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Using N-ethyl-N-nitrosourea mutagenesis in mice, we identified a mutant with increased resistance to viral infections because of the presence of hyperresponsive NK cells.

In mice, we identified an essential role for histone 3 lysine 9 (H3K9) dimethylation and the lysine dimethyltransferase G9a in cocaine-induced structural and behavioral plasticity.

Using chromatin interaction sequencing, massively parallel reporter assays (MPRA), and transgenic mice, we identified disease-linked, biallelic HAR mutations in active enhancers for CUX1, PTBP2, GPC4, CDKL5, and other genes implicated in neural function, ASD, or both.

Of 50 recordings (from 29 mice) we identified 9 ChAT+ neurons and 30 ChAT− neurons, leaving 11 neurons unclassified.

In a screening of 128 generation-3 (G3) mice, we identified a mouse mutant (p23-ST1) with enlarged brain ventricles that proved heritable (Supplementary Fig. S1).

In an application of the new model for genetic mapping of iQTL in mice, we identified five significant QTLs on chromosomes 1, 4, 9, and 15 for the overall survival time to hyperoxic acute lung injury (HALI).

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By combining data from a GWAS screening in >100,000 individuals of European ancestry, mediator lipidomics, and functional validation studies in mice, we identify the AA metabolome as an important regulator of cholesterol homeostasis.

Using the available experimental full-length cDNA data sets for human and mouse, we identified 78 lncRNAs that are either syntenically conserved between human and mouse, or that originate from the same protein-coding genes.

In a screen of potential guidance cues that are expressed at the midline along the rostral course of mDN axons and temporally coincide with their passage (at E12.5 E15.5 in the mouse), we identified Shh as a candidate.

In our studies of CPMV trafficking in mouse, we identified a 54 kD cell-surface CPMV binding protein that was expressed on cells with APC activity (MC57) as well as vascular endothelial cells.

In a retroviral insertion mutagenesis screen in the mouse, we identified GPR110 as an oncogene.

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