Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Teleocidin, a tumor promoter, inhibited the proliferation, enhanced cytokeratin assembly and increased the type III procollagen production of PLC/PRF/5 hepatoma cells. Teleocidin transiently increased the levels of c-fos and p53 mRNAs measured by reverse transcription and polymerase chain reaction. This was followed by a reduction of c-myc mRNA and an increase of cytokeratin mRNA. The level of p120 mRNA was not remarkably altered. Sequential alterations of the expression of c-fos, p53, c-myc and cytokeratin genes induced by teleocidin may be responsible for the morphological and functional changes of hepatoma cells induced by this tumor promoter.
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PMID:Co-ordinate expression of c-fos, p53 and cytokeratin genes during the alteration of growth of human hepatoma cells. mRNA levels measured by reverse transcription and polymerase chain reaction. 138 34

We have previously reported the isolation of several temperature-sensitive (ts) mutants of F9 cells. Further investigations showed that some mutants were induced to differentiate at non-permissive temperature of cell growth, accompanied by changes in the expression of various genes, whereas others were not. During the differentiation induced by shifting up to the non-permissive temperature, a rapid and transient decrease in both c-myc and p53 mRNA levels and rapid induction of c-jun mRNA were observed. These changes were specific in differentiation-inducible mutants and were not observed in a non-inducible mutant. In both types of mutants, the level of c-myc mRNA decreased in association with growth retardation at the non-permissive temperature. The p53 mRNA, however, showed specific increase in the differentiation-inducible ts mutants. These observations suggest distinct roles for p53 and c-myc from proliferation to differentiation in teratocarcinoma stem cells.
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PMID:c-myc and p53 gene expression in the differentiation of temperature-sensitive mutants of teratocarcinoma F9 cells. 146 50

L1210 cell lines, selected for resistance to deoxyadenosine due to the loss of allosteric inhibition of ribonucleotide reductase by dATP, had altered steady-state levels of the mRNAs for c-myc, fos, and p53. Wild-type L1210 cells had constitutive steady-state levels of c-myc and p53 with little or no fos mRNA. Two different deoxyadenosine-resistant cell lines (Y8 and ED2) had elevated steady-state levels of c-myc and fos but essentially no p53 mRNA. Hydroxyurea-resistant L1210 cells had the same levels of c-myc, fos, and p53 as the wild-type cells. There was no amplification of the gene for c-myc in the Y8 or ED2 cell lines. The half-life for c-myc mRNA was essentially the same in the wild-type and the Y8 and ED2 cells. Nuclear runoff experiments showed that the rates of transcription for c-myc in the Y8 and ED2 cells were elevated and could account for the increased steady-state levels of c-myc in these two cell lines. The transcription rate for p53 mRNA was not decreased in the Y8 and ED2 cells and therefore did not account for the loss of the steady-state levels of p53 in the cells. Cycloheximide treatment of the Y8 and ED2 cells resulted in a marked increase in the steady-state p53 mRNA level, indicating that a protein which was rapidly turned over was responsible for the extremely short half-life of p53 mRNA in these two cell lines.
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PMID:Altered steady-state levels of the messenger RNAs for c-myc and p53 in L1210 cell lines resistant to deoxyadenosine. 155 Nov 29

Mouse F9 teratocarcinoma cell lines can be induced to differentiate into either parietal endoderm or embryoid bodies which contain visceral endoderm-like cells. The nature of the early molecular events involved in these two differentiation pathways has not yet been fully elucidated. Moreover, since the process of differentiation is often accompanied by changes in cell growth, it is often difficult to determine which of the events that do occur during the early stages of differentiation are a direct result of the process of differentiation and which events are indirect results that occur as a consequence of altered cell growth. In the experiments reported here we have attempted to distinguish between these two possibilities by examining the patterns of expression of a representative group of growth-associated genes (i.e., c-myc, p53, and histone H3) when F9 cell aggregates are induced to differentiate into embryoid bodies containing visceral endoderm. By analysis of the patterns of growth-associated gene expression in both retinoic acid treated and nontreated F9 cell aggregates, we were able to classify early events as differentiation-specific events (events which occurred only following retinoic acid treatment of aggregates) or nondifferentiation-specific events caused by reduction in cell growth (events which occurred even when aggregates were not treated with retinoic acid). Our results show that F9 cells differentiated into embryoid bodies containing visceral endoderm-like cell exhibit an early reduction in both growth and c-myc mRNAs which is neither retinoic acid-specific nor differentiation-specific. However, following this initial response to aggregation, constant levels of c-myc mRNA are maintained despite continued reduction in growth. Thus, it appears that alteration in c-myc expression is a differentiation-specific event along the pathway to formation of visceral endoderm. Interestingly, however, the nature and time course of this alteration in c-myc expression in F9 cells' differentiation into visceral endoderm is different from that observed in F9 cells differentiated into parietal endoderm.
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PMID:Molecular analysis of early growth-associated events during the differentiation of F9 cells into embryoid bodies. 213 1

We have used a system of nutritional manipulation to investigate whether hepatocytes of the normal liver can be primed for replication in vivo. In this system, rats that are denied protein for 3 days undergo a burst of hepatic DNA synthesis and mitosis when they are refed amino acids, while normally fed or starved rats do not respond. To determine if hepatocytes of protein deprived (PD) rats have been "primed" for replication, we examined changes in protooncogene expression in livers of PD rats to see if they would mimic the pattern of gene expression that is induced early after partial hepatectomy. c-jun, c-myc, and p53 mRNAs were elevated in livers of PD rats, while c-fos and c-ras genes were not expressed. The administration of amino acids to PD rats stimulated hepatic DNA synthesis in a shorter period than is required after partial hepatectomy and induced p53 and c-ras expression. In culture, hepatocytes from PD rats had higher levels of c-myc mRNA, underwent morphological changes more rapidly, and reached maximum rates of DNA synthesis earlier than normal hepatocytes. In both normal and primed hepatocyte cultures, transforming growth factor alpha stimulated DNA synthesis more effectively than epidermal growth factor. We conclude that hepatocytes pass through a priming stage before they proliferate and that replicative competence without DNA synthesis can be induced in hepatocytes in the normal liver.
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PMID:Induction of replicative competence ("priming") in normal liver. 220 69

To address the role of c-fos proto-oncogene we constructed a plasmid that allows constitutive expression of RNA complementary to c-fos mRNA, and stably introduced this plasmid into F9 embryonal carcinoma cells. Some F9 clones expressing c-fos antisense RNA had a reduced basal level of c-fos mRNA, and were unable to induce a c-fos mRNA as well as its protein when stimulated with phorbol ester or with interferon (IFN). Nevertheless, the ability to induce major histocompatibility class I genes following IFN treatment was not impaired in these clones. Clones expressing c-fos antisense RNA grew as rapidly as control F9 cells, and underwent differentiation after retinoic acid treatment. Unexpectedly, constitutive expression of c-myc mRNA was reduced on average by 10-fold in clones expressing c-fos antisense RNA. However, expression of the p53 gene and heat shock gene hsp 70 was not affected in these clones, indicating the existence of a specific regulatory linkage between c-fos and c-myc genes. Cycloheximide treatment led to induction of a large amount of c-fos mRNA in clones expressing c-fos antisense RNA as well as in control F9 clones. The amount of c-fos antisense RNA was also increased by cycloheximide treatment. We postulate that c-fos antisense RNA blocks expression of the endogenous c-fos gene by accelerating the degradation of c-fos mRNA and that cycloheximide treatment interferes with this degradation.
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PMID:Constitutive expression of c-fos antisense RNA blocks c-fos gene induction by interferon and by phorbol ester and reduces c-myc expression in F9 embryonal carcinoma cells. 245 69

To study the function of proto-oncogene c-fos, we prepared an antisense plasmid that expresses in mammalian cells c-fos antisense RNA which is complementary to the endogenous c-fos mRNA. Upon transfection into undifferentiated F9 EC cells, the antisense plasmid directed constitutive expression of a large amount of c-fos antisense RNA. These cells were very low in the basal level of c-fos message and were unable to induce c-fos message when stimulated with interferon or phorbol ester. The failure to induce c-fos message led to the blockade of c-fos protein expression in these cells. Thus, these cells represented a c-fos defective phenotype. The blockade of c-fos gene expression seen in antisense-cells could be caused by rapid degradation of the c-fos message, since c-fos mRNA expression was rescued in these cells when treated with protein synthesis inhibitor, cycloheximide. We found that expression of c-myc gene was down-regulated in c-fos antisense-cells: Although control undifferentiated F9 cells constitutively expressed a high level of c-myc message, the antisense cells had a much lower amount of c-myc mRNA. Since p53 and heat shock gene 70 were expressed at comparable levels in control and antisense cells, c-myc gene expression appears to be regulated by c-fos gene in F9 EC cells. Lastly, these antisense cells grew as rapidly as control F9 cells and underwent differentiation after retinoic acid treatment, indicating that c-fos expression is not a prerequisite for differentiation of F9 cells.
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PMID:c-fos antisense RNA blocks expression of c-fos gene in F9 embryonal carcinoma cells. 246 66

The induction of murine erythroleukemia cells (MELC) to terminal differentiation by hexamethylene bisacetamide (HMBA) is accompanied by changes in the levels of c-myb and c-myc mRNA, and in p53 protein levels. We simultaneously examined the effects of HMBA on modulation of c-myb, c-myc and p53 mRNA and protein levels, and examined the relationship between these changes and commitment to terminal cell division. In MELC cultured with HMBA, c-myb protein levels paralleled c-myb mRNA levels except at 24h, when the protein level was equivalent to the level in control cultures, whereas the mRNA had decreased. The c-myc protein paralleled c-myc mRNA throughout induction. The p53 mRNA and protein behaved in a discordant fashion. The p53 protein decreased to very low levels between 4 and 8 h and remained low, while the mRNA, which initially decreased, reaccumulated by 24 and 48 h. Transfer of MELC after 12 to 48 h of culture with HMBA to medium without inducer resulted in rapid (less than 3 h) reaccumulation of the c-myb mRNA, c-myb protein, and p53 protein, and cessation of recruitment of cells to commitment. Cells already induced to commit to terminal differentiation continued to express the differentiated phenotype.
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PMID:Modulation of the c-myb, c-myc and p53 mRNA and protein levels during induced murine erythroleukemia cell differentiation. 264 54

Cell lines have been permanently established from BALB/c3T3 cells that constitutively express either the murine p53, the human IGF-1 gene, or both (Gai et al., 1988). The derivative cell lines grow well in platelet-poor plasma or in serum-free medium supplemented with the appropriate growth factors, while BALB/c3T3 cells do not grow in platelet-poor plasma, nor do they grow in serum-free medium unless supplemented with both platelet-derived growth factor and insulin (or IGF-1). In BALB/c3T3 cells, steady-state levels of c-myc mRNA decrease promptly and sharply once the cells are transferred to platelet-poor plasma. In the derivative cell lines, constitutively expressing p53, IGF-1, or both, c-myc mRNA levels remain elevated and actually increase when the cells are transferred to platelet-poor plasma. In serum-free medium, the c-myc mRNA levels decreased in BALB/c3T3 cells, as well as in the derivative cell lines. However, in the latter cell lines, but not in BALB/c3T3, the addition of platelet-poor plasma or insulin again increased the expression of c-myc. The increase in c-myc mRNA levels could be partially explained by an increase in transcription. These results indicate that in certain cell lines the expression of c-myc mRNA can be induced by insulin or platelet-poor plasma.
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PMID:Regulation of c-myc mRNA levels by insulin or platelet-poor plasma. 269 56

Stimulation of beta-adrenoreceptors in rat parotid acinar cells in vitro by the beta-adrenergic agonist isoproterenol induces steady-state levels of c-fos mRNA and c-fos protein in these cells. A dramatic increase in the steady-state levels of c-fos mRNA was observed at 60 min, followed by a decrease at 2 h with a second peak at 4 h. c-fos induction in rat parotid acinar cells in vitro seems to be mediated by cAMP. Increased levels of p53 and c-myc mRNA were detected only at 60 min. c-abl and c-sis were also induced by isoproterenol but in a pattern different from that seen with c-fos. c-abl was the only oncogene in rat parotid gland which showed increased expression after chronic isoproterenol treatment of rats. In rat parotid acinar cells we observed no correlation between DNA synthesis and c-fos induction.
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PMID:Regulation of proto-oncogenes in rat parotid acinar cells in vitro after stimulation of beta-adrenergic receptors. 284 68


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