Boon Chuan Low

This study identifies a mechanism where invading cells and tissue barriers coordinate to rupture barriers through intercellular adhesions and subcellular contractility, challenging existing models of collective invasion.

This study identifies fibrillar adhesions as the primary integrin complexes that respond to matrix topography, forming independently of focal adhesions.

This study shows that HIF-1α activation defines the SASP across different stressors, independent of micronuclei-induced cGAS/Sting activation.

This study identifies ZO-2 as a scaffolding protein that regulates Hippo signaling by facilitating LATS1-mediated phosphorylation and inactivation of YAP.

This study identifies BNIP-2 as a key organizer of focal adhesion nanostructure that enhances signaling and traction force, essential for cardiomyocyte differentiation.

The paper identifies ZO-2 as a scaffold that promotes LATS1-YAP complex formation at tight junctions, leading to YAP phosphorylation and cytoplasmic retention in response to cell density.

This study identifies actomyosin contractility as a mechanism driving bile regurgitation in obstructive cholestasis by forming vesicles that relieve biliary pressure.