Disease relevance of Thrsp

• Identification of genes enhanced by protein-calorie malnutrition by differential display polymerase chain reaction (expression of fibrinogen B beta chain, B cell translocation gene 1 and thyroid hormone responsive protein genes) [1].
• The gene is highly homologous to the rat Spot 14 ortholog and located on a chromosomal region implicated in human obesity [2].
• Furthermore, whereas in liver or epididymal fat, hypothyroidism resulted in an 80% fall in S14 mRNA, in brown fat the level of this sequence increased a further 3-fold [3].
• In vivo genomic footprinting of thyroid hormone-responsive genes in pituitary tumor cell lines [4].
• The presumption is that the prokaryotic (E. coli) ribosomal proteins, S10, S12, and S14, possess antigenic determinants also present in eukaryotic (rat liver) ribosomal proteins; the rat liver proteins have not yet been identified [5].

Psychiatry related information on Thrsp

• Septal-diagonal band grafts improved open field habituation (within trial decline of ambulatory activity) and radial maze learning; the former was observed only in S16 rats, whereas the latter was observed only in S14 rats [6].

High impact information on Thrsp

• The highest density of S-14 section labeling occurred over A cells, which under conditions of maximum labeling (37 degrees C for 60 min) contained five times as many ARG as did B cells [7].
• Monolayer cultures of rat islet cells were incubated with [125I-Tyr11]S-14 (S-14 section) or [125I-Leu8, D-Trp22, Tyr25]S-28 (S-28 section) in the presence or absence of excess unlabeled peptides [7].
• Opposing effects of glucagon and triiodothyronine on the hepatic levels of messenger ribonucleic acid S14 and the dependence of such effects on circadian factors [8].
• Moreover, the data suggest the hypothesis that T3 may act on S14 gene expression by antagonizing factors that inhibit its transcription [8].
• In an attempt to identify such a molecule, I characterized the molecular forms of S-28(1-12)-like immunoreactivity (S-28(1-12) LI) in the rat pancreas and compared the relative amounts of these forms with those of S-14-like immunoreactivity (S-14 LI) [9].

Chemical compound and disease context of Thrsp

• Expression of a thyroid hormone-responsive recombinant gene introduced into adult mice livers by replication-defective adenovirus can be regulated by endogenous thyroid hormone receptor [10].
• However, replacement of the 21-bp S14 ChoRE with the authentic MLTF binding site from the adenovirus major late promoter failed to elicit the glucose response [11].
• 4. Hypothyroidism resulted in a reduction in myocardial alpha-MHC and hepatic Spot 14 mRNAs, in contrast to amiodarone, whilst hypothyroidism and amiodarone both exerted stimulatory influences on beta-MHC mRNA [12].
• Effect of hypothyroidism and thyroid hormone treatment of the rat on hepatic Spot 14 and thyroxine binding prealbumin mRNAs [13].

Biological context of Thrsp

• Dietary carbohydrate and thyroid hormone (T3) interact to regulate rat liver S14 gene expression [14].
• Analysis of S14 chromatin structure showed that starvation of hypothyroid rats inhibited the formation of three DNase I-hypersensitive sites flanking the 5'-end of the S14 gene (Hss-1 at -65 to -265 base pairs; Hss-2 at -1.2 kilobases and Hss-3 at -2.67 kilobases) [14].
• Spot 14 is a 17-kDa protein expressed in lipogenic tissues and is postulated to play a role in thyroid hormone stimulation of lipogenesis [2].
• Site-directed mutagenesis confirmed the identity of a candidate DR-4 thyroid hormone response element within this fragment that is similar, but not identical, to the two rat Spot 14 thyroid hormone response elements [2].
• The structure of DNAase I hypersensitive site 1 (Hss-1), located adjacent to the 5' end of the rat liver S14 gene, is regulated by tissue-specific factors, and its formation correlates with the transcriptional activation of the S14 gene [15].

Anatomical context of Thrsp

• The thyroid hormone responsive protein (THRP) is a novel gene product that remains responsive to thyroid hormone (TH) in the cerebral cortex of adult rats [16].
• The experiments showed that proteins S2, S3, S4, S6, S7, S13, and S14 in the small subunit of rat liver ribosomes are located at the ribosomal interface in close proximity to 28S rRNA [17].
• Polyunsaturated fatty acids inhibit S14 gene transcription in rat liver and cultured hepatocytes [18].
• To investigate the cellular site at which T3 acts to induce this hepatic mRNA, we made parallel measurements of the relative levels of spot 14 mRNA and nuclear precursor RNA and of the rate of gene transcription after treatments designed to alter the thyroid status of rats [19].
• All HpaII/MspI sites and most HhaI sites either within or flanking the S14 gene were undermethylated in liver and lactating mammary gland [20].

Associations of Thrsp with chemical compounds

• Northern blot analysis revealed that THRP, highly expressed in the brain in a tissue-specific manner, was induced by PCM and that cysteine supplementation abolished the THRP induction [1].
• We have isolated and characterized a rat gene coding for spot 14 mRNA: a hepatic product induced rapidly by thyroid hormone [21].
• Both T3 and sucrose were required to restore S14 run-on activity and mRNAS14 to euthyroid-fed levels within 4 h [14].
• To further document THRP-induced cytotoxicity, the cells were either transfected with pSVL (empty vector)+pSV2neo (neomycin resistance vector for cell labeling), pSVL-THRP+pSV2neo, or pSVL-THRP+pc-Abl (cAbl tyrosine kinase expressing vector)+pSV2neo [16].
• To study the effects of THRP on neuronal cell survival, primary neurons cultured from rats at embryonic day 19 were treated with either 10(-7) mol L(-1) 3,5,3'-triiodothyronine (T(3)), or 10(-7) mol L(-1) L: -thyroxine (T(4)) [16].

Other interactions of Thrsp

• In rat liver, triiodothyronine (T3) and dietary carbohydrate induce the expression of the genes coding for malic enzyme (ME) (EC 1.1.1.40) and S14 protein [22].
• Despite the absence of COX-1 and -2 expression in primary hepatocytes, prostaglandins (PGE2 and PGF2alpha) suppressed fatty acid synthase, l-pyruvate kinase, and the S14 protein mRNA, while having no effect on acyl-CoA oxidase or CYP4A2 mRNA [23].
• Despite the fact that RC3 expression in vivo is thyroid hormone-dependent, no evidence for the presence of a thyroid hormone responsive element was found within the 2.4 kbp flanking region analyzed and thyroid hormone did not increase reporter activity after cotransfection of suitable constructs with thyroid hormone receptor expression vectors [24].
• Hepatic fatty acid synthase and Spot-14 are insulin/glucose-dependent genes [25].
• 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 [26].

Analytical, diagnostic and therapeutic context of Thrsp

• Northern and/or reverse transcription-polymerase chain reaction (RT-PCR) analyses revealed that PCM increased the expression of fibrinogen B beta chain, B cell translocation gene I (BTGI) and thyroid hormone responsive protein (THRP) mRNAs [1].
• The relative abundance of the 9,000-11,000 mol wt S-28(1-12) LI material was unchanged following removal of S-14 LI from pancreatic extracts by affinity chromatography before gel filtration [9].
• Quantitative electron microscopic autoradiography was used for comparing the binding of labeled somatostatin-14 (S-14) and somatostatin-28 (S-28 section) to islet cells [7].
• Isolation of a thyroid hormone-responsive gene by immunoprecipitation of thyroid hormone receptor-DNA complexes [27].
• The time course of induction of the nuclear precursor to spot 14 mRNA after intramuscular injection of T3 displayed a very short lag period of between 10 and 20 min [28].

References