Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.108 (TAT)
 2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biochemical functions of human livers were studied using fetal hepatocytes in primary culture. Immunocytochemical staining showed that albumin was not expressed in any fetal hepatocytes, whereas alpha-fetoprotein was detected in almost all the cells. Tryptophan 2,3-dioxygenase (TO, EC 1.13.11.11.) activity was not induced in the presence of 10(-7) M dexamethasone and 10(-7) M glucagon, but the activity of tyrosine aminotransferase (TAT, EC 2.6.1.5.) was elevated about 35 fold under the same conditions. These results suggest that the TAT and alpha-fetoprotein genes are activated in human fetal liver at 14 to 20 weeks of gestation.
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PMID:Studies on the expression of liver-specific functions of human fetal hepatocytes in primary culture. 244 88

The effect of insulin on the abundance of mRNAs coding for tyrosine aminotransferase (TAT; EC 2.6.1.5), tryptophan oxygenase (TO; EC 1.13.1.12), and P-enolpyruvate carboxykinase(GTP) (PEPCK; EC 4.1.1.32) was examined in primary cultures of adult rat hepatocytes and in FTO-2B rat hepatoma cells by Northern blot analysis using RNA probes made from SP6-cDNAs. Insulin (10(-11)-10(-7) M), which has been reported to induce TAT and decrease the activity of TO, did not change the levels of TAT mRNA and TO mRNA in hepatocytes regardless of the presence of other inducers. In the same cells, dexamethasone increased TAT mRNA up to 19-fold and TO mRNA up to 15-fold, and 8pClPhS-cAMP (CPT-cAMP) raised the level of TAT mRNA up to 36-fold. The abundance of TO mRNA was not altered by CPT-cAMP. In contrast to TAT mRNA and TO mRNA, the level of PEPCK mRNA was dramatically decreased by insulin in the same hepatocytes. The sensitivity to this inhibitory effect of insulin was enhanced by dexamethasone and reduced by CPT-cAMP. FTO-2B hepatoma cells, which do not express detectable levels of TO mRNA, showed responses similar to those of hepatocytes, except that insulin caused a moderate reduction in TAT mRNA, but only in the presence of CPT-cAMP. The PEPCK mRNA in FTO-2B cells was suppressed by insulin in a manner closely resembling the effects in hepatocytes in the present study and in H4IIE hepatoma cells previously reported.
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PMID:Regulation of gene expression in rat hepatocytes and hepatoma cells by insulin: quantitation of messenger ribonucleic acid's coding for tyrosine aminotransferase, tryptophan oxygenase, and phosphoenolpyruvate carboxykinase. 287 68

In vitro antiglucocorticoids (cortexolone and progesterone) were evaluated as in vivo antagonists of dexamethasone-induced increases in liver tyrosine amino transferase (TAT; EC 2.6.1.5), tryptophan oxygenase (TPO; EC 1.13.1.12), and glycogen deposition. Cortexolone antagonized the TPO and glycogen responses to dexamethasone in the liver of adrenalectomized rats but did not significantly influence the induced TAT activity. Progesterone, although toxic at levels approaching those used for cortexolone, was capable of antagonizing the glycogen increase. A new antagonist, 6 beta-bromoprogesterone, was found to be nontoxic and was more potent than cortexolone in blocking the TPO and glycogen responses. These results demonstrate that in vivo antiglucocorticoid activity can be evaluated and suggested significant differences between the sensitivity of TAT induction and that of glycogen or TPO.
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PMID:Antiglucocorticoids: in vivo assay and evaluation of cortexolone, progesterone, and 6-beta-bromoprogesterone. 610

Tyrosine aminotransferase (TAT; L-tyrosine:2-oxoglutarate aminotransferase, EC 2.6.1.5) from rat liver is subject to glucocorticoid, cAMP, and developmental control. To study the underlying regulatory mechanisms, the TAT structural gene was isolated from a lambda bacteriophage rat DNA library. Heteroduplex analysis revealed that the 2.4-kilobase-long TAT mRNA is encoded by a gene that extends over 11 kilobases and is interrupted by 11 introns. To characterize the presumptive control region, the DNA sequence around the 5' end of the gene was determined and the start site of transcription was identified by nuclease S1 protection experiments. A short sequence homology in an equivalent position relative to the cap site was detected between TAT and tryptophan oxygenase, another glucocorticoid-controlled gene from rat liver. This sequence is related to the sequence 5' T-G-T-T-C-T 3' found in regions of the long terminal repeat of mouse mammary tumor virus, which has been shown to interact with the glucocorticoid receptor [Scheidereit, C., Geisse, J., Westphal, H. M. & Beato, M. (1983) Nature (London) 304, 749-752].
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PMID:Isolation and characterization of the rat tyrosine aminotransferase gene. 614 18