Biochemical and Biophysical Research Communications
Reversible G1 arrest of a human Burkitt lymphoma cell line(Raji) induced by tunicamycin
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Biological and structural characterization of glycosylation on ephrin-a1, a preferred ligand for EPHA2 receptor tyrosine kinase
2013, Journal of Biological ChemistryCitation Excerpt :To further confirm the glycosylation on eA1, U-251 MG [eA1](+) cells were grown in the presence of tunicamycin to block the synthesis of all N-linked glycoproteins (23). As tunicamycin is known to causes cell cycle arrest in G1 phase (24), we observed a reduction in the amount of total eA1 in the cell lysates, which was produced in non-glycosylated form (Non Gly-eA1) in accordance with the smaller size of the protein (Fig. 2B). Non-glycosylated eA1 was no longer detected in the media of tunicamycin-treated cells, in sharp contrast to eA1-WT (Fig. 2B), demonstrating that N-glycosylation is critical for proper eA1 folding and/or release.
Expression profiling and biochemical analysis suggest stress response as a potential mechanism inhibiting proliferation of polyamine-depleted cells
2012, Journal of Biological ChemistryCitation Excerpt :However, because cells containing both deficiencies are not available, we cannot rule out the existence of additional causes for the establishment of growth arrest in polyamine-depleted cells. Stressed cells are usually growth-arrested at the G1 phase of the cell cycle (40, 41, 43, 64), as we demonstrate here for polyamine-depleted cells. The G1 arrest in polyamine-depleted cells was associated with increased transcription of p21 and Gadd45a, decreased transcription of Cdk2, E2f1, Pcna, cyclins A and E, and most profoundly with decreased levels of the cyclin D1 protein, a regulator of the Cdks required for G1/S transition, whose decline was demonstrated to suffice for arresting cellular proliferation (40, 65).
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