![]()
|
|
||||||||
J. Biol. Chem., Vol. 262, Issue 5, 2116-2120, 02, 1987
TA Gasiewicz and PA Bauman
The characteristics of the Ah receptor from rat liver were investigated
following the incubation of cytosol with [3H]2,3,7,8-tetrachlorodibenzo-
p-dioxin (TCDD) under various conditions, and using DEAE- and DNA-
Sepharose chromatography and sucrose density gradient centrifugation. These
studies indicated that the Ah receptor can exist in three distinct forms in
vitro that are dependent on the presence or absence of TCDD and the
duration and temperature of incubation. The unoccupied receptor was
distinguished by its elution from DEAE-Sepharose columns at 0.20-0.23 M
NaCl and lack of affinity for DNA-Sepharose. Following the incubation of
the unoccupied receptor with [3H]TCDD, two occupied forms were
distinguished based on their overall surface charges and affinities for
DNA. One of these forms was predominant following short incubations (2 h)
with [3H]TCDD at a low temperature (0 degree C) and was characterized by
having the same elution profile on DEAE-Sepharose as the unoccupied form,
but demonstrated some affinity for DNA. Another occupied form was
predominant following an incubation for a longer time (20 h, 0 degree C) or
at an elevated temperature (2 h, 20 degrees C). This form had an overall
surface charge that was less negative and a greater affinity for DNA. These
changes in receptor characteristics were dependent on the presence of TCDD
and were not accompanied by apparent changes in the sedimentation
coefficients of the two occupied forms. Anion exchange chromatography of
the [3H]TCDD-receptor complex extracted from hepatic nuclei of
[3H]TCDD-treated rats indicated that the ligand-induced change of the
unoccupied receptor to a less negatively charged form had occurred in vivo.
These results indicated a biochemical heterogeneity of the Ah receptor and
suggested the occurrence of a ligand- and temperature-dependent
transformation process in vivo and in vitro.
Heterogeneity of the rat hepatic Ah receptor and evidence for transformation in vitro and in vivo
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
Technorati What's this?
This article has been cited by other articles:
![]() |
A. B. Okey An Aryl Hydrocarbon Receptor Odyssey to the Shores of Toxicology: The Deichmann Lecture, International Congress of Toxicology-XI Toxicol. Sci., July 1, 2007; 98(1): 5 - 38. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Joiakim, P. A. Mathieu, A. A. Elliott, and J. J. Reiners Jr. Superinduction of CYP1A1 in MCF10A Cultures by Cycloheximide, Anisomycin, and Puromycin: A Process Independent of Effects on Protein Translation and Unrelated to Suppression of Aryl Hydrocarbon Receptor Proteolysis by the Proteasome Mol. Pharmacol., October 1, 2004; 66(4): 936 - 947. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Joiakim, P. A. Mathieu, C. Palermo, T. A. Gasiewicz, and J. J. Reiners Jr. THE JUN N-TERMINAL KINASE INHIBITOR SP600125 IS A LIGAND AND ANTAGONIST OF THE ARYL HYDROCARBON RECEPTOR Drug Metab. Dispos., November 1, 2003; 31(11): 1279 - 1282. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. C. Henry, A. S. Kende, G. Rucci, M. J. Totleben, J. J. Willey, S. D. Dertinger, R. S. Pollenz, J. P. Jones, and T. A. Gasiewicz Flavone Antagonists Bind Competitively with 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) to the Aryl Hydrocarbon Receptor But Inhibit Nuclear Uptake and Transformation Mol. Pharmacol., April 1, 1999; 55(4): 716 - 725. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |