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Acute Neurite Retraction Elicited by Diverse Agents Is Prevented by Genistein, a Tyrosine Kinase Inhibitor
Author(s) -
Smalheiser Neil R.
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb03573.x
Subject(s) - genistein , neurite , lysophosphatidic acid , tyrosine kinase , protein kinase c , microbiology and biotechnology , biology , piceatannol , extracellular , phorbol , tyrosine kinase inhibitor , neuroscience , chemistry , in vitro , pharmacology , signal transduction , endocrinology , biochemistry , receptor , genetics , cancer , resveratrol
The retraction of axonal branches is a prominent feature of nervous system development and function. Although various biological and pathological signals can elicit retraction, little is known regarding their underlying mode of action. An in vitro assay using NG108–15 cells was used to demonstrate that rapid‐onset neurites exposed acutely to trypsin, serum, lysophosphatidic acid, extracellular ATP, the phorbol ester phorbol 12‐myristate 13‐acetate, and nocodazole were all protected from retraction by the tyrosine kinase inhibitor genistein. This finding indicates that a common (genistein‐sensitive) cellular event is involved in integrating the influence of multiple extrinsic and intrinsic signals and in regulating whether or not neurites will execute a retraction response.