scholarly journals Adenovirus type 2 activates cell cycle-dependent genes that are a subset of those activated by serum.

1985 ◽  
Vol 5 (11) ◽  
pp. 2936-2942 ◽  
Author(s):  
H T Liu ◽  
R Baserga ◽  
W E Mercer
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Histone H3 ◽  
Adenovirus Type ◽  
3T3 Cells ◽  
Cycle Dependent ◽  
Cellular Dna ◽  
Adenovirus Type 2

We have studied a panel of 10 genes and cDNA sequences that are expressed in a cell cycle-dependent manner in different types of cells from different species and that are inducible by different mitogens. These include five sequences (c-myc, 4F1, 2F1, 2A9, and KC-1) that are preferentially expressed in the early part of the G1 phase, three genes (ornithine decarboxylase, p53, and c-rasHa) preferentially expressed in middle or late G1, and two genes (thymidine kinase and histone H3) preferentially expressed in the S phase of the cell cycle. We have studied the expression of these genes in nonpermissive (tsAF8) and semipermissive (Swiss 3T3) cells infected with adenovirus type 2. Under the conditions of these experiments, adenovirus type 2 infection stimulates cellular DNA synthesis in both tsAF8 and 3T3 cells. However, four of the five early G1 genes (c-myc, 4F1, KC-1, and 2A9) and one of the late G1 genes (c-ras) are not induced by adenovirus infection, although they are strongly induced by serum. The other sequences (2F1, ornithine decarboxylase, p53, thymidine kinase, and histone H3) are activated by both adenovirus and serum. We conclude that the cell cycle-dependent genes activated by adenovirus 2 are a subset of the cell cycle-dependent genes activated by serum. The data suggest that the mechanisms by which serum and adenovirus induce cellular DNA synthesis are not identical.

Adenovirus type 2 activates cell cycle-dependent genes that are a subset of those activated by serum

1985 ◽  
Vol 5 (11) ◽  
pp. 2936-2942
Author(s):  
H T Liu ◽  
R Baserga ◽  
W E Mercer
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Histone H3 ◽  
Adenovirus Type ◽  
3T3 Cells ◽  
Cycle Dependent ◽  
Cellular Dna ◽  
Adenovirus Type 2

We have studied a panel of 10 genes and cDNA sequences that are expressed in a cell cycle-dependent manner in different types of cells from different species and that are inducible by different mitogens. These include five sequences (c-myc, 4F1, 2F1, 2A9, and KC-1) that are preferentially expressed in the early part of the G1 phase, three genes (ornithine decarboxylase, p53, and c-rasHa) preferentially expressed in middle or late G1, and two genes (thymidine kinase and histone H3) preferentially expressed in the S phase of the cell cycle. We have studied the expression of these genes in nonpermissive (tsAF8) and semipermissive (Swiss 3T3) cells infected with adenovirus type 2. Under the conditions of these experiments, adenovirus type 2 infection stimulates cellular DNA synthesis in both tsAF8 and 3T3 cells. However, four of the five early G1 genes (c-myc, 4F1, KC-1, and 2A9) and one of the late G1 genes (c-ras) are not induced by adenovirus infection, although they are strongly induced by serum. The other sequences (2F1, ornithine decarboxylase, p53, thymidine kinase, and histone H3) are activated by both adenovirus and serum. We conclude that the cell cycle-dependent genes activated by adenovirus 2 are a subset of the cell cycle-dependent genes activated by serum. The data suggest that the mechanisms by which serum and adenovirus induce cellular DNA synthesis are not identical.

scholarly journals Adenovirus type 5 induces progression of quiescent rat cells into S phase without polyamine accumulation.

1982 ◽  
Vol 2 (10) ◽  
pp. 1295-1298 ◽  
Author(s):  
B F Cheetham ◽  
D C Shaw ◽  
A J Bellett
Keyword(s):  
Dna Replication ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Ornithine Decarboxylase ◽  
Adenovirus Type ◽  
S Phase ◽  
Polyamine Biosynthesis ◽  
Adenosylmethionine Decarboxylase ◽  
Cellular Dna ◽  
Adenovirus Type 5

Adenovirus type 5 induces cellular DNA synthesis and thymidine kinase in quiescent rat cells but does not induce ornithine decarboxylase. We now show that unlike serum, adenovirus type 5 fails to induce S-adenosylmethionine decarboxylase or polyamine accumulation. The inhibition by methylglyoxal bis(guanylhydrazone) of the induction of thymidine kinase by adenovirus type 5 is probably unrelated to its effects on polyamine biosynthesis. Thus, induction of cellular thymidine kinase and DNA replication by adenovirus type 5 is uncoupled from polyamine accumulation.

Control of thymidine kinase mRNA during the cell cycle

1987 ◽  
Vol 7 (8) ◽  
pp. 2925-2932
Author(s):  
D L Coppock ◽  
A B Pardee
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Gene Transcription ◽  
Half Life ◽  
Mammalian Cells ◽  
Mrna Degradation ◽  
S Phase ◽  
3T3 Cells

To investigate the mechanism which controls the onset of DNA synthesis, we examined the regulation of thymidine kinase (TK) and its mRNA in the cell cycle. TK activity provides a useful marker for the onset of the S phase in mammalian cells. The present analysis of regulation of TK mRNA in BALB/c 3T3 cells showed that (i) the increase in TK activity depended on the availability of TK mRNA, (ii) the level of TK mRNA between G0 and S increased more than 20-fold, (iii) the rate of run-on TK transcription increased at most 2- to 4-fold between the G0 and S phases, (iv) the half-life of TK mRNA was greater than 8 to 12 h in the S and M phases and decreased as cells entered quiescence, (v) the TK mRNA increase was fully blocked by inhibition of protein synthesis by only 60%, (vi) this inhibition was completely effective for up to about 10 h following serum addition and progressively much less effective when the drugs were added later. These results suggest that the appearance of TK mRNA at the beginning of the S phase in serum-stimulated 3T3 cells is controlled not only by the rate of gene transcription but importantly also by the decreased rate of mRNA degradation. Similar mechanisms may be involved in regulation of the onset of DNA synthesis and the increase in TK mRNA since both are controlled in a manner consistent with a requirement for a labile protein.

scholarly journals Investigation on Cell Proliferation with a New Antibody against Thymidine Kinase 1

2001 ◽  
Vol 23 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Naining Wang ◽  
Qimin He ◽  
Sven Skog ◽  
Staffan Eriksson ◽  
Bernhard Tribukait
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Thymidine Kinase ◽  
Specific Marker ◽  
Thymidine Kinase 1 ◽  
C Terminus ◽  
Proliferation Activity ◽  
Cycle Dependent ◽  
Cellular Dna ◽  
Archival Specimens

The cytosolic thymidine kinase 1 (TK1) is one of the enzymes involved in DNA replication. Based on biochemical studies, TK1 is activated at late G1 of cell cycle, and its activity correlates with the cell proliferation. We have developed a polyclonal anti‐TK1 antibody against a synthetic peptide from the C‐terminus of human TK1. Using this antibody, here we demonstrate the exclusive location of TK1 in the cytoplasm of cells. Cell cycle dependent TK1 expression was studied by simultaneous fluorescence staining for TK1 and bromodeoxyuridine, by using elutriated cells, and by quantitation of the amount TK1 in relation to the cellular DNA content. TK1, which was strongly expressed in the cells in S+G2 period, raised at late G1 and decreased during mitosis. The amount of TK1 increased three folds from late G1 to G2. TK1 positive cells were demonstrated in areas of proliferation activity of various normal and malignant tissues. The new anti‐TK1 antibody works in archival specimens and is a specific marker of cell proliferation.

scholarly journals Control of thymidine kinase mRNA during the cell cycle.

1987 ◽  
Vol 7 (8) ◽  
pp. 2925-2932 ◽  
Author(s):  
D L Coppock ◽  
A B Pardee
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Gene Transcription ◽  
Half Life ◽  
Mammalian Cells ◽  
Mrna Degradation ◽  
S Phase ◽  
3T3 Cells

To investigate the mechanism which controls the onset of DNA synthesis, we examined the regulation of thymidine kinase (TK) and its mRNA in the cell cycle. TK activity provides a useful marker for the onset of the S phase in mammalian cells. The present analysis of regulation of TK mRNA in BALB/c 3T3 cells showed that (i) the increase in TK activity depended on the availability of TK mRNA, (ii) the level of TK mRNA between G0 and S increased more than 20-fold, (iii) the rate of run-on TK transcription increased at most 2- to 4-fold between the G0 and S phases, (iv) the half-life of TK mRNA was greater than 8 to 12 h in the S and M phases and decreased as cells entered quiescence, (v) the TK mRNA increase was fully blocked by inhibition of protein synthesis by only 60%, (vi) this inhibition was completely effective for up to about 10 h following serum addition and progressively much less effective when the drugs were added later. These results suggest that the appearance of TK mRNA at the beginning of the S phase in serum-stimulated 3T3 cells is controlled not only by the rate of gene transcription but importantly also by the decreased rate of mRNA degradation. Similar mechanisms may be involved in regulation of the onset of DNA synthesis and the increase in TK mRNA since both are controlled in a manner consistent with a requirement for a labile protein.

Restricted replication of adenovirus type 2 in mouse balb/3T3 cells

1986 ◽  
Vol 87 (3-4) ◽  
pp. 241-264 ◽  
Author(s):  
G. Silverstein ◽  
W. A. Strohl
Keyword(s):  
Adenovirus Type ◽  
3T3 Cells ◽  
Adenovirus Type 2

Incomplete particles of adenovirus type 2 III. Viral and cellular DNA sequences in incomplete particles

Virology ◽  
1977 ◽  
Vol 76 (1) ◽  
pp. 365-379 ◽  
Author(s):  
Sian Tjia ◽  
Ellen Fanning ◽  
Jochen Schick ◽  
Walter Doerfler
Keyword(s):  
Dna Sequences ◽  
Adenovirus Type ◽  
Cellular Dna ◽  
Adenovirus Type 2

Adenovirus type 5 induces progression of quiescent rat cells into S phase without polyamine accumulation

1982 ◽  
Vol 2 (10) ◽  
pp. 1295-1298
Author(s):  
B F Cheetham ◽  
D C Shaw ◽  
A J Bellett
Keyword(s):  
Dna Replication ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Ornithine Decarboxylase ◽  
Adenovirus Type ◽  
S Phase ◽  
Polyamine Biosynthesis ◽  
Adenosylmethionine Decarboxylase ◽  
Cellular Dna ◽  
Adenovirus Type 5

Adenovirus type 5 induces cellular DNA synthesis and thymidine kinase in quiescent rat cells but does not induce ornithine decarboxylase. We now show that unlike serum, adenovirus type 5 fails to induce S-adenosylmethionine decarboxylase or polyamine accumulation. The inhibition by methylglyoxal bis(guanylhydrazone) of the induction of thymidine kinase by adenovirus type 5 is probably unrelated to its effects on polyamine biosynthesis. Thus, induction of cellular thymidine kinase and DNA replication by adenovirus type 5 is uncoupled from polyamine accumulation.

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