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Mouse models lacking the α3- or γ2-chain of laminin-332 have been developed and a spontaneous ß3-knockout mouse exists, but all die shortly after birth.
Indeed, they have proved to be essential elements in normal physiology, as shown by mouse models lacking these proteins, that evidence several developmental abnormalities and pathological features.
We therefore used two different conditional mouse models lacking Prkg1 in the nervous system.
Further tests in mouse models lacking the specific epithelial receptor will permit more targeted examination of the complex interplays between the pathogen and the lung epithelium.
To characterize the influence of PRKG1 on sleep and circadian rhythmicity in mammals, we analyzed two different mouse models lacking functional PRKG1 in the brain.
Support for these activity-dependent roles of AChR derives from in vivo studies of mouse models lacking synaptic organizers such as agrin or MuSK, showing apparently normal myofiber growth and survival [4], [7].
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The coexpression of RET/PTC 3 and E7 in transgenic mouse models lacks any cooperative effect in the neoplastic transformation of thyroid cells and the E7-induced thyroid phenotype is dominant with respect to the RET/PTC3 one.
We generated a mouse model lacking both collagen IX and COMP to study the potential complementary role of these proteins in skeletal development.
In order to explore this we have utilised an APOE 'humanised' mouse model lacking the mouse APOE gene with human APOEε3 or ε4 knocked in.
Similarly, long-term EE improves memory and reduces astrogliosis and brain degeneration in a mouse model lacking the presenilin genes [77].
Furthermore, a transgenic mouse model lacking white adipose tissue (male A-ZIP/F-1), exhibits reduced fertility independent of leptin and testosterone levels [59], suggesting a potential role for stored fatty acids in the production of viable sperms.
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