Yongho Bae

This study identifies Myo9b's role in regulating epithelial brush border microvilli through RhoA signaling and shows that a disease variant disrupts microvilli formation in human cells.

This study identifies maladaptive Piezo1 mechanotransduction as a driver of smooth muscle aging in the gut, showing it impairs contractility and contributes to gastrointestinal dysfunction.

This paper develops a biomimetic scaffold system to enhance rotator cuff enthesis regeneration by replicating native tissue properties and integrating with conventional suture anchors.

This study identifies survivin as a key oncogenic driver in renal cell carcinoma, showing its roles in cell cycle, migration, and mitochondrial function, and suggests it as a therapeutic target.

This study shows ATF6α regulates lung aging and remodeling in specific cell types, with distinct effects on epithelial mitochondrial function and pericyte fibrosis.

This study identifies ARHGAP18 as a RhoA effector that forms a complex with YAP to coordinate Hippo and Rho pathways in regulating actin cytoskeleton and epithelial polarity.

This paper develops a tunable vascular dECM platform to study stiffness-driven vascular remodeling and identifies YAP and survivin as regulators of VSMC mechanotransduction.

This study identifies survivin as a mechanosensitive regulator linking ECM stiffness to GBM growth and matrisome remodeling, suggesting it as a therapeutic target.

This study shows survivin enhances VSMC migration in stiff environments, suggesting it could be a therapeutic target for arterial stiffness-related diseases.

This study investigates how epigenetic mechanisms regulate meniscus cell migration under inflammation, revealing zonal differences and potential therapeutic targets.

This study shows that FAK and p130Cas modulate early transcription and metabolism in response to substrate stiffness using RNA sequencing in mouse cells.

The paper analyzes gene expression and protein networks in vascular injury models to show similarities with cardiovascular disease mechanisms.