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Homozygous mutant mice express normal Scarb1 mRNA levels and are fertile.
The muscles of mdx mice express normal amounts of mRNA for the DAPC components, thus suggesting post-transcriptional regulation.
We confirmed that lung AECs from TLR-9-/ mice express normal levels of TLR7 and TLR8, for instance (data not shown).
Leheste et al. initially reported that approximately 10% of the proximal tubular cells of these mice express normal levels of megalin [ 12], and Motoyoshi et al. reported residual megalin expression in 35 50% of proximal tubular cells [ 23].
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Using the Zurich 1 PrPKO and matched wild type (Wt) mice expressing normal levels of PrP as experimental models, we demonstrate that PrPKO mice show a phenotype of systemic iron deficiency and altered iron homeostasis compared to Wt controls.
Genetic or siRNA-mediated PrPC depletion in these studies delayed or even prevented disease, while still replicating PrPSc to levels seen in wild type mice expressing normal levels of PrPC.
Furthermore, IRflox/flox Pf4-Cre+ mice expressed normal levels of IR in liver and skeletal muscle.
Results indicate that mutant mice expressing lower HO-1 had fewer lung metastases compared to mice expressing normal HO-1.
Transgenic mice expressing normal forms of human APP (HuAPPwt mice) or tau (ALZ17 mice), and transgenic rats expressing a mutated form of human APP (APP21 rats).
We hypothesized that this is due to a signaling defect as platelets from mutant mice expressed normal levels of integrin αIIbβ3.
Exposure of transgenic mice to maneb and paraquat showed a higher level dopaminergic neurotoxicity in mice with doubly mutated α-synuclein compared with mice expressing normal wild-type human α-synuclein (Thiruchelvam et al. 2004).
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