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In an inducible, conditional mouse line lacking NMDARs in DA neurons, the insertion of GluA2-lacking AMPARs and conditioned place preference were dissociated.
Recently, another mouse line lacking Kidins220 was described, where heterozygous mice displayed a 30 40% reduction in the protein levels of Kidins220.
Recently, a new mutant mouse line lacking the orphan G protein-coupled receptor GPR-88 was reported to recapitulate hyperactivity-related ADHD-like symptoms (Quintana et al, 2012), further offering novel molecular mechanisms and molecular targets for ADHD research.
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Recently, we reported on the characterization of mouse lines lacking UPF2 in various hematopoietic compartments [13].
We used a gene-targeting approach to generate mouse lines lacking either Tph1 or Tph2, and then crossbred the two lines to produce animals lacking both genes.
Yet, studies of mouse lines lacking Dp427 or all dystrophins only showed mild cognitive impairments and failed to unveil the specific contribution of Dp71 to neuronal function and to the genesis of MR [12] [14].
Several mouse lines lacking LAR-RPTP-binding postsynaptic organizers have been reported.
As selective death of specific neuronal subpopulations were reported in mouse lines lacking NT or their receptors, we asked whether the lack of Kidins220 specifically affected one or more of these populations.
To investigate whether mitochondrial morphology and functions were specifically dependent on the expression of these isoforms, we analyzed muscle cryosections and tissue lysates derived from isoform-specific knockout mouse lines, lacking either P1b (P1b-KO) (10) or P1d P1d-KOO) (14), while expressing the other isoforms of plectin.
The first line of evidence came from our study of another mutant mouse line specifically lacking the GluR1-S831 site (GluR1-S831A mutant).
This mouse embryonic fibroblast cell line lacking expression of Src, Yes, and Fyn has been used in previous studies to explore the role of Src in ouabain-induced stimulation of the EGFR/Src Ras ERK pathway.
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