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. 2018 Aug 9;8:11935. doi: 10.1038/s41598-018-29817-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Mechanism driving differential biomechanics. (A) Schematic depicting formation of PGCCs and underlying cytoskeletal features that drive their stiffness. Upregulated actin stress bundles increase overall cell stiffness in PGCCs. RhoA-ROCK1 and actin network disruption leads to significant loss of cell stiffness. However, nuclear mechanics are less responsive to RhoA-ROCK1 inhibition but stiffness is fully restored to non-PGCC levels after actin disruption. (B) Summary table of inhibitor studies of PGCCs normalized to non-PGCCs, highlighting increased cytoplasmic sensitivity to inhibitors and nuclear sensitivity to actin disruption.