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Although molecular genetic alterations have been characterized in human astrocytomas, many of the mice engineered with these mutations do not develop astrocytomas.
USH1C (Usher) mice, engineered with a human USH1C mutation, exhibit these multi-sensory deficits by circling behavior and lack of response to sound.
To assess telomerase as a cancer therapeutic target and determine adaptive mechanisms to telomerase inhibition, we modeled telomerase reactivation and subsequent extinction in T cell lymphomas arising in Atm−/− mice engineered with an inducible telomerase reverse transcriptase allele.
Immunosignaturing, a technology that employs antibody binding to a random-sequence peptide microarray, generates profiles that distinguish transgenic mice engineered with familial AD mutations (APPswe/PSEN1-dE9) from non-transgenic littermates.
We demonstrate that these in vivo murine-matured autologous CD3+ T cells from humans (MATCH) can be collected from the mice, engineered with lentiviral vectors, reinfused into the mice, and detected in multiple lymphoid compartments at stable levels over 50 days after injection.
In contrast to mice engineered with constitutive deletions of GluR2 [16] our conditional knockout mice showed no motor, sensory or motivational changes and they exhibited normal acquisition of several hippocampus-independent learning tasks.
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Sections double stained for Fluoro-Jade and NF-κB activity (using a mouse engineered with a NF-κB responsive promoter driving a LacZ gene to produce beta galactosidase) demonstrated neuronal degeneration only in regions sparsely showing NF-κB activity, and those demonstrating NF-κB activity failed to degenerate.
These models and others (e.g., the TRAMP mouse engineered with an activatable SV40 T antigen [ 40]) of prostate carcinogenesis invariably involve oncogene activation.
But scientists have already worked with mice engineered to mimic 5-HTT variations in humans.
They set up an experiment to compare normal mice that produce the binding proteins with mice engineered to lack them.
In particular, we describe our findings with mice engineered to contain a point mutation, N265M, in the β3 subunit of the GABAA receptor.
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