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Intercrossing of these mice with p53-deficient mice completely rescued the progenitor cell defect, thus accounting for the frequent co-occurrence and adverse impact of TP53 defects in myelodysplasia with isolated 5q- 121
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Assays of stroma and thylakoid fractions showed no detectable GCL and GS activity in the lumen (unpublished data)
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Therefore, inhibition of PI3K results in reduced glucose uptake in skeletal muscle and adipose tissue
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