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Exercise in mouse models causes neurogenesis in the dentate gyrus.
Global constitutive activation of ACVR1 in mouse models causes embryonic lethality; however, transgenic mice containing a Cre-inducible constitutively active allele (ALK2 Q207D) have been developed (Fukuda et al., 2006).
For example, posttranscriptional control of tumor necrosis factor-α (TNF-α) expression has been extensively reported, and increased expression of TNF-α, caused by impaired control of its mRNA degradation, leads to just over twofold increase in mRNA half-life which, in mouse models, causes severe autoimmune disease (7, 8, 32).
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The ablation of Paneth cells in several mouse models caused recoverable loss of Lgr5+ stem cells (Sato et al., 2011).
Previous research showed that 1 enhanced the cellular and humoral immunity in mice, and increased the phagocytic activity of macrophages in immune-depression mouse models caused by massive doses of hydrocortisone and hydroxycarbamide [ 12].
Loss of Wnt1 or β-catenin in mouse models caused severe abnormalities in midbrain and cerebellar development by preventing specification of the midbrain hindbrain boundary (McMahon and Bradley, 1990; Thomas and Capecchi, 1990; Schuller and Rowitch, 2007).
It has been demonstrated that glucose transporter (GLUT1) deficiency in a mouse model causes a diminished cerebral lipid synthesis.
A lack of GP130 in T cell specific conditional gp130 deficient mice models causes the activation of Th2 and regulatory T cell pathways [70].
Disrupting the Mdm2 and Mdm4 interaction using knockin mice models causes embryonic lethality that can be completely rescued by the concomitant loss of p53, suggesting that Mdm2 and Mdm4 heterodimerization is critical to inhibit p53 activity during embryogenesis.
Prenatal cocaine exposure in a mouse model caused a decrease in both GABA neuron migration from the basal to the dorsal forebrain and radial neuron migration in the dorsal forebrain.
Heterozygous deletion of Becn1 in an AD mouse model caused increased neurodegeneration, decreased autophagy, and disruption of the lysosomal system [41].
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