|
|
|
|||||||
|
|||||||||
J. Biol. Chem., Vol. 275, Issue 27, 20255-20259, July 7, 2000
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From the Although transforming growth factor-
Overexpression of a Nuclear Protein, TIEG, Mimics Transforming
Growth Factor-
Action in Human Osteoblast Cells*
§,§,,,, and
Department of Biochemistry and Molecular
Biology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota
55905 and the ¶ Division of Endocrine, Reproductive, and
Developmental Toxicology, Chemical Industry Institute of
Toxicology, Research Triangle Park, North Carolina 27709
(TGF-)
is a growth factor with many known regulatory activities in many
different cell types, its intracellular signaling pathway is still not
fully understood. A TGF--inducible early gene (TIEG) was
discovered and shown by this laboratory to be a 3-zinc finger
transcription factor family member; its expression is rapidly induced
in cells treated with TGF-. To ascertain whether TIEG plays a major
role in the TGF- pathway, human osteosarcoma MG-63 cells were stably transfected either with an expression vector containing a TIEG cDNA
or with the vector alone. Clones that contain only the vector express
normal levels of TIEG mRNA and protein and display the same
patterns of gene expression and levels of cell proliferation as the
nontransfected, non-TGF--treated parental cells. However, transfected cells that overexpress TIEG mRNA and protein
(TIEG-6 and TIEG-7) display changes that mimic those of MG-63
cells treated with TGF-, i.e. increased alkaline
phosphatase activity, decreased levels of osteocalcin mRNA and
protein, and decreased cell proliferation. The degree of these changes
correlated with the level of TIEG expressed in the cell lines. TGF-
treatment of the overexpressed cells showed no added effects. These
findings and other published reports support a primary role of TIEG as
a transcription factor in the TGF- signaling pathway.
*
This work was supported by National Institutes of Health
(NIH) Grant AR43627, the Howard Wagner Cancer research Fund, the Mayo
Foundation, and NIH Training Grant Awards HD07108 (to G. G. R.) and
CA09441 (to K. M. W.).The costs of publication of this article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of
Biochemistry and Molecular Biology, 1601A Guggenheim Bldg., Mayo
Clinic, 200 First Street S.W., Rochester, MN 55905. Tel.: 507-284-2480; Fax: 507-284-2053; E-mail: spelsberg.thomas@mayo.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  J. R. Hawse, M. Subramaniam, D. G. Monroe, A. H. Hemmingsen, J. N. Ingle, S. Khosla, M. J. Oursler, and T. C. Spelsberg Estrogen Receptor {beta} Isoform-Specific Induction of Transforming Growth Factor {beta}-Inducible Early Gene-1 in Human Osteoblast Cells: An Essential Role for the Activation Function 1 Domain Mol. Endocrinol., July 1, 2008; 22(7): 1579 - 1595. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Alvarez-Rodriguez, M. Barzi, J. Berenguer, and S. Pons Bone Morphogenetic Protein 2 Opposes Shh-mediated Proliferation in Cerebellar Granule Cells through a TIEG-1-based Regulation of Nmyc J. Biol. Chem., December 21, 2007; 282(51): 37170 - 37180. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Hwa, R. C. Fry, A. Sivaraman, P. T. So, L. D. Samson, D. B. Stolz, and L. G. Griffith Rat liver sinusoidal endothelial cells survive without exogenous VEGF in 3D perfused co-cultures with hepatocytes FASEB J, August 1, 2007; 21(10): 2564 - 2579. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Subramaniam, G. Gorny, S. A. Johnsen, D. G. Monroe, G. L. Evans, D. G. Fraser, D. J. Rickard, K. Rasmussen, J. M. A. van Deursen, R. T. Turner, et al. TIEG1 Null Mouse-Derived Osteoblasts Are Defective in Mineralization and in Support of Osteoclast Differentiation In Vitro Mol. Cell. Biol., February 1, 2005; 25(3): 1191 - 1199. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Ganss and A. Jheon ZINC FINGER TRANSCRIPTION FACTORS IN SKELETAL DEVELOPMENT Critical Reviews in Oral Biology & Medicine, September 1, 2004; 15(5): 282 - 297. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. D. Noti, A. K. Johnson, and J. D. Dillon The Zinc Finger Transcription Factor Transforming Growth Factor {beta}-Inducible Early Gene-1 Confers Myeloid-specific Activation of the Leukocyte Integrin CD11d Promoter J. Biol. Chem., June 25, 2004; 279(26): 26948 - 26958. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Dyrskjot, M. Kruhoffer, T. Thykjaer, N. Marcussen, J. L. Jensen, K. Moller, and T. F. Orntoft Gene Expression in the Urinary Bladder: A Common Carcinoma in Situ Gene Expression Signature Exists Disregarding Histopathological Classification Cancer Res., June 1, 2004; 64(11): 4040 - 4048. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. C. Fleet, L. Wang, O. Vitek, B. A. Craig, and H. J. Edenberg Gene expression profiling of Caco-2 BBe cells suggests a role for specific signaling pathways during intestinal differentiation Physiol Genomics, March 18, 2003; 13(1): 57 - 68. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Johnsen, M. Subramaniam, D. G. Monroe, R. Janknecht, and T. C. Spelsberg Modulation of Transforming Growth Factor beta (TGFbeta )/Smad Transcriptional Responses through Targeted Degradation of TGFbeta -inducible Early Gene-1 by Human Seven in Absentia Homologue J. Biol. Chem., August 16, 2002; 277(34): 30754 - 30759. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |