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Therefore, to evaluate the consequences of the interaction of ClpX with FtsZ in vivo, we created M. tuberculosis strains expressing altered levels of ClpX from the inducible tetracycline promoter and characterized them with respect to growth, viability and Z-ring structures.
Therefore, careful characterization of the expression of the other p53 family members, including the individual isoforms of p63 and p73, is necessary in mouse models expressing altered levels of p53 in order to understand the complex interplay and potential compensation between the p53 family members in processes that regulate longevity.
Specifically, we tested mutants constructed in NCTC8325-4 S. aureus strain, expressing altered levels of autolysins (Δ arlR), lacking the major autolysin (Δ atl) or factors that modulate autolysin activity (Δ fmtA), producing non-O-acetylated peptidoglycan with increased susceptibility to lysozyme (Δ oat), or producing altered WTAs lacking attached β-O-GlcNAc (Δ tarS) or D-alanyl residues (Δ dltA).
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This model is supported by the finding that when mammalian and yeast cells are genetically engineered to express altered levels of the Cu transporters they exhibit altered sensitivity to Pt drugs and are defective in intracellular Pt accumulation due to altered uptake and/or efflux rates.
We found that T98G BTSCs express altered levels of many nuclear receptors compared with the glioma cells (Table 1).
We next proceeded to determine whether aging oocytes express altered levels of enzymes involved in CoQ biosynthesis.
Our antiestrogen-resistant cell lines did not express altered levels of EGFR, HER-2/neu, ErbB-3 and ErbB-4.
We show for the first time that BTSCs express altered levels of nuclear receptors compared with glioma cells.
These results suggest that BTSCs express altered levels of nuclear receptors, which may serve as novel therapeutic targets for the treatment of brain tumour.
We found that BTSCs express altered levels of many nuclear receptors compared with glioma, which are currently under investigation in our laboratory.
nSSL-BMS treatment leads to lower levels of cerebral inflammation, expressed by altered levels of corresponding cytokines and chemokines.
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