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Expression of the SM‐20 Gene Promotes Death in Nerve Growth Factor‐Dependent Sympathetic Neurons
Author(s) -
Lipscomb Elizabeth A.,
Sarmiere Patrick D.,
Crowder Robert J.,
Freeman Robert S.
Publication year - 1999
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 - 10.1046/j.1471-4159.1999.0730429.x
Subject(s) - nerve growth factor , programmed cell death , apoptosis , gene expression , biology , microbiology and biotechnology , ly294002 , endocrinology , immediate early gene , medicine , sympathetic nervous system , gene , kinase , phosphatidylinositol , receptor , biochemistry , blood pressure
Sympathetic neurons undergo apoptosis when deprived of nerve growth factor (NGF). Inhibitors of RNA or protein synthesis block this death, suggesting that gene expression is important for apoptosis in this system. We have identified SM‐20 as a new gene that increases in expression in sympathetic neurons after NGF withdrawal. Expression of SM‐20 also increases during neuronal death caused by cytosine arabinoside or the phosphatidylinositol 3‐kinase inhibitor LY294002. In addition, SM‐20 protein synthesis is elevated in NGF‐deprived neurons compared with neurons maintained with NGF. Importantly, expression of SM‐20 in sympathetic neurons causes cell death in the presence of NGF. These results suggest that SM‐20 may function to regulate cell death in neurons.