| 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 |
Cell Growth & Differentiation, Vol 4, Issue 12 985-991, Copyright © 1993 by American Association of Cancer Research
ARTICLES |
LE Ostrowski, TE Gray, SH Randell and P Nettesheim
Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.
It has been previously reported (R. W. Steigerwalt et al., Mol. Carcinog., 5:32-40, 1992) that primary cultures of rat tracheal epithelial (RTE) cells and immortalized RTE cell lines produce three mRNA transcripts [2.5, 1.9, 1.4 kilobases (kb)] which hybridize to a murine transforming growth factor beta 1 (TGF-beta 1) complementary DNA probe. In this report, we show that the 1.9- and 1.4-kb transcripts are not detectable by Northern analysis of resting adult trachea but are induced in regenerating tracheal grafts and tumors formed from transformed RTE cells. Northern analysis of the TGF-beta 1 transcripts with subclones of the murine complementary DNA demonstrate that the 1.4-kb transcript lacks much of the 5' untranslated region (UTR). RNase protection analysis was used to map the transcriptional start site of the 1.4-kb transcript to within 30-40 base pairs of the first ATG codon. No differences in the coding or 3' UTR were detected between the 1.4-kb and the 2.5-kb transcripts. Although RTE cells produce a 1.9-kb TGF-beta 1 mRNA, we were unable to detect a previously reported unique 3' UTR, which we found to be almost identical to a rat mitochondrial ATPase sequence. Because the 1.4-kb transcript is missing most of the long GC-rich 5' UTR, it may be translated at a different rate than the 2.5- and 1.9-kb transcripts, or it may code for an intracellular form of TGF-beta 1. The 1.4-kb transcript has been observed under several conditions of injury or stress and, therefore, may be an important component of the TGF-beta 1 response to these conditions.
This article has been cited by other articles:
![]() |
D. Fraser, L. Wakefield, and A. Phillips Independent Regulation of Transforming Growth Factor-{beta}1 Transcription and Translation by Glucose and Platelet-Derived Growth Factor Am. J. Pathol., September 1, 2002; 161(3): 1039 - 1049. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Morrisey, R. A. Evans, L. Wakefield, and A. O. Phillips Translational Regulation of Renal Proximal Tubular Epithelial Cell Transforming Growth Factor-{beta}1 Generation by Insulin Am. J. Pathol., November 1, 2001; 159(5): 1905 - 1915. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. D. Potdar, K. L. Andrews, P. Nettesheim, and L. E. Ostrowski Expression and regulation of gamma -glutamyl transpeptidase-related enzyme in tracheal cells Am J Physiol Lung Cell Mol Physiol, November 1, 1997; 273(5): L1082 - L1089. [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 |