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As mentioned above, sites enriched in the TAF4 mutant have no specific location although a small number are associated with upregulated genes.
However, the function of A20 appears to be complex, since a recent study reveal that knockin mice expressing a DUB-inactive A20 mutant have no defect in NF-κB activation by TNF or LPS, suggesting a DUB-independent function of A20 [ 33].
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Interestingly, the pac mutant has no trichome phenotype (Carey et al.[2004]).[2004]
A TTG2-disrupted mutant has no trichomes (Johnson et al. 2002).
The ppi4 mutant had no obvious phenotype (Hiltbrunner et al. 2004).
The rcn11 mutant has no mutation in the RCN1/OsABCG5 gene and rcn11 has no effect on RCN1/OsABCG5 gene expression.
On the other hand, the D77I mutant had no detectable activity toward phenolic acid methyl esters and feruloylated arabinoxylan.
This GCV-selected mutant had no mutation in the UL54 but had an amino acid alteration at codon M460V of UL97, which conferred resistance to GCV.
Furthermore, in trans complementation of each mutation by introduction of a plasmid containing the intact deleted gene rescued the deficiency of each mutation, whereas introduction of the empty vector into each mutant had no significant effect (Fig. 3).
Unlike the Δppk2 mutant, the ppk1 mutant has no survival defect under aerobic conditions [15], [16].
This likely functional redundancy could explain why the ΔlytM mutant has no obvious phenotype.
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