| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
ARTICLES |
Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center; and Departments of Medicine (W.B., M.A.T., P.J.G., B.A.R.) and Neurology (B.A.R.), University of Miami School of Medicine, Miami, Florida 33125
Address all correspondence and requests for reprints to: Wayne Balkan, Geriatric Research, Education, and Clinical Center (11 GRC), Miami Veterans Affairs Medical Center, 1201 Northwest 16th Street, Miami, Florida 33125. E-mail: wbalkan{at}mednet.med.miami.edu
TRH, an amidated tripeptide secreted by certain hypothalamic neurons, is a principal regulator of TSH secretion and thyroid hormone release. TRH is also produced by other neurons in the central nervous system, where it appears to function as a neuromodulator or neurotransmitter, and by certain endocrine cells, where it may act as an autocrine or paracrine factor. The genomic organization of the rat TRH (rTRH) gene is well understood; however, the domains of the rTRH gene that regulate expression are less well characterized. We observed that the region between -47 and +6 of the rTRH gene (relative to the transcription start site at +1) was active in CA-77 cells, a medullary thyroid carcinoma cell line model of TRH production, but was not active in transgenic mice. Inclusion of most of exon 1 (84 out of 103 bp; -47 to +84) increased promoter activity in CA-77 cells and was active in transgenic mice, principally in tissues that normally express the TRH gene. Further lengthening of the 5' end to -243, -547, or -776 retained this expression in TRH-producing tissues in transgenic mice, while further increasing activity in CA-77 cells. These results suggest that cis element(s) located within exon 1 are necessary for the expression of the rTRH gene in vivo.
This article has been cited by other articles:
 |
|
 |
|
  A Cote-Velez, L Perez-Martinez, M Y Diaz-Gallardo, C Perez-Monter, A Carreon-Rodriguez, J-L Charli, and P Joseph-Bravo Dexamethasone represses cAMP rapid upregulation of TRH gene transcription: identification of a composite glucocorticoid response element and a cAMP response element in TRH promoter J. Mol. Endocrinol., February 1, 2005; 34(1): 177 - 197. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. J Teede, F. S Dalais, and B. P McGrath Dietary soy containing phytoestrogens does not have detectable estrogenic effects on hepatic protein synthesis in postmenopausal women Am. J. Clinical Nutrition, March 1, 2004; 79(3): 396 - 401. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Guissouma, S. M. Dupre, N. Becker, E. Jeannin, I. Seugnet, B. Desvergne, and B. A. Demeneix Feedback on Hypothalamic TRH Transcription Is Dependent on Thyroid Hormone Receptor N Terminus Mol. Endocrinol., July 1, 2002; 16(7): 1652 - 1666. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Becker, I. Seugnet, H. Guissouma, S. M. Dupre, and B. A. Demeneix Nuclear Corepressor and Silencing Mediator of Retinoic and Thyroid Hormone Receptors Corepressor Expression Is Incompatible with T3-Dependent TRH Regulation Endocrinology, December 1, 2001; 142(12): 5321 - 5331. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. A. Nillni and K. A. Sevarino The Biology of pro-Thyrotropin-Releasing Hormone-Derived Peptides Endocr. Rev., October 1, 1999; 20(5): 599 - 648. [Abstract] [Full Text]
|
|
|
|
 |
|
 H. Guissouma, M. T. Ghorbel, I. Seugnet, T. Ouatas, and B. A. Demeneix Physiological regulation of hypothalamic TRH transcription in vivo is T3 receptor isoform specific FASEB J, December 1, 1998; 12(15): 1755 - 1764. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
