Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.1.21 (thymidine kinase)
 7,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the clinical applications of serum thymidine kinase (TK) activity, we compared the results obtained with this parameter with those of other liver function tests in 27 patients with acute viral hepatitis and 16 normal controls. In those in the acute stage, the serum TK activity increased significantly to 55.5 +/- 66.5 U/L. There was no significant correlation between serum TK activity and findings for serum albumin, bilirubin, alkaline phosphatase or r-glutamyl transpeptidase. However, it did correlate significantly well with the serum activity of aspartate aminotransferase (AST) (r = 0.621, P < 0.01), alanine aminotransferase (ALT) (r = 0.551, P < 0.01), and lactate dehydrogenase (LDH) (r = 0.620, P < 0.01). Serum TK activity reached higher than 70 U/L in 8 of 11 patients with hepatitis A; however, no patients with the other types of hepatitis reached such a high level. During the recovery stage, the serum TK activity decreased significantly to 5.9 +/- 1.7 U/L (P < 0.01), and did not correlate with AST, ALT, LDH or other conventional liver function parameters. The data suggest that an elevation of serum TK in patients with acute viral hepatitis results from hepatocellular damage. A marked elevation of serum TK activity may thus provide a marker for acute hepatitis A infection.
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PMID:Elevated serum thymidine kinase activity in patients with acute viral hepatitis. 844 Apr 24

The mouse cytochrome oxidase (COX) Vb promoter contains three sequence motifs with partial or full consensus for YY-1 and GTG factor binding and a CArG box, located between positions -480 and -390. Individually, all three motifs stimulated transcription of the TKCAT promoter, and bound distinctly different proteins from the liver and differentiated C2C12 nuclear extracts. Collectively, these motifs, together with the downstream flanking sequence, -378 to -320, suppressed the transcription activity of heterologous promoters, thymidine kinase-chloramphenicol acetyltransferase (TKCAT) and COXIV/CAT. The transcription activities of both TKCAT and COXIV/CAT constructs were induced 3-4-fold during induced myogenesis of C2C12 cells. The downstream CArG-like motif binds transcription factor YY-1, while the upstream YY-1-like motif binds to a yet unidentified factor. Co-expression with intact YY-1, but not that lacking the DNA binding domain suppressed the transcriptional activity. Mutations targeted to the CArG-like motif abolished the suppressive effect of the negative enhancer and the inducibility of the promoter during myogenic differentiation. Our results suggest that the activity of the negative enhancer may determine the level of expression of the COX Vb gene in different tissues.
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PMID:Regulation of murine cytochrome oxidase Vb gene expression in different tissues and during myogenesis. Role of a YY-1 factor-binding negative enhancer. 903 8

The chromosomal complements of somatic cell pig-mink hybrids was determined by a new approach. This approach includes microdissection of metaphase chromosomes, generation of chromosome and region-specific DNA libraries, and fluorescence in situ hybridization of these libraries with pig lymphocyte chromosomes. The studied hybrid cells were shown to contain two small acrocentric chromosomes and a microchromosome of porcine origin. Identification of these chromosomes by differential GTG-staining was impossible. Chromosome isolation by a micromanipulation technique followed by DNA amplification in TOPO-DOP polymerase chain reaction provided chromosome-specific DNA libraries of the rearranged chromosomes. Based on these libraries, the labeled DNA probes were prepared and hybridized to pig chromosomes. This allowed us to determine the origin of the material contributing to the hybrid cell chromosomes. One of these chromosomes contained five pig chromosomal regions: 15cen-q2; 6q21-q23; 13q21; 13q22; 7q25-qter, while the other contained the following pig chromosomal regions: 4p12-p13; 16q12-q14; 12pter-p15. The microchromosome contained the Xp11-Xq11 region. The minimal size of the revealed chromosomal regions was about 3 to 4 x 10(6) bp. Segregation analysis of the thymidine kinase gene 1 (TK1), which was earlier localized to the pig 12p region, and the hybrid cell pig chromosomes in the hybrid subclones suggested that TK1 gene can be assigned to 12p15-pter. The results obtained demonstrate the efficiency of the applied approach in its detailed and reliable description of complex chromosomal rearrangements in hybrid clones, when differential chromosome staining failed to identify these chromosomes.
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PMID:[A new approach to the analysis of complex chromosomal rearrangements in cell hybrids]. 958 54

We report the first mutational study of thymidine kinase 1 (TK1) performed in human solid tumors. We sequenced cDNAs representing the complete coding region of TK1 in human breast (n=22) and colorectal (n=26) cancer. Codon 106 near the ATP binding site constantly differed (ATG --> GTG; Met --> Val) from the one deposited by Bradshaw and Deininger in the Genbank database (Accession number NM_003258). Silent polymorphisms at codon 11 (CCC --> CCT; Pro --> Pro) and codon 75 (GCG --> GCA; Ala --> Ala) were frequently detected in tumors as well as in normal tissues. In breast cancer the two polymorphisms were observed in 63.6% of the samples analyzed. No significant association could be found between polymorphisms and TK activity. In colorectal cancer the incidence of the two changes was 73.1% and 69.2%, respectively. Interestingly, one colon cancer with high cytosolic TK activity displayed two missense mutations located in and near the putative phosphorylation site by tyrosine kinase (s) (TAT --> CAT; Tyr --> His) and by cAMP-, cGMP-dependent protein kinase (TAC --> TGC; Tyr --> Cys), respectively; adjacent normal mucosa showed no mutation. This may open new avenues that imply TK1 activity in tumor cell proliferation.
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PMID:Mutation analysis in the coding sequence of thymidine kinase 1 in breast and colorectal cancer. 1269 56