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This would be consistent with the detection of occasional mutant cells showing weak Gata4 staining.
T 1/2 in the mother part of yos9Δ mutant cells was 13.3 ± 4 s and 18.8 ± 7.4 s in hrd3Δ mutant cells, showing that Kar2-sfGFP dynamics were significantly slower than in the mother part of unstressed wild type cells (t 1/ 2 = 8.1 ± 2.2 s).
Thus, sorafenib, 885-A and PLX4720 all induced BRAF binding to CRAF in NRAS or KRAS mutant cells, but not in BRAF mutant cells, showing that BRAF inhibition per se did not induce this binding; it only occurred when BRAF was inhibited in the presence of oncogenic RAS.
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Finally, ~16% of mutant cells showed division defects (Figs 2b and S2d,e).
NF1 mutant cells show activation of RAS/MAPK signaling, so a counter-screen in RAS mutant carcinoma cells was performed to exclude common RAS-pathway driven genes.
In addition, analysis of DNA plasmids recovered from Ku86 mutant cells showed an increased use of microhomologies at the nonhomologous end joining junctions, and displayed a significantly higher frequency of DNA insertions compared to control cells.
Indeed, delg mutant cells showed an identical COX activity compared to control (Fig. 5B).
In contrast, delg null mutant cells showed a strong decrease in staining.
In addition, Δctf4 and Δelg1 mutant cells show partially overlapping phenotypes.
As seen in Fig. 2D, delg mutant cells showed a strong reduction in NAO.
In contrast, the elongated and deformed ssn8 mutant cells showed uneven cellular organization.
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