CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gutmann, D. H.
Right arrow Articles by Snider, W. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gutmann, D. H.
Right arrow Articles by Snider, W. D.

Cell Growth & Differentiation, Vol 6, Issue 3 315-323, Copyright © 1995 by American Association of Cancer Research


ARTICLES

Expression of the neurofibromatosis 1 (NF1) isoforms in developing and adult rat tissues

DH Gutmann, RT Geist, DE Wright and WD Snider
Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

The neurofibromatosis 1 (NF1) gene encodes a large M(r) approximately 250,000 phosphoprotein, the expression of which in adult tissues is limited to neurons, Schwann cells, oligodendrocytes, adrenal medulla, and leukocytes. The presence of two alternatively spliced exons (23a and 48a) in the NF1 gene allow for the generation of four possible neurofibromin isoforms. Type 1 neurofibromin contains neither 23a or 48a exon sequences, while type 2 neurofibromin contains only the 23a exon insertion. Previous studies have demonstrated that types 1 and 2 neurofibromin might have different functional properties relative to microtubule association and GTPase-activating protein activity towards p21-ras. To determine the normal pattern of expression of these NF1 isoforms, the adult and developmental expression of types 1 and 2 NF1 was examined. Herein, we demonstrate that NF1 mRNA is expressed at varying levels in adult tissues and is developmentally regulated during embryogenesis. Neurons in the central nervous system express predominantly type 1 NF1. Using mouse neocortical cultures enriched for neurons or glial cells, type 1 NF1 predominance was demonstrated in neurons, while type 2 NF1 predominated in glial cells. In contrast to central nervous system neurons, neurons expressing the type 2 NF1 isoform were identified in the developing dorsal root ganglia and spinal cord by in situ hybridization using a type 2-specific oligonucleotide probe. The elucidation of the differential expression pattern of these two NF1 isoforms during development and in adult life provides the foundations for future studies aimed at determining the functions of these neurofibromin isoforms.


This article has been cited by other articles:


Home page
Mol. Cell. Biol.Home page
M. N. Hinman, A. Sharma, G. Luo, and H. Lou
Neurofibromatosis Type 1 Alternative Splicing Is a Key Regulator of Ras Signaling in Neurons
Mol. Cell. Biol., June 15, 2014; 34(12): 2188 - 2197.
[Abstract] [Full Text] [PDF]


Home page
J. Clin. Pathol.Home page
D. Marrero, R. Peralta, A. Valdivia, A. De la Mora, P. Romero, M. Parra, N. Mendoza, M. Mendoza, D. Rodriguez, E. Camacho, et al.
The neurofibromin 1 type I isoform predominance characterises female population affected by sporadic breast cancer: preliminary data
J. Clin. Pathol., May 1, 2012; 65(5): 419 - 423.
[Abstract] [Full Text] [PDF]


Home page
NeurologyHome page
P. Balestri, R. Vivarelli, S. Grosso, L. Santori, M. A. Farnetani, P. Galluzzi, G. P. Vatti, F. Calabrese, and G. Morgese
Malformations of cortical development in neurofibromatosis type 1
Neurology, December 23, 2003; 61(12): 1799 - 1801.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1995 by the American Association of Cancer Research.