John Paul Kennelly

Endoplasmic Reticulum Associated Lipolysis Regulates Hepatic Fat Synthesis and Turnover

This study identifies AADAC as a regulator of hepatic lipid metabolism, showing its role in suppressing lipid synthesis and preventing MASLD under overnutrition.

Lipid- and protein-directed photosensitizer proximity labeling captures the cholesterol interactome

This paper introduces POCA, a photosensitizer-based proximity labeling method that captures both protein and lipid interactomes with high spatiotemporal resolution.

NK2R signaling governs intestinal lipid mobilization and mucosal inflammation

This study identifies NK2R as a key regulator of intestinal lipid metabolism and mucosal inflammation, showing bidirectional effects on lipid mobilization and immune responses.

T cell cholesterol transport is a metabolic checkpoint that links intestinal immune responses to dietary lipid absorption

This study identifies Aster-A as a cholesterol transporter in T cells that regulates immune signaling and metabolic responses by controlling membrane cholesterol levels.

Cholesterol Metabolism in a Murine Model of Vertical Sleeve Gastrectomy

This study shows that vertical sleeve gastrectomy in mice reduces plasma cholesterol without weight loss by enhancing bile acid synthesis and hepatobiliary elimination.

Dietary control of peripheral adipose storage capacity through membrane lipid remodelling

This study shows that PPARγ controls adipose tissue expansion by regulating LPCAT3, which affects membrane lipid composition and triglyceride storage, linking dietary n-6 PUFAs to energy balance.

Cholesterol binding to VCAM-1 promotes vascular inflammation

The paper identifies cholesterol binding to VCAM-1 as a mechanism promoting vascular inflammation by stabilizing VCAM-1 and enhancing immune cell recruitment.

Flow-Mediated Modulation of the Endothelial Cell Lipidome

This study examines how different blood flow patterns alter the lipidome of human aortic endothelial cells and identifies stimulus-specific lipid reprogramming in response to pro-inflammatory agonists.