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To investigate whether mmi1W112A affects any of the transcripts that are upregulated in mmi1∆ and/or erh1∆ cells, we compared the transcriptomes of WT and mutant cells using RNA-seq.
To do this, the DN-DaPKC transgene was expressed specifically in ept,H99 mutant cells using the MARCM technique [35].
To distinguish between these two possibilities, we first investigated the localization of two spindle assemble checkpoint proteins, Mad2 and Bub1, in wild-type and mutant cells using chromosomally integrated GFP-tagged versions of these genes driven by their native promoter.
The barrier strength was measured in wild-type, gcn5∆ mutant and bud6∆ mutant cells, using Nup49-GFP as a reporter.
Concomitantly, a sharp increase of ubiquitinated proteins and Lamp2 levels was detected in mutant cells using immunoblot analysis (Fig. 2G).
We next examined the cell and nuclear morphology of wild type and mutant cells using DAPI to stain DNA.
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In contrast, Abd-B was expressed ectopically in nuclei of expulsed ph mutant follicular cells using either the ph0 allele (Figure 8C C″, encircled) or the transgenic RNAi construct targeting ph (Figure 8D D″, yellow arrowhead).
To further evaluate these findings, we blocked p53 in Hs294T (wild-type p53) and SM-Mel-28 (mutant p53) cells using the p53-specific inhibitor pifithrin-α (PTF-α) (Komarov et al, 1999).
This study assessed whether the structurally diverse MDM2 p53 antagonists, MI-63, NDD0005, and RG7388 are also able to modulate MDR-1 function, particularly in p53 mutant neuroblastoma cells, using XTT-based cell viability assays, western blotting, and liquid chromatography mass spectrometry analysis.
We evaluated the adhesive effects of hepaCAM and its extracellular domain truncation mutant on T24 cells using cell adhesion and detachment assays.
To test this idea, we employed FRET to measure the protein-protein interactions of HAND1 and HAND1 point mutants in HEK293 cells using YFP and CFP fusion proteins and laser scanning confocal microscopy.
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