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. 2022 Oct 21;11(20):3317. doi: 10.3390/cells11203317

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Small GTPase/cytoskeletal regulation of thrombin-induced NF-κB activation. Thrombin activation of PAR-1 stimulates RhoA/Rho-associated kinase (ROCK) signaling, nonmuscle myosin light-chain kinase (nmMLCK) activity, and autophagic flux. RhoA/ROCK activates LIM kinase 1 (LIMK1), which acts to phosphorylate IKKβ, causing release of RelA/p65 from IκBα. In parallel, LIMK1 causes phosphorylation and inactivation of cofilin-1 to induce actin cytoskeleton reorganization. Thrombin also activates nmMLCK, which acts in concert with LIMK1/cofilin-1 to promote actin–myosin interaction. Generation of actin–myosin stress fibers by this mechanism facilitates the nuclear translocation of released RelA/p65. Induction of autophagy via Beclin-1 and ATG7 also contributes to cofilin-1 phosphorylation and stress fiber formation. Cofilin-1 phosphorylation is tightly regulated by engagement of slingshot-1Long (SSH-1L), a cofilin-1 phosphatase.