Neil E. Humphreys

This study shows that mice with a germ-line deletion of a Csf1r enhancer lack specific macrophages but maintain normal physiology and can be replenished by donor cells.

This study shows that LBR nucleoplasmic domains regulate X-chromosome solubility and nuclear organization during neural differentiation in mouse cells.

The paper engineers a compact Cas9 ortholog, enCme2, for efficient in vivo gene editing via single AAV delivery, showing high specificity and minimal off-target activity.

This study identifies TRIM66 as a key factor enforcing monogenic expression of olfactory receptors through epigenetic silencing of super-enhancers, impacting axonal projections and behavior.

The paper generates a Ym1 deficient mouse using CRISPR-Cas9 in CB6 embryos and validates the absence of Ym1 protein without affecting related chitinase genes.

This study shows that reducing OGT activity in mice causes embryonic lethality proportional to the reduction in O-GlcNAc modification, with milder reductions causing developmental delays and retrovirus activation.

This study investigates a kinase-dead Csf1r mutation in mice, showing it causes dominant-negative effects on CSF1R signaling and impacts macrophage development and brain microglia.

This paper develops a CSF1R-FRed transgenic mouse that specifically labels mononuclear phagocyte system cells, showing high expression in monocytes, macrophages, and dendritic cells while excluding other lineages.

The paper reports a CRISPR-Cas9-induced deletion and reinsertion event in the mouse Csf1r promoter, highlighting the need for copy number analysis to confirm genomic edits.

The paper re-evaluates the efficiency of a CRISPR-Cas9 method for generating conditional knockout alleles in mice, finding very low success rates and high rates of undesired alleles.