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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.
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).
Interestingly, Roberts et al. reported that Apcmin/+ mice carrying an EGFR mutation with a marked reduction in EGFR activity had a 90% reduction in intestinal tumor compared with Apcmin/+ mice expressing normal EGFR [ 31].
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).
Similar(54)
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.
Furthermore, IRflox/flox Pf4-Cre+ mice expressed normal levels of IR in liver and skeletal muscle.
We hypothesized that this is due to a signaling defect as platelets from mutant mice expressed normal levels of integrin αIIbβ3.
We confirmed that lung AECs from TLR-9-/ mice express normal levels of TLR7 and TLR8, for instance (data not shown).
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