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We also found that CD133+ isolated from the nine AT/RT patients expressed severe deletion of chromosome 22q11 (Figure 1; Table 1), and these cells further demonstrated a self-renewal capability, rapid growth rate, and multipotential to differentiate into three germ layers (Figures 2 & 3).
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The fraction of mutants with severe deletions in the Hprt locus after exposure to oxygen ions increases from 65% at 60 keV/μm up to a maximum (100%) at 300 keV/μm and declines with higher LET values to 75% at 750 keV/μm.
These defects became progressively more severe with deletion of more modules from CipA and most severe for the CipA-ΔCBM-1 and CipA-ΔCBM-2 strains, in which the CBM is deleted.
However, the penalty is not severe if deletions and insertions constantly occur in the same locations.
However, due to severe sequential deletions in the sequenced O 3/4 strains, a possible impact of this prophage on O 3/4 pathogenicity and elevated ampicillin resistance remains questionable.
Interestingly, in developing airways defects in Clara cells differentiation were similar between Pofut1/Shh-Cre and Rbpj/Shh-Cre mutants [37]; however, defects in neuroendocrine cells differentiation were more severe in Pofut1 deletion than in Rbpj deletion and it was ascribed to a marginal reduction of Hes1 expression by Rbpj deletion [38].
Histological analysis revealed pronounced, severe apoptosis and deletion of spermatocytes in testes with conditionally deleted Hsp90α, similar to what was observed in the conventional Hsp90α KO mice.
We hypothesized that excision of exon 3 (BcorΔ3) would result in a frame shift and a premature stop codon that should cause severe carboxy-terminal deletion of the BCOR protein and/or elimination of the mRNA by nonsense-mediated decay (Figure 1C).
Our observations in a T cell-specific model provide strong evidence that a severe thymic clonal deletion defect is sufficient to cause autoimmune pathology.
To explore why loss of Esrrb has more severe consequences than deletion of Nanog, we utilized the ChIP-seq compendium to compare profiles of Nanog, Oct4, Sox2, Tcf3, and Esrrb.
Although the phenotype of the H4G94P mutant in yeast is more severe than the deletion of ASF1 alone, given the importance of the C-terminal tail of H4 within the Asf1-H3/H4 structure [ 23, 24], we were interested in whether the H4G94P mutant protein altered the structure of the Asf1-H3/H4 complex.
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