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Related Experiment Video

Updated: Jan 24, 2026

Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells

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Published on: July 30, 2020

Time-Variant SRC Kinase Activation Determines Endothelial Permeability Response.

Jennifer E Klomp¹, Mark Shaaya¹, Jacob Matsche¹

¹Department of Pharmacology, The University of Illinois College of Medicine, 835 S. Wolcott Avenue, Chicago, IL 60612, USA.

Cell Chemical Biology

|May 28, 2019

Summary

SRC kinase activation has dual effects on endothelial barriers. Immediate SRC activation enhances barrier function by stabilizing adherens junctions, while prolonged activation increases permeability through VE-cadherin phosphorylation.

Keywords:

Kinase LYN SRC VE cadherin adherens junctions cell migration endothelial barrier function endothelial cells inducible kinase reticular junctions

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Published on: June 7, 2022

Area of Science:

Cell biology
Biochemistry
Vascular biology

Background:

The tyrosine kinase SRC is traditionally thought to increase endothelial permeability by promoting adherens junction disassembly.
Endothelial barrier integrity is crucial for regulating transport and preventing inflammation.

Purpose of the Study:

To investigate the time-dependent effects of SRC kinase activation on endothelial barrier function.
To elucidate the specific mechanisms by which SRC influences endothelial adherens junctions and permeability.

Main Methods:

Utilized a chemical biology approach for temporal control of SRC activation.
Analyzed VE-cadherin phosphorylation at specific tyrosine residues (Y731 and Y685).
Observed changes in adherens junction morphology and endothelial barrier permeability.

Main Results:

Transient SRC activation led to enhanced endothelial barrier function.
Enhanced barrier function correlated with VE-cadherin accumulation at adherens junctions and formation of reticular adherens junctions.
SRC-mediated barrier enhancement required VE-cadherin phosphorylation at Y731.
Prolonged SRC activation resulted in VE-cadherin phosphorylation at Y685, increasing endothelial permeability.

Conclusions:

SRC kinase exerts time-variant effects on endothelial barrier function.
Differential phosphorylation of VE-cadherin at Y731 and Y685 by SRC dictates barrier enhancement or disruption.
Temporal control of SRC signaling is critical for fine-tuning endothelial barrier function.