Anthony R Isles

The paper shows reduced PWS gene expression in mouse placenta leads to a 25% loss of fetal endothelial cells critical for nutrient transfer.

This study shows that combining dCas9 and Cas9 improves viability and reduces off-target effects when editing genes linked to viability or paralogous clusters.

The paper introduces PCAN, a resource integrating high-throughput phenotyping of mouse models for Prader-Willi syndrome to evaluate phenotypes and therapeutic strategies.

This study investigates the effects of Setd1a haploinsufficiency in mice, finding sex-dependent behavioral changes relevant to schizophrenia and suggesting limitations in antipsychotic efficacy.

The paper analyzes scRNA-seq data from multiple mouse tissues to show imprinted genes are enriched in stem and endocrine cell types.

The paper identifies Magel2 as an imprinted gene critical for parenting behavior by linking its expression in galanin neurons to behavioral deficits in null mice.

The paper systematically investigates imprinted gene expression in the mouse brain at single-cell resolution, finding over-representation in neurons and specific brain regions.

The paper compares gene expression in two mouse models of Prader-Willi Syndrome to identify molecular differences associated with psychotic illness versus schizophrenia.

The paper shows that reduced EHMT1 activity decreases NRSF/REST protein, leading to abnormal neuronal gene expression and neurodevelopmental issues in human iPSCs.

This study shows that mice lacking paternal expression of Grb10 exhibit increased risk-taking behavior in specific tasks, supporting the idea that imprinted genes influence risk tolerance oppositely based on parental origin.

This study examines information processing deficits in a mouse model of Ehmt1 haploinsufficiency, showing abnormalities in sensory-motor gating and electrophysiological responses.

The paper shows that mice lacking paternal Grb10 make fewer impulsive choices, suggesting imprinted genes influence impulsive behavior and may contribute to pathological conditions.