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Gelsolin overexpression enhances neurite outgrowth in PC12 cells
Author(s) -
Furnish Elizabeth J.,
Zhou Wei,
Cunningham Casey C.,
Kas Josef A.,
Schmidt Christine E.
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)03078-2
Subject(s) - gelsolin , neurite , microbiology and biotechnology , nerve growth factor , motility , actin , cytoskeleton , actin cytoskeleton , chemistry , biology , cell , in vitro , biochemistry , receptor
The rational design of therapies for treating nerve injuries requires an understanding of the mechanisms underlying neurite extension. Neurite motility is driven by actin polymerization; however, the mechanisms are not clearly understood. One actin accessory protein, gelsolin, is involved with remodeling the cytoskeleton, although its role in cell motility is unclear. We report a two‐fold upregulation of gelsolin upon differentiation with nerve growth factor. Cells that were genetically modified to overexpress gelsolin have longer neurites and a greater neurite motility rate compared to controls. These data suggest that gelsolin plays an important role in neurite outgrowth.

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