HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cifuentes, M. E. Articles by Hod, Y. Search for Related Content PubMed PubMed Citation Articles by Cifuentes, M. E. Articles by Hod, Y. Social Bookmarking                      What's this?

J. Biol. Chem., Vol. 266, Issue 3, 1557-1563, 01, 1991

Hormonal control of 6-phosphofructo-2-kinase/fructose-2,6- bisphosphatase gene expression in rat hepatoma cells

ME Cifuentes, C Espinet, AJ Lange, SJ Pilkis and Y Hod
Department of Physiology and Biophysics, State University of New York, Stony Brook 11794-8661.

The hormonal control of 6-phosphofructo-2-kinase/fructose-2,6- bisphosphatase gene expression was studied in the rat hepatoma cells, FTO-2B. In contrast to another hepatoma cell line (HTC), the enzyme in FTO-2B cells displays both kinase and bisphosphatase activities. As in rat liver, the mRNA in FTO-2B cells is 2.2-kilobases in length. However, the 5' region of the mRNA differs from the mRNA in the liver in that it contains sequences unique to 6-phosphofructo-2- kinase/fructose-2,6-bisphosphatase mRNA from skeletal muscle. These results suggest that the mRNA in FTO-2B cells may represent an additional alternative splicing product of the 6-phosphofructo-2- kinase/fructose-2,6-bisphosphatase gene. Exposure of FTO-2B cells to media containing either insulin (10(-7) M) or dexamethasone (10(-6) M) induced about a 10-fold increase in the level of 6-phosphofructo-2- kinase/fructose-2,6-bisphosphatase mRNA within 6-10 h of hormone treatment. The concentrations of insulin or dexamethasone giving half- maximal stimulation were 10(-9) M and 2 x 10(-8) M, respectively, and dibutyryl cyclic AMP (5 x 10(-7) M) completely prevented the increase in enzyme mRNA induced by these hormones. Exposure of cells to glucose- free medium abolished the insulin-mediated enhancement in 6- phosphofructo-2-kinase/fructose-2,6-bisphosphatase mRNA, but not that induced by dexamethasone. No alteration in the degradation rate of 6- phosphofructo-2-kinase/fructose-2,6-bisphosphatase mRNA was noted when cells were treated with insulin. Run-on transcription assays with isolated nuclei showed an increase in the relative transcription rate of the gene in cells treated with either insulin or dexamethasone. The time course of transcription activation preceded the increase in the level of the mRNA, indicating that the main mechanism for the induction of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase expression by insulin and dexamethasone is mediated by stimulation of gene transcription.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				D. J. Klemm, W. J. Roesler, T. Boras, L. A. Colton, K. Felder, and J. E-B. Reusch Insulin Stimulates cAMP-response Element Binding Protein Activity in HepG2 and 3T3-L1 Cell Lines J. Biol. Chem., January 9, 1998; 273(2): 917 - 923. [Abstract] [Full Text] [PDF]

				D. Mitanchez, B. Doiron, R. Chen, and A. Kahn Glucose-Stimulated Genes and Prospects of Gene Therapy for Type I Diabetes Endocr. Rev., August 1, 1997; 18(4): 520 - 540. [Abstract] [Full Text] [PDF]