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Targeted deletion of PTEN in the mouse leads to constitutive activation of the PI3K/AKT pathway.
Genetic ablation of Scleraxis in the mouse leads to defective differentiation of limb muscle tendons [31].
In contrast with the LR asymmetry requirement of dmrt2a in zebrafish, the loss of Dmrt2 in mouse leads to embryonic somite patterning defects [15].
The combined inactivation of Dlx5 and Dlx6 in the mouse leads to a lower-to-upper jaw transformation, with vibrissae forming also in the lower jaw [39], [40].
First, ablation of the AVE of the mouse leads to a loss of Hesx expression in the anterior neural folds of the mouse (although other markers assessed were normal) [60].
Dystrophin is one of the best characterized DGC proteins and its absence in humans and the mdx mouse leads to a destabilization of the DGC, sarcolemmal fragility, myofiber degeneration and muscle weakness [3].
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Absence of these proteins in knockout mice leads to susceptibility to lung infection and emphysema.
Accordingly, its overexpression in transgenic mice leads to pulmonary hypertension along with pathologic muscularization of small pulmonary arteries [81].
Our results indicate that partial loss of Smad7 function in mice leads to compromised bone formation and enhanced bone resorption.
Experimental airway allergy in mice leads to increased activity in specific hypothalamic and amygdaloid nuclei, and behavioral changes.
Suppression of SOCS-3 activity leads to activation of STAT3, which when activated in keratinocytes in transgenic mice leads to the development of psoriasis (Sonkoly et al., 2007).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com