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Non-infected, mutant RBCs display slight but significantly increased membrane deposition of hemichromes accompanied by low-grade but distinct enhancement of phagocytic uptake [20], [22], [23].
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Other protection mechanisms probably concur with this based on enhanced ring-phagocytosis of mutant RBCs underscored here.
G6PD deficient red cells (G− RBCs) display a failure of the protective response to oxidant stress, which leads to irreversible oxidation of glutathione [1], [2], [4] [6].
WNT7A mutant mice display several Müllerian duct derivative abnormalities.
Pax3 mutant mice display absence of muscular diaphragm.
Vmat2 heterozygous mutant mice display a depressive-like phenotype.
Meanwhile, c30f12.4 mutant worms display a shortened lifespan.
In addition, the mutant mice display a microphthalmia phenotype.
cenp-metaΔ mutant cells display a mitotic delay.
Hence, Hem/Kette/Nap1 mutant GMCs display symmetric, rather than asymmetric division.
A percentage of gnz mutant embryos display gastrulation defects; homozygous Cripto null mutants display gastrulation defects (Ding et al., 1998).
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