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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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A single cysteine, Cys-64, is essential for assembly of tenascin-C hexabrachions

TL;DR: The results show that trimers are an intermediate of tenascin-C assembly and that Cys-64 is essential for formation of hexabrachions, and that monomers were the major extracellular form.
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A simple nanoscale interface directs alignment of a confluent cell layer on oxide and polymer surfaces

TL;DR: In this method, a volatile zirconium alkoxide complex is first deposited at reduced pressure onto a surface pattern that is prepared by photolithography; the substrate is then heated to thermolyze the organic ligands to form surface-bound zIRconium oxide patterns.
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Mechanistic insights into the cellular effects of a novel FN1 variant associated with a spondylometaphyseal dysplasia.

TL;DR: Immunofluorescence and immunoblotting analyses show that mutant fibroblasts assemble significantly lower amounts of FN matrix than wild‐type cells, and mutant FN was preferentially retained within the endoplasmic reticulum.
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The cartilage-specific (V+C)- fibronectin isoform exists primarily in homodimeric and monomeric configurations.

TL;DR: The unique dimerization pattern of (V+C)(-) fibronectin is consistent with this isoform having specialized functional properties in situ that are important for either the structural organization and biomechanical properties of cartilage matrix or regulation of a chondrocytic phenotype.
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mig-38, a novel gene that regulates distal tip cell turning during gonadogenesis in C. elegans hermaphrodites

TL;DR: RNAi depletion of both mig-38 and ina-1 enhanced the loss of turning phenotype indicating a genetic interaction between these genes, and a model to explain the dual role of MIG-38 in motility and turning is proposed.