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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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Development of hybrid scaffolds with natural extracellular matrix deposited within synthetic polymeric fibers.

TL;DR: A novel hybrid extracellular matrix-synthetic scaffold biomaterial is fabricated by cell-mediated deposition of ECM within an electrospun fiber mat that promoted cell adhesion and spreading and stimulated new ECM assembly by stem cells and tumor cells.
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A cell-assembled, spatially aligned extracellular matrix to promote directed tissue development

TL;DR: A nanometer thick, micron scale-patterned interface on a polymeric material directs fibroblast proliferation into a highly aligned, confluent cell monolayer that is maintained throughout a decellularization process.
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Rapid intracellular assembly of tenascin hexabrachions suggests a novel cotranslational process.

TL;DR: Examination of the biosynthesis of tenascin and its assembly into hexabrachions using pulsechase labeling of U-138 MG human glioma cells provides evidence for a novel co-translational mechanism ofTenascin assembly which would be facilitated by its length and by the amino-terminal location of the assembly domain.
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Probing the conformation of the fibronectin III1-2 domain by fluorescence resonance energy transfer.

TL;DR: A conformation-dependent mechanism for the regulation of FN matrix assembly by III1–2 is proposed and mutations of key charged residues resulted in conformational changes that exposed binding sites for the N-terminal 70-kDa FN fragment.
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Stimulatory effects of advanced glycation endproducts (AGEs) on fibronectin matrix assembly.

TL;DR: Results indicate that cells respond to AGEs by increasing matrix assembly and that RAGE is involved in this response, which raises the possibility that the accumulation of ECM during the progression of fibrosis may be enhanced by cell interactions with A GEs on a glycated ECM.