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We demonstrate that STX-T plays an essential role in the fast recycling of transferrin receptor and STX-T-deficiency mice are lethal with iron deficiency anemia.
Survivin is essential in suppressing apoptosis during mouse development, Survivin null mice are lethal at early embryonic stage (Uren et al., 2000).
TNF Receptor Associated Factor-2 (TRAF2) is one of those molecules which its role is controversial and not well defined yet 4. Since TRAF2 knock-out mice are lethal at birth, we have established various conditional and tissue specific TRAF2 knock-out to study the role of TRAF2 in different tissues.
CASK knockout mice are lethal but show no dramatic synaptic alterations except increased neuroligin protein levels and higher spontaneous event frequency at glutamatergic synapses [57], consistent with our data and a subtle role in synaptic protein organization.
In contrast, the Dicer-knockout mice are lethal by extensive internal hemorrhage at the later embryonic stage [ 47].
Only homozygous Elovl4-null and Elov4 knock-in mice are lethal due to epidermal permeability barrier defects.
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MOF is essential for mammalian embryonic development and unlike the male-specific lethality in Drosophila, deletion of Mof in mice is lethal for both sexes (Gupta et al., 2008; Thomas et al., 2008).
Knockout of either p68 or p72 in mice is lethal (E11.5 or P2, respectively) and double knockout animals show earlier lethality without obvious specific degeneration of organogenesis [ 103].
Deletion of RagA in adult mice is lethal.
Ablated or defective Runx2 expression in mice is lethal as there is an absence of osteoblasts and bone in such animal models [27], [30], [31].
Administration of high-dose CpdA to mice was lethal while treatment of EAE with low to intermediate amounts of CpdA dissolved in water significantly ameliorated the disease.
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