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- W4313366106 abstract "Abstract Recruitment of neutrophils in appropriate numbers at vascular sites of inflammation is critical for innate immune surveillance. LFA-1 adhesive bonds that support neutrophil deceleration and arrest under fluid shear, also function to mechanotransduce signals that spatially localize calcium flux necessary to guide transendothelial migration. We set out to characterize how bond tension acting on high-affinity LFA-1/ICAM-1 bonds transduce intracellular signaling in a manner proportional to the shear force acting on adherent cells. A sequential set of events beginning with a shift to high affinity of LFA-1 that binds ICAM-1, a buildup of tension, and assembly of adaptor proteins that terminate in spatial linkage to the CRAC channel Orai-1. Utilizing microfluidic vascular mimetic flow chamber, we observed that force catalyzed integrin clustering and calcium flux in a Kindlin-3 dependent manner. Kindlin-3 has a dual role as a mechanical anchor that links to adaptors that assemble Orai-1 mediated calcium influx and as a support for LFA-1 membrane clustering. RACK1 deficient neutrophils retained the capacity for integrin clustering but lacked calcium signaling. Utilizing a molecular platform that regulates the force acting on LFA-1 bonds we determined the characteristic bond tension necessary to transduce signaling. Forces between 33 and 54 pN were sufficient to support LFA-1 binding to Kindlin-3 and promote integrin clustering. As this characteristic force completed a macromolecular complex constituted of RACK1/Orai1 signaling complex competent to transduce calcium influx. We identify a molecular circuit catalyzed by a well-defined force that may represent the necessity to assemble Kindlin-3 to intracellular LFA-1 domains." @default.
- W4313366106 created "2023-01-06" @default.
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- W4313366106 date "2019-05-01" @default.
- W4313366106 modified "2023-09-26" @default.
- W4313366106 title "Bond tension on neutrophil LFA-1 regulates membrane calcium flux from the outside-in" @default.
- W4313366106 doi "https://doi.org/10.4049/jimmunol.202.supp.64.13" @default.
- W4313366106 hasPublicationYear "2019" @default.
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