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Importantly, the meiotic phenotype of dfp1-r35 suggests that disruption in prDSB formation is not its only defect, because rec12Δ mutants, which are completely defective for prDSB formation, nevertheless complete both meiotic divisions in with a normal timing and transcriptional program.

In Traf6 −/− cells, Q145N but not 2ED MAVS was completely defective in inducing IFNβ, but this defect was rescued by ectopic expression of WT but not C70A TRAF6.

Cytosolic extracts from Traf6 −/− primary MEF cells were severely, albeit not completely, defective in supporting IRF3 dimerization and IκBα phosphorylation in vitro, and these defects were rescued by adding back wild-type TRAF6.

"Maybe there's completely defective thinking [in the conventional view]," he says in the film.

Consistent with the result in Malt1 KO MEF cells, both CARMA3-deficient and BCL10-deficient cells were completely defective for NF-κB activation upon doxorubicin treatment.

The resulting constructs are functional, stably maintained under conditions where the original constructs are unstable, completely defective for conjugative transfer, and transferred via electroporation.

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Similar(6)

We found that, contrary to previous reports, rde-4 mutant animals are not completely RNAi defective.

Before testing whether cross-presentation could prime MCMV-specific CD8+ T cells, we needed to confirm that the ΔgL virus was completely spread defective.

We found that the nuclear RNAi and the FBF-1-mediated adaptation pathways function in parallel, such that double mutants are completely adaptation defective.

In line, other studies demonstrate that some of the PSEN1 FAD mutants, unlike wild-type human PSEN1 (hPSEN1) and its catalytically inactive forms, are unable to fully rescue altered Wnt signaling in PSEN-deficient cells [ 33] or completely alleviate defective epidermal growth factor receptor (EGFR) turnover in lysosomes, in a similar context [ 116].

The phenotype of both vertebrate cell lines is remarkably different: While ATG13−/− cells are completely autophagy defective, ULK1−/− ULK2−/− cells do not display any impairment of the autophagic pathway, indicating that ATG13 plays an essential role in autophagy induction, while ULK1/2 kinase activity is dispensable in this cell line.

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