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Cells expressing Cep290 carrying the missense mutation R1747Q in mouse exhibited a defective Sonic hedgehog (Shh) signalling response, mislocalisation of the Shh receptor Smoothened (Smo), and dysregulation of ciliary protein mobility, which ultimately disrupted the proliferation of cerebellar granule progenitors (CGPs).
The heterozygous mouse exhibited a well-circumscribed syndrome of behavioral abnormalities, consisting primarily of a decreased fear response and an increase in defensive aggression, in the absence of any measured cognitive deficits.
The skin of RASSF9−/− mouse exhibited a significant epidermal thickening.
A LIPHlpd1 Knock Out mouse exhibited a complex multifactorial phenotype including retarded hair growth [12].
Fig. 5A shows that an identified GHRH neuron in an adult male somatostatin knockout mouse exhibited a spontaneous firing rate of ∼0.9 Hz under control conditions, increasing to ∼3.3 Hz upon addition of 10 nM ghrelin to the external solution.
The PRAKO mouse, like the PRKO mouse, exhibited a infertility phenotype.
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In addition, the BLM-injected Ninj1 KO mice exhibited a mild fibrotic phenotype, as compared to WT mice.
JZL184-treated mice exhibited a broad array of CB1-dependent behavioral effects, including analgesia, hypothermia and hypomotility.
Glomus cells from partially HIF-1α deficient mice exhibited a normal sensitivity to hypoxia.
In this variable light-dark condition, wild-type mice exhibited a gradual adaptation manifested by a continuing compression of their α activity.
Knockout mice exhibited a dramatic 85% decline in intramuscular NAD content, accompanied by fiber degeneration and progressive loss of both muscle strength and treadmill endurance.
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