Disease relevance of AF348365

• The herpes simplex virus thymidine kinase gene promoter contains a novel thyroid hormone response element [1].

High impact information on AF348365

• We report here the identification of thyroid hormone response elements (TREs) that consist of a direct repeat, not a palindrome, of the half-sites [2].
• Response of hepatic mitochondrial alpha-glycerophosphate dehydrogenase and malic enzyme to constant infusions of L-triiodothyronine in rats bearing the Walker 256 carcinoma. Evidence for divergent postreceptor regulation of the thyroid hormone response [3].
• Retinoic acid receptors are ligand-dependent transcription factors that stimulate gene transcription from promoters containing retinoic acid or thyroid hormone response elements [4].
• These results demonstrate that, although necessary, the thyroid hormone response element is not sufficient for complete thyroid hormone regulation of this gene in vivo [5].
• The 161-bp sequence upstream of the transcription start site, which contains a TATA box, a CCAATT box, and a thyroid hormone response element, was transcriptionally active but not thyroid hormone responsive [5].

Biological context of AF348365

• Transfection experiments with the luciferase reporter gene revealed that thyroid hormone response sequences are located within the 5'-flanking regions of each alpha-isoform gene.(ABSTRACT TRUNCATED AT 250 WORDS)[6]
• When a complex thyroid hormone response element composed of both direct and inverted repeat hexamers was tested, these two ligands activated gene expression synergistically [7].
• Since other members of this family of nuclear receptors also have been shown to use varying arrangements of the traditional hexamer sequence as response elements, we examined whether the octamer sequence was specific as a thyroid hormone response element [8].
• By transfection and in vitro receptor binding analyses, we have identified two thyroid hormone response elements, A1 (-295/-268) and B1 (+207/+227) [9].
• The response to the liganded thyroid hormone receptor (TR) was mediated by an unusual thyroid hormone response element located between -1000 and -987 relative to the transcription start site [10].

Anatomical context of AF348365

• 3,5,3'-L-triiodothyronine (thyroid hormone)-induced protein-DNA interactions in the thyroid hormone response elements and cell type-specific elements of the rat growth hormone gene revealed by in vivo dimethyl sulfate footprinting [11].
• Delineation of three different thyroid hormone-response elements in promoter of rat sarcoplasmic reticulum Ca2+ATPase gene. Demonstration that retinoid X receptor binds 5' to thyroid hormone receptor in response element 1 [12].
• The enhancer involved is distinct from the thyroid hormone response element of the 'malic' enzyme promoter and is partly homologous with that which mediates transcriptional activation of peroxisomal acyl-CoA oxidase by peroxisome proliferators [13].
• Responsiveness to thyroid hormone is enhanced in rat hepatocytes cultured as spheroids compared with that in monolayers: altered responsiveness to thyroid hormone possibly involves complex formed on thyroid hormone response elements [14].
• Thyroid hormone response of slow and fast sarcoplasmic reticulum Ca2+ ATPase mRNA in striated muscle [15].

Associations of AF348365 with chemical compounds

• This region, at nucleotide position -465/-432, contains an array of thyroid hormone response half-sites that bind preferentially T3R as heterodimers with retinoid X receptor and whose deletion causes loss of the T3-dependent repression [16].
• Three elements were found to be essential for supporting the glucose response: a thyroid hormone-response element between -1522 and -1494, an accessory factor site between -1421 and -1392, and the ChoRE between -1450 and -1425 [17].
• Distance-dependent interactions between basal, cyclic AMP, and thyroid hormone response elements in the rat growth hormone promoter [18].
• Thyroid hormone response elements differentially modulate the interactions of thyroid hormone receptors with two receptor binding domains in the steroid receptor coactivator-1 [19].
• Genes with appropriate response elements will show amplification of the thyroid hormone response by 9-cis-retinoic acid in the presence of retinoid X receptors; other thyroid hormone-responsive genes will be influenced by retinoid X receptors, but not 9-cis-retinoic acid [7].

Physical interactions of AF348365

• Triiodothyronine (T3) activates rat liver S14 gene transcription through T3 receptors (TRbeta) binding distal thyroid hormone response elements located between -2.8 and -2.5 kilobase pairs upstream from the transcription start site [20].

Other interactions of AF348365

• The time course of the T3 effect in liver and pituitary in vivo and the lack of any effect in vitro suggests that this action is indirect, and not as a result of interaction between the T3 receptor and the putative thyroid hormone response element on the rat 11 beta-HSD gene [21].
• This induction of CPT-I alpha gene expression requires the thyroid hormone response element in the promoter and sequences within the first intron [22].
• Thyroid hormone receptors (TRs) are ligand-dependent nuclear transcription factors that are encoded by two different genes, TR alpha and TR beta, and bind to thyroid hormone response elements (TREs) in the promoters of thyroid hormone (T3)-regulated genes [23].
• T3 regulation of SERCA1 expression is mediated by a complex thyroid hormone response element that may serve to provide a greater range of response in interaction with nuclear receptor partners or cell-specific transcription factors [24].
• The most potent of these thyroid hormone response elements, R3, increased the 2-fold background T3 stimulation of the thymidine kinase promoter to nearly 6-fold [24].

Analytical, diagnostic and therapeutic context of AF348365

• 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 [25].
• Sequence analysis suggested the presence of three thyroid hormone response elements, TRE-1 (-602/-589), TRE2 (-411/-396), and TRE3 (-376/-350) [26].
• Stimulation of DNA-binding was demonstrated in electrophoretic mobility shift assays for a specific RXR-containing protein complex with a DR+4 thyroid hormone response element of the human type 1 5'DI promoter using nuclear extracts from GH3 cells treated with 3,5-T2 [27].

References