Antony D. Adamson

This study uses reporter mice to visualise NLRP3 inflammasomes in vivo, revealing their localisation, organisation, and cellular sources.

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.

The paper shows that oscillatory co-expression of HES1 and HES5 allows hybrid states in a bistable transcription factor motif by enabling phase-locking and entrainment.

This study disrupts the nuclear localisation sequence of endogenous IL-1α in mice and examines its effects on inflammatory responses, finding no significant changes in LPS-induced transcriptional signatures or IL-1 release.

This study shows that GSK-3β regulates axonal microtubule organisation via Shot and Tau, and misregulation causes microtubule disorganisation linked to neurodegeneration.

This study uses hPSCs to model MED with MATN3 mutations, revealing altered matrix organisation and upregulated cholesterol biosynthesis pathway.

The paper identifies 508 CKD-associated genetic loci, prioritizes 651 kidney genes, and highlights novel CKD genes like CA12 with functional consequences.

The paper corrects a TYR variant associated with albinism in patient-derived iPSCs to create a model for studying pigmentation biology.

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 identifies gene regulatory networks driving periderm formation in early skin development using single-cell multiome and spatial transcriptomics data.

The paper investigates collagen fibril formation in fibroblasts, showing it occurs at the plasma membrane independently of secretion and involves endocytosis.

This study evaluates AAV9 transduction efficiency in Alport syndrome podocytes, finding enhanced transduction in Alport podocytes both ex vivo and in vivo.

This study examines how colonic inflammation affects the intestinal circadian clock and immune function, finding altered clock function and new oscillations in regulatory T cells.

This study identifies a selective vulnerability of cerebral vascular smooth muscle cells to NOTCH3 variants in small vessel disease and shows that PDE5 inhibition can rescue the dysfunction.

This study investigates how lysosome positioning affects NLRP3 inflammasome activation in HeLa and macrophage cells, finding that peripheral lysosome positioning enhances inflammasome activation.

The paper identifies biallelic RCC1 variants causing an acute axonal neuropathy triggered by infection, with mechanistic overlap with ALS and GBS.

This study identifies HAND1's concentration-dependent role in specifying cardiac and extraembryonic progenitors from human pluripotent stem cells.

The paper identifies ERRFI1 as a novel gene involved in psoriasis and psoriatic arthritis by showing its regulation by a non-coding risk variant at 1p36.23 through enhancer activity in keratinocytes.

The paper introduces DExCon, DExogron, and LUXon methods to control endogenous gene expression using CRISPR-Cas9, enabling on-demand activation and analysis of Rab11 family members.

The paper quantifies circadian interactions and protein abundance to reveal mechanisms maintaining the circadian clock's operational stability.

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.

The paper identifies spatially periodic HES5 microclusters in the mouse spinal cord during neurogenesis, showing their dynamic regulation by Notch signaling and their role in progenitor differentiation.

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.

This study uses Capture Hi-C and CRISPR activation to identify KLF4 as a target gene in the 9q31 psoriasis risk locus, linking GWAS variants to functional interactions.

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.

The paper uses CRISPR-Cas9 to tag collagen-I with Dendra2 for live imaging, showing cells synthesize, migrate on, and interact with collagen fibrils.