Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-3-25
pubmed:abstractText
Neuronatin was recently cloned from neonatal rat brain (Biochem, Biophys. Res. Commun., 201 (1994) 1227-1234). In subsequent studies, we noted neuronatin mRNA was brain-specific and that there were two alternatively spliced forms, alpha and beta (Brain Res., 690 (1995) 92-98). Furthermore, on sequencing the human neuronatin gene, it was determined that the alpha-form was encoded by three exons, and the beta-form was encoded by the first and third exons only (Genomics, 33 (1996) 292-297). The middle exon was spliced out in the beta-form. The human neuronatin gene is located in single copy of chromosome 20q 11.2-12 (Brain Res., 723 (1996) 8-22). These studies called for an understanding of the function of this gene. Therefore, we studied the expression of neuronatin in PC12 cells, an established model of neuronal growth and differentiation. Neuronatin mRNA expression was found to be abundant in undifferentiated PC12 cells. Treatment with nerve growth factor (NGF), resulting in neuronal differentiation, was associated with a downregulation of neuronatin mRNA expression. Removal of NGF was associated with a return of neuronatin mRNA levels towards baseline. These effects appear to be specific for NGF as they were not seen with transforming growth factor, epidermal growth factor, 12-O-tetradecanoylphorbol-13-acetate or dexamethasone. Although, basic fibroblast growth factor also reduced neuronatin mRNA levels, the effect was less pronounced than with NGF. The NGF-induced decreased in neuronatin mRNA occurred even in the presence of protein and RNA syntheses inhibitors. Of the two spliced forms, only the alpha-form was expressed in PC12 cells. In conclusion, we report the presence of neuronatin mRNA in PC12 cells, and that NGF downregulates its expressions. These findings provide a basis for investigating the role of neuronatin in neuronal growth and differentiation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Cycloheximide, http://linkedlifedata.com/resource/pubmed/chemical/Dactinomycin, http://linkedlifedata.com/resource/pubmed/chemical/Fibroblast Growth Factor 2, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins, http://linkedlifedata.com/resource/pubmed/chemical/NNAT protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Nerve Growth Factors, http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Nnat protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Nucleic Acid Synthesis Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Protein Synthesis Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
738
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
32-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Neuronatin mRNA in PC12 cells: downregulation by nerve growth factor.
pubmed:affiliation
Department of Neurology/K-11, Henry Ford Health Sciences Center, Detroit, MI 48202, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't