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On the contrary, loss of RPTPσ in mice causes an enhancement in novel object recognition memory (Horn et al., 2012).
In mice, an engineered null mutation in mice causes an increase in 5-HTP accumulation in vivo [103].
ZO-1 deficiency in mice causes an embryonic lethal phenotype associated with defected yolk sac angiogenesis and apoptosis of embryonic cells [31].
Because ΔFosB overexpression in mice causes an enhancement of bone formation [29], [30], the increase in ΔFosB in response to mechanical stress may play an important role in the stimulation of bone formation by mechanical stress.
Our data indicate that a CNV found in the largest extant mouse RI panel, a large inbred strain panel, an outbred laboratory mouse population and wild-caught mice causes an eQTL for Glo1.
For example, irradiating mice causes an accumulation of senescent cells, which promote increased growth and metastasis of transferred tumor cells.
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Lee, A. W. et al. (NEGR1 Functional inactivation of the genome-wide association study obesity gene neuronal growth regulator 1 in mice causes a body mass phenotype.
The paralog Zfhx1a (a.k.a. Zeb1) when knocked out in mice causes a cleft palate phenotype with 100% penetrance [59], [60].
In summary, this study demonstrated that an additional Fas deficiency in ApcMin/+ mice causes a dramatic increase in the number of intestinal tumors.
The lack of Rab27a in Ashen mice causes a defect in vesicle tethering to the PM, as well as in exocytosis of LG [18], [20], [22].
Disruption of GLP-1 signaling in mice causes a significantly decreased sensitivity to sweet tastants, and increased sensitivity to umami and sour tastants.
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