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By using an atrbohD/F double mutant we demonstrate here that dark-induced H2O2 formation occurs by a similar mechanism in Arabidopsis.

Using the glycolate-accumulating ΔglcD1 mutant, we demonstrate enhanced 13C partitioning into the glycolate pool under conditions favouring photorespiration and enhanced 13C partitioning into the glycine pool of the glycine-accumulating ΔgcvT mutant.

Using this HSF1 CE2 deletion mutant we demonstrate that Hsf1 activation, and hence thermal adaptation, contributes significantly to the virulence of C. albicans.

Through comparisons of 3 D movement between wild‐type ookinetes and a cytoskeleton‐knockout mutant we demonstrate that perturbation of cell shape changes motion from helical to broadly linear.

Further, using complementation assays in an Escherichia coli mutant we demonstrate functional replacement of a pantothenate biosynthesis enzyme, 2-dehydropantoate 2-reductase (E.C. 1.1.1.169), by an endosymbiont gene, ilvC, encoding a substrate ambiguous enzyme.

By comparing a methicillin-resistant S. aureus (MRSA) strain with an isogenic Staphopain A mutant, we demonstrate that Staphopain A is the only secreted protease with activity towards CXCR2.

Similar(54)

Using the ΔTK ErbB1 mutant we demonstrated that the tyrosine kinase domain, although not essential for ErbB1/nucleolin interaction, is crucial for ErbB1 activation induced by nucleolin.

Regarding the Cj-E116Q mutant, we demonstrated that Mn2+ was not able to restore its catalytic activity.

Using a dominant-negative AP-2 mutant, we demonstrated that simultaneous interference with both, AP-2α and AP-2γ leads to a decrease in proliferation and induction of apoptosis in N202.1A breast cancer cells.

By using a dominant negative p73 mutant we demonstrated that genotoxin-induced apoptosis relies on p73 activation and importantly, that p73 activation is required for Noxa expression in our cells.

Using a panel of CIITA mutants, we demonstrate that cytoplasmic CIITA increases Gag-Pol polyprotein levels.

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