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Jean E. Schwarzbauer

Researcher at Princeton University

Publications -  154
Citations -  12375

Jean E. Schwarzbauer is an academic researcher from Princeton University. The author has contributed to research in topics: Fibronectin & Extracellular matrix. The author has an hindex of 58, co-authored 149 publications receiving 11529 citations. Previous affiliations of Jean E. Schwarzbauer include Massachusetts Institute of Technology & University of Washington.

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Fibronectin fibril alignment is established upon initiation of extracellular matrix assembly

TL;DR: In this paper, the authors investigated the initiation of fibronectin (FN) matrix assembly using fibroblasts that assemble parallel ECM fibrils and found that matrix assembly sites, where FN fibrillogenesis is initiated, were oriented in parallel at the cell poles.
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Transcriptionally regulated cell adhesion network dictates distal tip cell directionality.

TL;DR: It is suggested that directional changes in cell migration rely on the precise gene regulation of adhesion, by means of cbp‐1 and let‐607, which coordinate a gene network that is necessary for integrin‐mediated adhesion.
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Nanomaterials can Dynamically Steer Cell Responses to Biological Ligands

TL;DR: A monotonic relationship is found between the nanocarrier cytointernalization rate and the cell migration rate, suggesting the possibility of designing biointerfacial features for the dynamic control of cell migration.
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New mechanism of fibronectin fibril assembly revealed by live imaging and super-resolution microscopy

TL;DR: Fn1 fibrils have long been viewed as continuous fibers composed of extended, periodically aligned Fn1 molecules, however, live imaging and single-molecule localization microscopy (SMLM) are inconsistent with this traditional view and show that Fn1fibrils are composed of roughly spherical nanodomains containing 6-11 Fn1 dimers.
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Functional characterization of KIN-32, the Caenorhabditis elegans homolog of focal adhesion kinase.

TL;DR: The results show that reduced levels of expression or absence of the FERM domain do not affect viability, fertility, or anatomy in C. elegans, and possibly KIN‐32 activity in general, appears to be dispensable for normal C. Edwards physiology.