Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.1.1.17 (ornithine decarboxylase)
6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the regulation of proliferation of lung alveolar epithelial type 2 cells, we have established a cell line derived from neonatal type 2 cells by transfection with the SV40 large T antigen gene. We find that this cell line, designated SV40-T2, displays the same post-transcriptional control of expression of proliferation-related genes, including c-myc, ornithine decarboxylase, thymidine kinase, and histone, that we have previously described in primary isolates of type 2 cells (Clement et al., Proc. Natl. Acad. Sci. USA 87, 318-322, 1990). Both proliferating and nonproliferating SV40-T2 cells express these genes at high levels, but their translation products are only detected in proliferating cells. Using the histone gene as an example, we have found that regulation of expression occurs at the level of transcription and of mRNA turnover, as previously described in other mammalian systems. However, in addition, regulation of expression also occurs at the level of translation of the histone mRNA, because its protein product is not detectable in nonproliferating SV40-T2 cells. We have analyzed the steps which are potentially involved in this translational regulation of histone gene expression in SV40-T2 cells. In both proliferating and nonproliferating cells, histone mRNA was found to be efficiently transported from the nucleus to the cytoplasm and to associate with the translationally active heavy polysomal fractions. These results indicate that control of histone gene expression (and perhaps that of other proliferation-related genes) in lung epithelial cells may involve either rapid and selective degradation of histone protein or binding factor(s) which modulate translational efficiency of histone mRNA.
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PMID:SV40T-immortalized lung alveolar epithelial cells display post-transcriptional regulation of proliferation-related genes. 171 83

The effects of 5-fluorouracil (FUra) treatment on thymidine kinase (TKase) activity were examined in vivo in CD8F1 mice bearing first generation CD8F1 mouse mammary tumors. TKase activity was not affected by low dose FUra25 (25 mg/kg), a dose which substantially inhibited thymidylate synthase (TSase), but was severely inhibited 24 hr following treatment with FUra100, a weekly maximally tolerated dose, as judged by activity measurements and labeling of DNA with [3H]thymidine. The amount of (FU)RNA was increased markedly with increasing FUra dose from 0.4 nmol/mg DNA at FUra25 to 2.2 nmol/mg DNA at FUra100. At FUra100, TKase activity gradually declined over 24 hr to less than 10% of the control value, remained low for a further 48 hr, and then was gradually restored to control levels by 168 hr. The loss of TKase activity followed the incorporation of FUra into RNA which peaked at 4-5 hr. TKase activity was not restored by removal of endogenous inhibitors but was restored by treatment with uridine. TKase activity was not inhibited by therapeutic levels of methotrexate (300 mg/kg). TKase from murine colon 38 carcinoma was also severely inhibited, but the activity from colon 26 was only partially (50%) inhibited. Ornithine decarboxylase was also inhibited by FUra100 treatment in the CD8F1 tumor. These results demonstrate that certain short-lived, proliferation-related enzymes are affected by FUra doses higher than those required for TSase inhibition, and this effect appears to correlate with incorporation of FUra into RNA. Thus, in some tumors high doses of FUra can inhibit salvage as well as de novo synthesis of thymidylate providing an increased block of DNA synthesis and increased therapeutic advantage.
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PMID:Loss of murine tumor thymidine kinase activity in vivo following 5-fluorouracil (FUra) treatment by incorporation of FUra into RNA. 172 9

When an 18-kDa cell surface sialoglycopeptide (SGP), isolated from intact bovine cerebral cortex cells, was incubated with exponentially growing Swiss 3T3 cells, cell proliferation was efficiently arrested. The inhibition was totally reversible since after removal of the SGP the arrested cells resumed their progress in the cell cycle in a synchronized manner for at least two divisions. Readdition of the GSP 4 h after reversal of the inhibition did not, however, affect the commitment of the cells to advance through metaphase, although progress through the cell cycle was once again inhibited after the cells reentered the G1 phase. The efficient nature of the SGP-mediated cell cycle arrest in G1 provided us with a basis to examine potential changes in the expression of several competence genes, and genes associated with mid and late G1, that have been implicated in cell cycle progression. Upon serum stimulation of quiescent Swiss 3T3 cells, the induction of c-myc and c-fos expression was not influenced by the SGP at concentrations highly inhibitory to cell cycling. Expression of JE was induced by serum, and the presence of the SGP had little effect on the expression of this growth-related gene. KC expression was not appreciably stimulated by serum although, surprisingly, the addition of the SGP resulted in a significant increase in expression. In addition, we learned that the SGP did not alter expression of ornithine decarboxylase, c-ras, or thymidine kinase, which are induced later than the genes associated with the initial stages of competence.
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PMID:Modulation of growth-related gene expression and cell cycle synchronization by a sialoglycopeptide inhibitor. 190 95

Ornithine decarboxylase (ODC) and thymidine kinase (TK) are enzymes important for DNA synthesis, a process that is critical for cell renewal and regeneration. As such, they already have been used as surrogate markers of regeneration in tissue. In the present study, the activity of these two enzymes in plasma of rats and regenerating hepatic tissue following a 70% hepatectomy were determined. The results demonstrate that the changes in these enzyme activities in plasma reflect the changes obtained in the liver tissue. Thus, blood levels of ODC and TK can be used as a less invasive and nondestructive means of monitoring the regenerative response of the liver and possibly other tissues.
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PMID:Relationship between plasma and hepatic cytosolic levels of ornithine decarboxylase (ODC) and thymidine kinase (TK) in 70% hepatectomized rats. 199 63

The hemopoietic growth factor interleukin 3 (IL-3) supports the survival and proliferation of multipotent and committed progenitor cells in vitro. To elucidate the molecular mechanisms triggered by IL-3 we studied the expression of cell cycle-related genes in a recently established human IL-3-dependent clone (M-07e). No changes in the level of expression of early (c-myc), mid (ornithine decarboxylase), or mid-late G1 (p53, c-myb) cell cycle genes were detected after restoration of IL-3 in deprived cells. The fact that only late G1-S-phase genes [proliferating cell nuclear antigen (PCNA) thymidine kinase (TK), histone H3] are modulated by IL-3 suggests that this factor may control human cell proliferation by acting at the G1-S boundary.
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PMID:Interleukin 3-dependent proliferation of the human Mo-7e cell line is supported by discrete activation of late G1 genes. 199 64

The role of conjugated bilirubin in liver regeneration after partial hepatectomy (PH) was studied in Gunn rats, in transport-mutant (TR-) rats, and in rats with extrahepatic biliary obstruction. Ornithine decarboxylase (ODC) and thymidine kinase (TK) activities in liver homogenates and immunohistochemistry of in vivo bromodeoxyuridine (BrdU) incorporation in hepatic DNA were followed as regeneration parameters at 24 and 48 hr after PH. The results relative to TK activity and BrdU incorporation were consistent with significantly delayed hepatic DNA synthesis in Gunn rats in comparison to control Wistar and TR- rats. This delay in DNA synthesis was not reflected in the hepatic ODC activity. After one week of complete common bile duct obstruction (CBO), an increased TK activity and BrdU incorporation was seen. PH following CBO resulted in a further increase in ODC activity and BrdU incorporation. TK activity did not change, however. These data relative to the regulation of hepatic DNA synthesis after PH in Gunn rats and in rats with extrahepatic biliary obstruction suggest a possible stimulatory role for conjugated bilirubin in hepatic regeneration; however, the normal hepatic DNA synthesis in TR- rats studied before PH and the subnormal DNA synthesis seen 24 hr after PH in TR- rats and in rats with CBO indicate that conjugated bilirubin does not stimulate hepatic DNA synthesis.
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PMID:Liver regeneration after partial hepatectomy in rats with defective bilirubin conjugation or biliary excretion. 200 68

8-(N,N-Diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), a putative inhibitor of intracellular calcium mobilization, causes a dose-dependent inhibition of serum-induced proliferation of arterial smooth muscle cells in culture. Neither early rise in cytosolic calcium concentration nor induction of early induced cell cycle dependent genes (c-fos, ornithine decarboxylase) are inhibited after serum stimulation in presence of 100 microM TMB-8. In contrast, expression of thymidine kinase, a gene normally induced in late-G1 phase, is entirely inhibited by TMB-8. Taken together with flow cytometry studies, these results indicate that TMB-8 blocks cell cycle progression in mid- or late-G1 phase by a mechanism not directly related to early responses to serum stimulation since TMB-8 is also effective when introduced several hours after serum stimulation.
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PMID:Influence of 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) on cell cycle progression and proliferation of cultured arterial smooth muscle cells. 200 73

Attempts have been made to use enzyme assays primarily in tissue, to predict risk of colon cancer in high risk colon cancer families, and in patients with polyposis. Efforts have also been made to predict recurrence in surgically "cured" cancer patients. The use of thymidine kinase, ornithine decarboxylase, LDH isoenzymes, and other enzymes for these purposes will be reviewed.
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PMID:Enzymes used in predicting high risk to colon cancer. 217 52

Thirteen patients who underwent 40% to 80% removal of their livers had blood samples drawn initially and daily on postoperative days 1 to 7. The enzyme marker of heightened polyamine metabolism, ornithine decarboxylase, and the indicator of DNA synthesis, thymidine kinase, were measured. In addition, the hormones (insulin, glucagon, estradiol and androgen), which in animals are known to reflect and possibly modulate regeneration, were measured. Changes in all these indices followed the same pattern as in rats, dogs and swine but at a slower rate. Ornithine decarboxylase and estradiol increased within 24 hr, but thymidine kinase and insulin rises did not become statistically significant until 3 to 5 days. Using these plasma or serum indices as surrogate measures of biochemical events in the liver itself, regeneration reached a maximum after 4 or 5 days. By computed tomography scan analysis, restoration of hepatic cell mass was not complete until 3 wk.
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PMID:Hormonal and enzymatic parameters of hepatic regeneration in patients undergoing major liver resections. 222 10

In 3T3 cells stimulated from quiescence by serum, impaired thymidine incorporation caused by inadequate supply of Zn2+ was associated with both decreased thymidine kinase activity and a comparable decrease in its mRNA concentration. In contrast, the amount of mRNA for ribosomal protein S6 was not affected, nor was the earlier increase in the activity of ornithine decarboxylase.
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PMID:A requirement for Zn2+ for the induction of thymidine kinase but not ornithine decarboxylase in 3T3 cells stimulated from quiescence. 226 79


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