Search

Your search keyword '"Hansjorg Keller"' showing total 4 results
Start Over Author "Hansjorg Keller"
4 results on '"Hansjorg Keller"'

1. Retinoid X Receptor β and Peroxisome Proliferator- Activated Receptor Activate an Estrogen Response Element

Author

Walter Wahli, Hansjorg Keller Ken Wang, Keiko Ozato, James H. Segars, Susan B. Nunez, and Jeffrey A. Medin

Subjects
Hormone response element, chemistry.chemical_classification, Reporter gene, Peroxisome proliferator-activated receptor, Estrogen receptor, Retinoid X receptor, Biology, Cell biology, body regions, Nuclear receptor, chemistry, Biochemistry, embryonic structures, lipids (amino acids, peptides, and proteins), Binding site, Receptor, hormones, hormone substitutes, and hormone antagonists
Abstract

Publisher Summary This chapter discusses a study suggesting that an estrogen-responsive DNA element (ERE) can be specifically activated by cotransfection of the retinoid X receptor (RXR) and peroxisome proliferator-activated receptors (PPAR) in the absence of the estrogen receptor (ER). The specific nucleotide sequence of the ERE differs from the canonical RXR and PPAR element in the orientation and number of nucleotide spaces between half-sites of the element. The cotransfection of RXR and PPAR caused an augmentation of ERE-dependent reporter activity in the presence or absence of either 9-cis-RA or arachidonic acid. Transfection of either RXR or PPAR alone resulted in activation less than that observed when both expression vectors were introduced. The capacity of a single coregulator (RXR) to promote a discriminatory function in DNA site targeting suggested that binding site specificity is conferred both by RXR and the respective nuclear receptor partner. The activation of the ERE-dependent reporter gene by PPAR depends on the RXR as deletion of the DBD of RXR reduces the observed reporter activity. The finding of the experiment explained in the chapter that PPAR and RXR activate an estrogen-responsive element suggests that the two receptors are involved in a mechanism to generate diversity and tissue-specific regulation of estrogen-responsive genes. The concept that receptors other than the ER control estrogen responsive genes is supported by the presence of natural EREs such as in the rat oxytocin promoter, where the ER, TR, RAR and a COUP-like factor have been suggested to control expression of the gene.

Published
1995

2. LIST OF CONTRIBUTORS

Author

Adriano Aguzzi, Tamara Alliston, Ali Arslan, Indrani C. Bagchi, Milan K. Bagchi, C. Wayne Bardin, Craig L. Best, Julie A. Blendy, Martha M. Bosma, Eugene P. Brandon, Robert E. Braun, D.D. Brown, Nail Burnashev, Jean S. Campbell, Nicholas A. Cataldo, Kevin J. Catt, Pierre Chambon, Anne Charru, J.H. Check, Mitchell I. Chemin, Khoi Chu, James H. Clark, Jeffrey W. Clemens, Timothy J. Cole, Orla M. Conneely, Pierre Corvol, Tamás Csikós, Mark Danielsen, Ying Qing Ding, Carl Djerassi, B. Eliceiri, Adria A. Elskus, Satish A. Eraly, Mark A. Fajardo, Susan L. Fitzpatrick, Victor Y. Fujimoto, J.D. Furlow, Dana Gaddy-Kurten, Ruth Ganss, Frederick W. George, Kirstin A. Gerhold, Paul A. Godfrey, Jonathan D. Graves, Lee M. Graves, L. Earl Gray, Joseph A. Hill, Bertil Hille, Lyann R. Hodgskin, Edith Hummler, David L. Hurley, Rejean L. Idzerda, Robert B. Jaffe, Amy M. Jensen, Xavier Jeunemaitre, A. Kanamori, William R. Kelce, Hansjorg Keller, Paul A. Kelly, John Kirkland, Georg Köhr, Yuri Kotelevtsev, Edwin G. Krebs, David J. Kulik, Thomas Kuner, Agnès Larcher, Mark A. Lawson, Keesook Lee, Diana Lefèbvre, Joanna M. Makris, Shaila Mani, Kelly E. Mayo, G. Stanley McKnight, Jeffrey A. Medin, Pamela L. Mellon, Emily Monosson, Lluis Montoliu, Hannah Monyer, Jaqueline K. Morris, Patricia L. Morris, Lata Murthy, Lynne V. Nazareth, Susan B. Nunez, Bert W. O'Malley, Yoshihiro Okuda, Keiko Ozato, Kathleen Creed Page, Carol J. Phelps, Ming Qi, Jason O. Rahal, Marilyn B. Renfree, Stéphane Richard, JoAnne S. Richards, Mario I. Romero, Elliott M. Ross, Florence Rozen, Radmila Runic, Peter N. Schlegel, Wolfgang Schmid, William T. Schrader, Jill M. Schumacher, Günter Schütz, Neena B. Schwartz, R. Schwartzman, Peter H. Seeburg, James Segars, Rony Seger, B.S. Shanis, Jean Sirois, Carolyn Smith, Florent Soubrier, Rolf Sprengel, George Stancel, Stanko S. Stojilkovic, Steven T. Suhr, Joyce Tay, Vilmos Thomazy, E. Brad Thompson, Philippe Touraine, Amy Tse, Frederick W. Tse, Kunihiro Tsuchida, Wylie Vale, Walter Wahli, Ken Wang, Z. Wang, Nancy L. Weigel, David B. Whyte, Jean D. Wilson, Patrick W. Wojtkiewicz, Shimin Zhang, and Hans H. Zingg

Published
1995

4. Peroxisome proliferator-activated receptors A link between endocrinology and nutrition?

Author

Keller H and Wahli W

Abstract

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily like the steroid, thyroid, or retinoid hormone receptors, which are ligand-activated transcription factors regulating gene expression. PPARs mediate the induction of the enzymes of the peroxisomal and microsomal fatty-acid oxidation pathways by hypolipidemic drugs such as clofibrate and are probably also involved in the gene expression of other lipid-metabolism-associated proteins that are controlled by fibrate hypolipidemic drugs. That PPARs play an important role in the regulation of lipid metabolism is reinforced by the discovery of their activation by physiologic concentrations of fatty acids. This observation raises the question of whether fatty acids are ligands of PPARs, which would imply that nutritional fatty acids can act like hormones.

Published
1993
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results