasts showed reduced responsiveness to T stimulated mRNA expression of mTOR vs. CON cells and T also reduced myostatin expression in PD myoblasts only.

Immunoblot analysis of cell lysates revealed that hPTP1B was expressed in all reconstituted cells (WT, D/A, and K/R) while mouse (m) PTP1B was expressed in Con cells and absent in KO cells (Fig. 1A).

They were also less adhesive to substrate and were more invasive compared to CON cells.

CON cells, on the other hand, were more migratory in the presence of a serum gradient.

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Similar(36)

Like NHU cells (not shown), NHU-Con cells showed some β-catenin/TCF activity, which was diminished in the presence of physiological calcium (Figure 4D).

These experiments showed that NHU-ECmut cells displayed consistently higher proliferation rates than NHU-Con cells in both low and physiological calcium conditions (Figure 4A).

Expression of active β-catenin was significantly decreased in β-catenin shRNA-expressing (NHU-β-cat-KD) cells when compared to control (NHU-Con) cells expressing control shRNA, as shown by immunoblotting experiments (Figure 5A).

As in NHU cells, the increased proliferation rate characteristic of cultures grown in physiological calcium was attenuated by LY294002 treatment in NHU-Con cells, whereas the inhibitor had little effect on the exponential growth rate in low calcium conditions.

However, NHU-β-cat-KD cell growth in physiological calcium was significantly reduced in comparison to cultures of NHU-Con cells (Figure 5B), indicating that β-catenin knock-down rendered NHU- β-cat-KD cells very sensitive to the LY294002 inhibitor and confirming the importance of PI3-K/AKT signalling in conditions that mimic E-cadherin engagement.

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