The nuclei of isolated rat hepatocytes were separable into three receptor compartments based upon their differential salt extractabilities: nucleoplasmic receptors (NP) extractable with 0.15 M KCl, high-salt extractable receptors (HSE) extractable with 0.4 M KCl, and salt-resistant receptors (SR) extractable with 0.4 M KCl/5 mM dithiothreitol. The receptor distribution among the three compartments was approximately NP, 45%; HSE, 30%; SR, 25%. The mean percent occupancy with endogenous T3 of the SR receptors (86%) was higher than the occupancies of the NP receptors (68%) and the HSE receptors (63%). When hepatocytes were pulsed with 3 nM [125I]T3 at 37 degrees C for brief intervals, receptor-[125I]T3 complexes were detectable in all three nuclear compartments within 15 sec. With increasing pulse intervals up to 120 sec, the receptor content of each nuclear compartment increased progressively and without evidence of preferential accumulation in any of the three compartments. To determine the life span and intercompartmental "migration" pattern of nuclear receptors, hepatocytes were pulsed with 3 nM [125I]T3 at 37 degrees C for 2.5 min or 5 min, followed by a chase with a 500-fold excess of nonlabeled T3. The population of receptor-[125I]T3 complexes generated during the pulse was serially recovered at increasing intervals after the chase. The complexes of each compartment dissociated with a half-life of approximately 3 min and manifested no predilection to accumulate in any of the compartments. Exposure of isolated hepatocytes to 3 nM T3 for 5 min or 10 min at 37 degrees C induced no change in the gross intercompartmental distribution of receptors compared to control hepatocytes incubated without T3.(ABSTRACT TRUNCATED AT 250 WORDS)
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http://dx.doi.org/10.1089/thy.1994.4.305 | DOI Listing |
Endocrinology
July 2013
Institut für Experimentelle Endokrinologie, Charité-Universitätsmedizin Berlin, D-13353, Berlin, Germany.
Mutations in monocarboxylate transporter 8 (MCT8; SLC16A2) cause the Allan-Herndon-Dudley syndrome, a severe X-linked psychomotor retardation syndrome. MCT8 belongs to the major facilitator superfamily of 12 transmembrane-spanning proteins and transports thyroid hormones across the blood-brain barrier and into neurons. How MCT8 distinguishes thyroid hormone substrates from structurally closely related compounds is not known.
View Article and Find Full Text PDFCent Eur J Public Health
June 2003
Institute of Endocrinology, Národní 8, 116 94 Prague, Czech Republic.
Iodine is an essential element with unique role in organism: it is indispensable component of thyroid hormones. After binding with specific nuclear receptor, T3/T4 induce transcription of genetic code via mRNA and regulate proteosynthesis in most tissues. Thyroid hormones regulate rate of metabolic processes and consequently development of organism.
View Article and Find Full Text PDFScand J Immunol
June 1989
Department of Microbiology and Biochemistry, Mount Sinai School of Medicine, New York, N.Y.
Cytolytic T lymphocytes (CTL) cause cytolysis of foreign or virus-infected syngeneic cells when recognition of the target plus major histocompatibility complex (MHC) occurs via the T-cell receptor (TCR). The recognition event leads to intimate contact between the two cells and activation of the cytolytic effector. Activation and target cell lysis can also occur in the presence of antibodies to the TCR.
View Article and Find Full Text PDFBiochimie
February 1989
Department of Medicine, University of Chicago, IL 60637.
Thyroid hormone nuclear receptor molecules have been characterized as proteins of approximately 49,000 molecular weight existing in cells attached to chromatin and with 4000-8000 copies per nucleus. They bind T3 with Ka of 0.2 X 10(10) l/mol and show microheterogeneity on isoelectric focusing.
View Article and Find Full Text PDFImmunol Ser
April 1991
Harvard Medical School, Dana Farber Cancer Institute, Boston, Massachusetts.
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