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We also show an image without transparent material to observe a defect in the fiber scintillator plate (Fig. 5(D)).
We did observe a defect in juvenile-to-adult phase transition in the cao/ch1 mutant under our growth conditions.
Therefore, amongst the maternal RNAs (representative of the various transport pathways) examined to date, we only observe a defect in maternal sqt RNA localization.
For example, we found that Lsd1 deletion with VavCre or Mx1Cre resulted in severe HSC differentiation and self-renewal defects resulting in complete loss of lineage-negative c-Kit+ myeloid progenitor cells, whereas Sprüssel et al. (2012) did not observe a defect in LT-HSCs.
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Similarly, we observed a defect in intestinal persistence in an enteropathogenic <i>E.
Most frequently, we observed a defect in muscles 6 and 7 whereby instead of running parallel, the two crossed, each appearing to insert improperly at the insertion site of the other (Figure 6B).
Using these cells, we observed a defect in PDGF-BB-induced Akt phosphorylation on Ser473, but also on Thr308.
We also observed a defect in the monoubiquitin conjugation to PTEN-SUMO1 complexes using in vitro assays.
Accordingly, we observed a defect in PPT formation starting at 10 nM abexinostat and this defect was only partially rescued by the downregulation of p53.
However, we and others have now observed a defect in cohesin loading in the absence of Chl1 (Laha et al. 2011).
In accordance with these results, we observed a defect in FANCD2 foci formation in USP1-depleted human cells (Fig. 4B and C).
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