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Query: UNIPROT:P06889 (
Mol
)
630,302
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Sepharose 4B column with antibody to tyrosine aminotransferase (E.C. 2.6.1.5) (
TAT
) covalently bound can selectively remove a specific fraction of
TAT
polysomes from rat liver homogenates. From the polysomes which was adsorbed by immunosorbent one may obtain mRNA containing a segment of poly-adenilate-rich residues, having sedimentation constant of 11--16S. This mRNA may program synthesis of the specific protein in a cell free system. Near 70% of the protein was synthesized in such a system, may react with the antibody to
TAT
.
Mol
Biol (Mosk)
PMID:Extraction of tyrosine aminotransferase mRNA by polyribosome immunosorption on sepharose 4B. 2 21
The influence of denaturation conditions upon the character of partial denaturation of DNA with random base distribution were thoroughly studied. Maps of partial DNA denaturation were obtained at T less than
TAT
for phage phiB DNA at pH 10.7 and 5.5; Tg9 DNA at pH 8.8; at T less than
TAT
for phiB DNA at pH 10.9 and Tg9 DNA at pH 8.8. The map quality was better when obtained at higher pH values; the peaks became sharper and higher against the background. We failed to obtain maps of partial denaturation at pH 5.5, T less than
TAT
. The improvement of the map quality and existence of the partial denaturation maps at T less than
TAT
at pH 10.9 were explained by the increase of primary melting probability of AT-rich DNA regions. At high pH the denaturation map quality was temperature independent. This was explained by a very weak temperature dependence of primary melting probability for all maps of equal quality. The map quality became worse, when the quantity of loops was increased.
Mol
Biol (Mosk)
PMID:[Nature of the easily melted portions of DNA with a quasi-random base sequence]. 2 79
HTC cell variants chosen for their lack of tyrosine aminotransferase (EC 2.6.1.5) (
TAT
) induction by glucocorticoids were tested for interrelated effects on other glucocorticoid responses:
TAT
induction by dibutyryl cyclic AMP (dBcAMP) +/- dexamethasone, glutamine synthetase (GS) induction, cyclic nucleotide phosphodieterase (PDE) suppression, inhibition of alpha-aminoisobutyric acid (AIB) uptake, inhibition of plasminogen activator (PA), and induction of mouse mammary tumor virus (MTV). Loss of
TAT
induction by steroid was accompanied by loss of
TAT
induction by dBcAMP and of PDE suppression by steroid. In addition, subclones of MTV-infected cells were examined for the effect of the virus on glutamine synthetase (GS) and
TAT
induction. The virus had no effect on their induction in wild-type cells and no effect on GS induction in the variants. One MTV-infected subclone from a
TAT
variant, however, showed significant return of
TAT
induction.
Mol
Cell Endocrinol 1979 Sep
PMID:Unlinked control of multiple glucocorticoid-induced processes in HTC cells. 3 58
DP-
TAT
-59, (Z)-2-(4-(1-(4-hydroxyphenyl)-2-(4-isopropylphenyl)-1-butenyl) phenoxy)-N, N-dimethylethylamine, has been reported to inhibit estrogen-stimulated growth of MCF-7 cells as well as rat uterus at lower concentrations than the hydroxymetabolite of tamoxifen (4-OH-TAM). In the present study, the growth of mouse Leydig cell tumor, B-1F cells were also more effectively inhibited by DP-
TAT
-59 than 4-OH-TAM. Additionally, the expression of estrogen responsive element ligated CAT gene transfected into B-1F cells was also suppressed by DP-
TAT
-59. Thus, the interaction of DP-
TAT
-59 with estrogen receptor (ER) was characterized and compared with that of 4-OH-TAM using immature rat and bovine uteri. The dissociation constant of DP-
TAT
-59 to ER of immature rat uterus was 0.24 nM and was similar to that of 4-OH-TAM (Kd = 0.20 nM) and estradiol (Kd = 0.29 nM). Using sucrose density gradients, the sedimentation constant of DP-
TAT
-59 with bovine uterus was 4.9S, which was similar to that of estradiol (5.1S) and 4-OH-TAM (5.3S). However, the elution profile of the DP-
TAT
-59-ER complex from a DEAE-Sephadex column was different for both estradiol-and 4-OH-TAM-ER complexes. These results suggest that ER forms different complexes with DP-
TAT
-59 than estradiol or 4-OH-TAM, while the ER binding affinity of these compounds are similar to each other.
J Steroid Biochem
Mol
Biol 1992 Nov
PMID:Interaction of DP-TAT-59, an active metabolite of new triphenylethylene-derivative (TAT-59), with estrogen receptors. 141 85
A certain nucleotide sequence in the promoter region of Vicia faba rRNA genes that specifically binds to a nuclear protein fraction has been identified by using a gel retardation assay and DNase I footprinting technique. The binding site of this protein fraction is located about 60 bp upstream from the initiation site of the pre-rRNA transcript. This location does not correspond with previously reported results on maize rRNA genes. However, both of the binding sites share a bi-partite consensus sequence,
TAT
-G(N)xCAGG. Methylation interference experiments show that two G residues in TATG and the complementary strand of CAGG are important for specific DNA-protein interaction. Furthermore, competition analyses using point-mutated synthetic DNAs show that two G residues in CAGG are essential for this interaction. Similar sequences are found in promoter regions of other plant and animal rRNA genes. We suggest that these sequences may be a cis-control element commonly involved in rRNA transcription.
Plant
Mol
Biol 1992 Dec
PMID:Characterization of nucleotide sequences that interact with a nuclear protein fraction in rRNA gene of Vicia faba. 146 30
The structural gene encoding liver-specific tyrosine aminotransferase (
TAT
; EC 2.6.1.5) was assigned to mouse chromosome 8 by screening a series of hybrid cell lines for retention of murine Tat-1 gene sequences by genomic Southern blotting. This assignment demonstrated that the Tat-1 structural gene was not syntenic with Tse-1, a chromosome 11-linked locus that negatively regulates
TAT
expression in trans (A. M. Killary and R. E. K. Fournier, Cell 38:523-534, 1984). We also showed that the fibroblast Tat-1 gene was systematically activated in hepatoma X fibroblast hybrids retaining fibroblast chromosomes 8 in the absence of chromosome 11 but was extinguished in cells retaining both fibroblast chromosomes. Thus, the
TAT
structural genes of both parental cell types were coordinately regulated in the intertypic hybrids, and the
TAT
phenotype of the cells was determined by the presence or absence of fibroblast Tse-1.
Mol
Cell Biol 1985 Sep
PMID:Chromosomal assignment and trans regulation of the tyrosine aminotransferase structural gene in hepatoma hybrid cells. 287 83
Tyrosine aminotransferase (
TAT
, EC 2.6.1.5) from the kinetoplastid, Crithidia fasciculata, was purified over 2000 fold to electrophoretic homogeneity. The native form of the enzyme had a molecular weight of approximately 100,000, whereas under denaturing conditions it produced two polypeptides of approximately 50,000 and 48,000, respectively. Absence of a reaction with the periodic acid-Schiff stain suggested that the crithidial enzyme was not a glycoprotein. It was relatively stable and remained active over a wide range of pH and temperature. It exhibited a broad substrate specificity and was able to utilize L-tyrosine, L-tryptophan, and L-phenylalanine as amino donors. Antiserum produced against partially purified crithidial tyrosine aminotransferase failed to inhibit the enzymatic activity. The same antiserum cross-reacted with a soluble extract from Trypanosoma brucei gambiense, but not with that from normal mouse liver, confirming evolutionary conservatism between the two protozoa.
Mol
Biochem Parasitol 1987 Aug
PMID:Purification and characterization of a tyrosine aminotransferase from Crithidia fasciculata. 289 Jan 1
The induction of tyrosine aminotransferase by a variety of steroids was studied in cells from a hepatoma tissue culture (HTC). We have defined a class of steroids that induce
TAT
synthesis to a higher level than optimal inducers described earlier; these are called supra-inducers. When
TAT
induction is compared with the binding of the steroids to the cytoplasmic receptor or to their binding in the whole cell, a good correlation between binding in vivo of the hormone and its induction capacity can be established, whereas such a correlation was not systematically observed in vitro. A very short exposure of HTC cells to either dexamethasone or corticosterone is sufficient to induce
TAT
. When the inducer is removed from the culture medium a few minutes after its administration, the intracellular hormone concentration decreases very rapidly but
TAT
will be synthesized at its maximal rate. Thus the hormones behave as a starting signal for the optimal synthesis of the enzyme, and their presence in the culture medium is not necessary throughout the entire induction period.
Mol
Cell Endocrinol 1981 May
PMID:Relations between steroid-cell contact, steroid-binding and induction of tyrosine aminotransferase. 611 76
All mitochondrial tRNAs in the protozoan Leishmania are believed to be encoded in the nuclear genome and imported selectively into the mitochondria by an as yet unknown mechanism. Previously, we reported that two tRNAs whose genes are tightly linked were imported by mitochondria. In contrast, a tRNA encoded by a lone tRNA gene was not detectable in mitochondria. The lone tRNA gene had flanking sequences that were different from the linked genes. These studies implied a possible correlation between tRNA gene organization and gene flanking sequence, and selective tRNA import into mitochondria. Here, we report the identification of a cluster of 10 tRNA genes and show the distribution of the corresponding tRNAs in cytosolic and mitochondrial fractions. tRNA(leu)(CAG) and tRNA2(arg)(TCG) are abundant in the cytosol, but relatively scarce in mitochondria. Conversely, tRNA(ile)(
TAT
) and tRNA1(lys)(TTT) are abundant in mitochondria, but relatively scarce in the cytosol. tRNA(val)(TAC) and tRNA2(thr)(TGT) are barely detectable in either cellular compartment, while tRNA(gln)(TTG), tRNA1(arg)(ACG), tRNA(gly)(TCC), and tRNA(trp)(CCA) are detected in approximately equal levels in both compartments. Sequencing of the 2600 bp that comprise the tRNA gene cluster also encoding the genes for 5S RNA and URNAB RNA indicates that nucleotide composition, length, and location of genes within the cluster do not clearly correlate with import characteristics. The unexpected presence of the tRNA(trp)(CCA)-gene transcript in mitochondria is also reported. Evidence suggests that this tRNA may have unidentified base modifications at the anticodon triplet.
Mol
Biochem Parasitol 1994 May
PMID:A nuclear tRNA gene cluster in the protozoan Leishmania tarentolae and differential distribution of nuclear-encoded tRNAs between the cytosol and mitochondria. 793 26
The pathway of gluconeogenesis is activated in liver shortly after birth and is controlled by glucagon and glucocorticoids, which stimulate, and insulin, which inhibits, the expression of genes coding for gluconeogenic enzymes. To understand the molecular basis of this cell type-specific and coordinate control, we analyzed the cis-regulatory elements of the tyrosine aminotransferase gene, which confer liver cell-specific expression in dependence of these hormones. The cAMP-responsive element (CRE) of the
TAT
gene is an essential element within a liver-specific enhancer and is recognized by the CRE-binding protein (CREB) in a phosphorylation-dependent manner. The glucocorticoid response is mediated by a complex regulatory unit comprised of the glucocorticoid receptor and other transcription factor-binding sites. Here, we show that both the cAMP- and glucocorticoid-inducible enhancers are targets for the antagonistic effects of insulin. The insulin-responsive sequences coincide with the CREB-binding site of the cAMP-responsive enhancer and a hepatocyte nuclear factor-3-binding site within the glucocorticoid-responsive unit. This design of the hormone-dependent enhancers reflects the molecular mechanism underlying the onset of tyrosine aminotransferase expression at birth when insulin levels decrease and concentrations of glucagon and glucocorticoids increase.
Mol
Endocrinol 1994 Jul
PMID:The cyclic adenosine 3',5'-monophosphate- and the glucocorticoid-dependent enhancers are targets for insulin repression of tyrosine aminotransferase gene transcription. 798 51
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