Area of research
Cell Biology · Molecular Biology
Research interest
Research interests include Protein Kinase Regulation and GTPase Signaling, Cellular Mechanics and Interactions, Cellular transport and secretion, and Cell Adhesion Molecules Research.
Protocol for quantifying the horizontal and vertical distribution of junctional proteins in fixed epithelial cells.
Critical-Size Muscle Defect Regeneration Using an Injectable Cell-Laden Nanofibrous Matrix: An Ex Vivo Mouse Hindlimb Organ Culture Study.
Immunomodulation Through Fibroblast-Derived Extracellular Vesicles (EVs) Within 3D Polycaprolactone-Collagen Matrix.
Quantification of horizontal and vertical distribution of junctional proteins in fixed epithelial cells
The Scribble-SGEF-Dlg1 complex regulates E-cadherin and ZO-1 stability, turnover and transcription in epithelial cells.
The Scribble/SGEF/Dlg1 complex regulates the stability of apical junctions in epithelial cells
ARHGAP17 regulates the spatiotemporal activity of Cdc42 at invadopodia.
Cell-based optimization and characterization of genetically encoded location-based biosensors for Cdc42 or Rac activity.
Quantification of ruffle area and dynamics in live or fixed lung adenocarcinoma cells.
Cell-based optimisation and characterisation of genetically encoded, location-based biosensors for Cdc42 or Rac activity
ARHGAP17 regulates the spatiotemporal activity of Cdc42 at invadopodia
FARP1, ARHGEF39, and TIAM2 are essential receptor tyrosine kinase effectors for Rac1-dependent cell motility in human lung adenocarcinoma.
ARHGEF26 enhances Salmonella invasion and inflammation in cells and mice.
Syndecan-4/PAR-3 signaling regulates focal adhesion dynamics in mesenchymal cells
P-REX1-Independent, Calcium-Dependent RAC1 Hyperactivation in Prostate Cancer.
SGEF forms a complex with Scribble and Dlg1 and regulates epithelial junctions and contractility.
Regulation of circular dorsal ruffles, macropinocytosis, and cell migration by RhoG and its exchange factor, Trio
Isolated nuclei adapt to force and reveal a mechanotransduction pathway in the nucleus
VAV3 mediates resistance to breast cancer endocrine therapy