Identification of multiple thyroid hormone response elements located far upstream from the rat S14 promoter.

Zilz, N D; Murray, Michael; Towle, Howard C.

doi:10.1016/s0021-9258(19)39048-9

Cited by 100 publications

(5 citation statements)

References 56 publications

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“…Other exceptions to our rule include the estrogen response element palindrome variably conferring negative or positive T 3 responsiveness depending on the individual study (Glass et al, 1988;Brent et al, 1989a;de Verneuil and Metzger, 1990;Holloway et al, 1990; our unpublished data), a reported TRE in the rGH gene intron (Sap et al, 1990), and the S14 gene TRE (Zilz et al, 1990). However, a reinterpretation of the S14 element (Howard Towle, personal communication) suggests it may conform to our model (Figure 10).…”

Section: Hre Diversitymentioning

confidence: 72%

Direct repeats as selective response elements for the thyroid hormone, retinoic acid, and vitamin D3 receptors

Umesono

Murakami

Thompson

et al. 1991

Cell

1,659

957

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Section: Hre Diversitymentioning

confidence: 72%

Direct repeats as selective response elements for the thyroid hormone, retinoic acid, and vitamin D3 receptors

Umesono

Murakami

Thompson

et al. 1991

Cell

1,659

957

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“…To determine whether the information from our studies have added to the knowledge of thyroid hormone action, we compared our results with those obtained from the study of other model genes that are also induced by T3, e.g., the rat S14, rat malic enzyme, and rat growth hormone genes. When the positive TREs are removed from the S14 and malic enzyme promoters, the activity of the deletional mutants is not inhibited by T3 (Zilz et al, 1990;Petty et al, 1990). However, removal of the positive TRE from the rat growth hormone gene uncovered a transient inhibitory element (TIE) that represses the activity of the deletional mutant in response to T3 (Wright et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

Identification of Functional Positive and Negative Thyroid Hormone-Responsive Elements in the Rat Apolipoprotein AI Promoter

Taylor¹,

Wishart²,

Lawless³

et al. 1996

Biochemistry

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Transcription of the antiatherogenic protein apolipoprotein AI is regulated by the thyroid hormone, L-triiodothyronine. Transient transfection and electrophoretic mobility shift assays were used to identify the cis-acting elements involved. In transient transfection assays, hormone bound to either thyroid hormone receptor alpha or beta exerts a positive effect through a thyroid hormone response element, site A (-208 to -193). In the absence of site A, liganded receptor alpha or beta have a negative effect on promoter activity. This negative effect is mediated by a 40 bp fragment spanning nucleotides -46 to -7. Closer examination of this region of the gene shows there to be a negative thyroid hormone response element at position -25 to -20 which is fused to the 3' end of the TATA element. Electrophoretic mobility shift assays show that bacterially expressed chicken or rat thyroid hormone receptor alpha 1 binds to site A, either as a homodimer or as a heterodimer with the human 9-cis-retinoic acid receptor alpha. In contrast, the negative thyroid hormone responsive element binds chicken thyroid hormone receptor alpha exclusively as a monomer. Site-directed mutagenesis of the negative thyroid hormone response element abolished the inhibitory effects of the hormone and increased basal promoter activity by up to 40-fold. These data suggest that functional positive and negative thyroid hormone response elements coexist within the rat apolipoprotein AI promoter and both elements contribute to the control of apolipoprotein AI gene expression.

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“…This finding suggests that THR and RAR may act on an overlapping set of genes; consistent with this inference, THR and RAR have been shown to bind and transactivate the same DNA sequences in certain cases (11,33,40,53,54,79). On the other hand, response elements specific for THR (TREs) and response elements specific for RAR (RAREs) have been identified and characterized in several genes (3,12,16,20,21,30,39,49,56,61,64,81,83,92). Presumably as a result of amino acid sequence similarities in their carboxy-terminal dimerization domains, THR and RAR are able to form heterodimers (32,84), making THR/RAR heterodimer-specific DNA binding also possible, although not yet demonstrated.…”

mentioning

confidence: 61%

Thyroid Hormone Receptor Can Modulate Retinoic Acid-Mediated Axis Formation in Frog Embryogenesis

Banker

Eisenman

1993

Molecular and Cellular Biology

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Thyroid hormone receptor acts as a hormone-dependent transcriptional transactivator and as a transcriptional repressor in the absence of thyroid hormone. Specifically, thyroid hormone receptor can repress retinoic acid-induced gene expression through interactions with retinoic acid receptor. (Retinoic acid is a potent teratogen in the frog Xenopus laevis, acting at early embryonic stages to interfere with the formation of anterior structures. Endogenous retinoic acid is thought to act in normal anterior-posterior axis formation.) We have previously shown that thyroid hormone receptor RNA (alpha isotype) is expressed and polysome-associated during Xenopus embryogenesis preceding thyroid gland maturation and endogenous thyroid hormone production (D. E. Banker, J. Bigler, and R. N. Eisenman, Mol. Cell. Biol. 11:5079-5089, 1991). To determine whether thyroid hormone receptor might influence the effects of retinoic acid in early frog development, we have examined the results of ectopic thyroid hormone receptor expression on retinoic acid teratogenesis. We demonstrate that microinjections of full-length thyroid hormone receptor RNA protect injected embryos from retinoic acid teratogenesis. DNA binding is apparently essential to this protective function, as truncated thyroid hormone receptors, lacking DNA-binding domains but including hormone-binding and dimerization domains, do not protect from retinoic acid. We have shown that microinjections of these dominant-interfering thyroid hormone receptors, as well as anti-thyroid hormone receptor antibodies, increase retinoic acid teratogenesis in injected embryos, presumably by inactivating endogenous thyroid hormone receptor. This finding suggests that endogenous thyroid hormone receptors may act to limit retinoic acid sensitivity. On the other hand, after thyroid hormone treatment, ectopic thyroid hormone receptor mediates teratogenesis that is indistinguishable from the dorsoanterior deficiencies produced in retinoic acid teratogenesis. The previously characterized retinoic acid-responsive gene, Xhox.lab2, can be induced by thyroid hormone in embryos ectopically expressing thyroid hormone receptor and is less responsive to retinoic acid in such embryos. The fact that both thyroid hormone and retinoic acid can affect overlapping gene expression pathways to produce abnormal embryonic axes and can regulate the same early-expressed gene suggests a model in which thyroid hormone receptor blocks retinoic acid receptor-mediated teratogenesis by directly repressing retinoic acid-responsive genes.

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Identification of multiple thyroid hormone response elements located far upstream from the rat S14 promoter.

Cited by 100 publications

References 56 publications

Direct repeats as selective response elements for the thyroid hormone, retinoic acid, and vitamin D3 receptors

Direct repeats as selective response elements for the thyroid hormone, retinoic acid, and vitamin D3 receptors

Identification of Functional Positive and Negative Thyroid Hormone-Responsive Elements in the Rat Apolipoprotein AI Promoter

Thyroid Hormone Receptor Can Modulate Retinoic Acid-Mediated Axis Formation in Frog Embryogenesis

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