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Updated: Sep 14, 2026

Efficient Production and Purification of Recombinant Murine Kindlin-3 from Insect Cells for Biophysical Studies
Published on: March 19, 2014
Kindlin-3 is a Regulator of Force-Regulated Activation of Integrin α4β7 by CCL25 During Lymphocyte Adhesion
Paimin Zhuo1, Zhiqing Luo1, Xianwen Luo1
1School of Biology and Biological Engineering, South China University of Technology, Guangzhou, 510006 China.
Purpose:
Lymphocyte recruitment to inflamed intestines in inflammatory bowel disease (IBD) critically depends on shearstress-regulated integrin α4β7/MAdCAM-1 interactions. However, the mechano-chemical coupling between the chemokine CCL25 and the intracellular adaptor Kindlin-3 in activating α4β7 under physiological flow remains unclear.
Methods:
Utilizing parallel-plate flow chamber assays combined with fluorescence microscopy and molecular perturbation, wedemonstrate that CCL25 triggers robust integrin α4β7 activation and stable lymphocyte adhesion only under physiological shear stress, a process regulated by Kindlin-3.
Results:
Mechanistically, Kindlin-3 acts as a force transmission hub, enabling CCL25 signaling to enhance α4β7-mediatedadhesion strengthening. Knockdown of Kindlin-3 specifi cally enhanced the force-sensitized, CCL25-induced activationof α4β7.
Conclusions:
This study reveals, for the first time, that Kindlin-3 is crucial for translating chemokine (CCL25) signals intobiomechanical activation of integrin α4β7 under shear flow. Our findings establish Kindlin-3 as a critical mechano-regulator of chemokine-induced integrin activation during lymphocyte homing, providing novel mechanistic insightsinto IBD pathogenesis and highlighting this pathway as a promising target for anti-adhesion therapeutics.
Supplementary Information:
The online version contains supplementary material available at https://doi.org/10.1007/s12195-026-00935-9.
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