JBC Advanced Glycation Endproducts

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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 reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bhat, M. K.
Right arrow Articles by Cheng, S.-y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bhat, M. K.
Right arrow Articles by Cheng, S.-y.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Volume 272, Number 46, Issue of November 14, 1997 pp. 28989-28993
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Tumor Suppressor p53 Is a Negative Regulator in Thyroid Hormone Receptor Signaling Pathways

(Received for publication, April 30, 1997, and in revised form, August 8, 1997)

Manoj Kumar Bhat , Chia-lin Yu , Nida Yap , Qimin Zhan Dagger , Yoshitaka Hayashi § , Prem Seth and Sheue-yann Cheng

From the  Laboratory of Molecular Biology, Medicine Branch and the Dagger  Laboratory of Molecular Pharmacology, NCI, National Institutes of Health, Bethesda, Maryland 20892-4255 and the § Department of Endocrinology and Metabolism, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan

Thyroid hormone nuclear receptors (TRs) are ligand-dependent transcription factors which regulate growth, differentiation, and development. The molecular mechanisms by which TRs mediate these diverse effects are unclear. One emerging hypothesis suggests that TRs could mediate these diverse effects via cooperation with different transcription factors/receptors. Indeed, we have recently shown that the human TR subtype beta 1 (h-TRbeta 1) interacts with the tumor suppressor p53. p53 is a transcription factor that plays a critical role in cell cycle regulation and tumor development. To assess the physiological relevance of the interaction of h-TRbeta 1 with p53, the present study addressed the question as to whether the functions of h-TRbeta 1 could be modulated by p53. We first compared the h-TRbeta 1-mediated transcriptional activity in two pairs of isogenic cell lines, RKO/RKO E6 and MCF-7/MCF-7 E6. RKO and MCF-7 cells are colon and breast carcinoma cell lines, respectively, that contain p53 but lack TRbeta 1. The isogenic RKO E6 and MCF-7 E6 cells are stable clones expressing high levels of papillomavirus type 16 E6 protein. In these cells, the level of p53 protein was lower than the parental cells. The impairment of p53 functions in these E6-containing cells led to an activation of TRbeta 1-mediated transcriptional activity. Furthermore, in a growth hormone-producing cell line in which the expression of the growth hormone gene is positively regulated by TRs, overexpression of the wild-type p53 led to repression in the expression of the growth hormone gene. Thus, TRs could cross-talk with p53 in its signaling pathways to regulate gene regulatory functions. The present findings further strengthen the hypothesis that mediation of the pleiotropic effects of T3 requires the cooperation of TRs with a large network of transcription factors.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 EndocrinologyHome page
R.-N. Chen, Y.-H. Huang, Y.-C. Lin, C.-T. Yeh, Y. Liang, S.-L. Chen, and K.-H. Lin
Thyroid Hormone Promotes Cell Invasion through Activation of Furin Expression in Human Hepatoma Cell Lines
Endocrinology, August 1, 2008; 149(8): 3817 - 3831.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Endocrinol.Home page
E. Kress, A. Rezza, J. Nadjar, J. Samarut, and M. Plateroti
The Thyroid Hormone Receptor-{alpha} (TR{alpha}) Gene Encoding TR{alpha}1 Controls Deoxyribonucleic Acid Damage-Induced Tissue Repair
Mol. Endocrinol., January 1, 2008; 22(1): 47 - 55.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
P.-J. Tai, Y.-H. Huang, C.-H. Shih, R.-N. Chen, C.-D. Chen, W.-J. Chen, C.-S. Wang, and K.-H. Lin
Direct Regulation of Androgen Receptor-Associated Protein 70 by Thyroid Hormone and Its Receptors
Endocrinology, July 1, 2007; 148(7): 3485 - 3495.
[Abstract] [Full Text] [PDF]

Home page
 Arch Otolaryngol Head Neck SurgHome page
M. Nelson, A. Hercbergs, L. Rybicki, and M. Strome
Association between development of hypothyroidism and improved survival in patients with head and neck cancer.
Arch Otolaryngol Head Neck Surg, October 1, 2006; 132(10): 1041 - 1046.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
Y.-H. Huang, C.-Y. Lee, P.-J. Tai, C.-C. Yen, C.-Y. Liao, W.-J. Chen, C.-J. Liao, W.-L. Cheng, R.-N. Chen, S.-M. Wu, et al.
Indirect Regulation of Human Dehydroepiandrosterone Sulfotransferase Family 1A Member 2 by Thyroid Hormones
Endocrinology, May 1, 2006; 147(5): 2481 - 2489.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
J.-I Chao, S.-H. Hsu, and T.-C. Tsou
Depletion of Securin Increases Arsenite-Induced Chromosome Instability and Apoptosis via a p53-Independent Pathway
Toxicol. Sci., March 1, 2006; 90(1): 73 - 86.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pharmacol.Home page
J.-I Chao and H.-F. Liu
The Blockage of Survivin and Securin Expression Increases the Cytochalasin B-Induced Cell Death and Growth Inhibition in Human Cancer Cells
Mol. Pharmacol., January 1, 2006; 69(1): 154 - 164.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
M. Puzianowska-Kuznicka, A. Krystyniak, A. Madej, S.-Y. Cheng, and J. Nauman
Functionally Impaired TR Mutants Are Present in Thyroid Papillary Cancer
J. Clin. Endocrinol. Metab., March 1, 2002; 87(3): 1120 - 1128.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
Y. Kamiya, M. Puzianowska-Kuznicka, P. McPhie, J. Nauman, S.-y. Cheng, and A. Nauman
Expression of mutant thyroid hormone nuclear receptors is associated with human renal clear cell carcinoma
Carcinogenesis, January 1, 2002; 23(1): 25 - 33.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
M. J. Wagner, M. Gogela-Spehar, R. C. Skirrow, R. N. Johnston, K. Riabowol, and C. C. Helbing
Expression of Novel ING Variants Is Regulated by Thyroid Hormone in the Xenopus laevis Tadpole
J. Biol. Chem., December 7, 2001; 276(50): 47013 - 47020.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
G. Barrera-Hernandez, K. S. Park, A. Dace, Q. Zhan, and S.-y. Cheng
Thyroid Hormone-Induced Cell Proliferation in GC Cells Is Mediated by Changes in G1 Cyclin/Cyclin-Dependent Kinase Levels and Activity
Endocrinology, November 1, 1999; 140(11): 5267 - 5274.
[Abstract] [Full Text]

Home page
 J. Biol. Chem.Home page
T. A. Awad, J. Bigler, J. E. Ulmer, Y. J. Hu, J. M. Moore, M. Lutz, P. E. Neiman, S. J. Collins, R. Renkawitz, V. V. Lobanenkov, et al.
Negative Transcriptional Regulation Mediated by Thyroid Hormone Response Element 144 Requires Binding of the Multivalent Factor CTCF to a Novel Target DNA Sequence
J. Biol. Chem., September 17, 1999; 274(38): 27092 - 27098.
[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 
Copyright © 1997 by the American Society for Biochemistry and Molecular Biology.