Feb 1, 2012 · In this study, we found that Mdm2 was stabilized and upregulated upon Actinomycin D (ActD) treatment in the p53-deficient H1299 cell line. This Mdm2 upregulation was not dependent on the ribosomal protein L11, an essential player in ribosomal stress-induced p53 activation, but did require a NEDDylation-dependent mechanism.

The interaction between p53 and Mdm2 proteins was detected by transfecting H1299 cells (p53 null) with plasmid constructs PCMV-HA-53 and PCMV-MDM2 wild-type or point mutants together with β-Gal for 24 h, followed by MG-132 treatment for 4 h.

Mitochondrial localization of ectopic FL-MDM2 in H1299 cells was further confirmed by immunogold labeling and transmission electron microscopy (TEM).

To examine this hypothesis in the absence of confounding p53-mediated effects, we evaluated ectopic MDM2 expression in a functionally-null p53 deficient human non-small cell lung cancer cell line, H1299.

Next-generation sequencing was performed upon ChIP with anti-MDM2 N20 antibody in H1299 cells expressing a shRNA targeting Mdm2 and in cells overexpressing MDM2-ΔAD mutant. Samples were processed in vitro to generate a library of short inserts of ∼250 bp.

Some tumor-derived cells, such as Saos-2, H1299 or U-2OS, are relatively insensitive to the growth-inhibitory effects of hMDM2. These observations suggest that hMDM2 overexpression in response to oncogenic stimuli would induce growth arrest in normal cells.

Jan 1, 2001 · The effect of excess mdm2 on p53-mediated apoptosis was investigated in two human-derived cell lines, H1299 and HeLa. In H1299 cells, overexpression of mdm2 resulted in effective protection from apoptosis.

Nov 13, 2020 · In an attempt to decipher the mechanisms that explain these two RB regulatory pathways, we studied the effect of increased concentrations of MDM2 on the levels of expression of exogenous RB in the p53 null cell line H1299 (human non‐small cell lung carcinoma) under normal cellular conditions.

Feb 1, 2012 · Here we report that Mdm2 is upregulated and stabilized in response to ribosomal stress in H1299 cells through a NEDDylation-mediated mechanism, and downregulation of Mdm2 increases the sensitivity of H1299 cells to ribosomal stress-induced cell death.

H1299 Control and H1299 NDI1 cells were transiently transfected with increased amounts of MDM2 WT, and this produced similar levels of MDM2 protein and apoptosis (Figure 5H), suggesting that the overall decrease in CI activity caused by MDM2 was unlikely to be the direct source of cellular stress.