Journal articles on the topic 'Fos oncogenes'
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1
Claycomb, W. C., and N. A. Lanson. "Proto-oncogene expression in proliferating and differentiating cardiac and skeletal muscle." Biochemical Journal 247, no. 3 (November 1, 1987): 701–6. http://dx.doi.org/10.1042/bj2470701.
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We have examined the expression of 13 proto-oncogenes in proliferating and terminally differentiated cardiac and skeletal muscle. Total RNA was prepared from intact ventricular cardiac-muscle tissue and from purified ventricular cardiac-muscle cells of neonatal and adult rats and from cultured proliferating and terminally differentiated L6A1 rat skeletal-muscle cells. cDNA probes for histone H4, thymidine kinase, myosin heavy chain and M-creatine kinase were used to assess cellular proliferation and differentiation. Oncogenes c-myc, c-raf, c-erb-A, c-ras-H, c-ski, and c-sis were expressed in both proliferating and differentiated cardiac muscle tissue and cells, whereas c-myb expression was not observed in either. c-src was expressed only in neonatal cardiac muscle tissue and cells. c-fms, c-abl, and c-ras-K were expressed in tissue from both neonatal and adult animals but only in purified cells from neonatal animals. c-fes/fps was expressed only in neonatal cardiac muscles cells. c-fos expression was not observed in cardiac-muscle tissue from either neonatal or adult rats, but surprisingly was abundantly expressed in freshly isolated cardiac-muscle cells from animals of both ages. These results emphasize that biochemical analysis using intact cardiac-muscle tissue may not necessarily reflect muscle-specific cell processes. They also show that the expression of c-fos can be activated by the cell isolation procedure. c-myc, c-ski, c-ras-H, c-ras-K, c-abl, c-raf and c-erb-A were expressed in both proliferating and terminally differentiated skeletal-muscle cells, whereas c-myb, c-fos, c-src and c-fms transcripts were observed only in proliferating cells. c-fes/fps and c-sis were not expressed in dividing or fused skeletal-muscle cells. These results demonstrate unique tissue and cell-specific patterns of proto-oncogene expression and suggest that these genes may be involved with the regulation of cellular proliferation and terminal differentiation in striated muscle.
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Introna, M., T. A. Hamilton, R. E. Kaufman, D. O. Adams, and R. C. Bast. "Treatment of murine peritoneal macrophages with bacterial lipopolysaccharide alters expression of c-fos and c-myc oncogenes." Journal of Immunology 137, no. 8 (October 15, 1986): 2711–15. http://dx.doi.org/10.4049/jimmunol.137.8.2711.
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Abstract Expression of the c-fos, c-myc, and c-fms proto-oncogenes has been studied in thioglycollate-elicited murine peritoneal macrophages after exposure to lipopolysaccharide (LPS). After incubation with LPS (20 ng/ml), a transient and rapid induction of the expression of c-fos and c-myc oncogenes could be observed, whereas the RNA levels for c-fms were not affected. Treatment with lipid A, the active moiety of the LPS molecule, increased the c-fos and c-myc expression to a comparable degree. Similar induction of c-fos and c-myc was observed after treatment with phorbol myristate acetate, suggesting that this effect of LPS on murine macrophages might be mediated through stimulation of protein kinase C. Under similar experimental conditions, LPS treatment of macrophages did not trigger DNA synthesis. Treatment with LPS blocked DNA synthesis in macrophages treated with L cell-conditioned medium containing colony-stimulating factor. Thus changes in c-fos and c-myc expression may be elements in the complex series of biochemical events that contribute to macrophage activation and are not necessarily related to induction or priming for cellular proliferation.
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Chrysovergis, Aristeidis, Vasileios Papanikolaou, Nicholas Mastronikolis, Despoina Spyropoulou, Maria Adamopoulou, Evangelos Tsiambas, Vasileios Ragos, et al. "C-Fos Digital Expression Analysis in Human PapillomavirusRelated Oral Squamous Cell Carcinoma." Asian Pacific Journal of Cancer Biology 6, no. 2 (May 14, 2021): 117–21. http://dx.doi.org/10.31557/apjcb.2021.6.2.117-121.
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Background: Fos Proto-Oncogene (c-Fos) represents a well analyzed gene involved in solid malignancies’ development and progression. The corresponding protein forms heterodimer with c-jun, a strong transcription factor. C-Fos/c-Jun complex influences critically the intracellular signal transduction to the nucleus. Our aim was to detect and evaluate c-Fos protein expression patterns in oral squamous cell carcinomas (OSCC) tissues. Materials and Methods: Fifty (n=50) formalin-fixed, paraffin-embedded primary OSCCs tissue sections were used. Immunohistochemistry and digital image analysis were implemented for identifying and evaluating c-Fos protein expression levels, respectively. Results: C-Fos protein over expression (moderate to high imunostaining intensity values) was observed in 28/50 (56%) tissue cores, whereas low expression rates were detected in the rest of the examined cases (22/50- 44%). C-Fos overall expression was strongly associated with the stage and grade of the examined tumors (p=0.014, p=0.003, respectively) and also with Human papillomavirus (HPV) persistent infection (p=0.004). c-Fos up regulation is frequently observed in OSCCs. Conclusion: C-Fos high expression levels are correlated with an aggressive phenotype (advanced stage/lymph node metastasis) in patients with OSCC, especially in HPV positive cases, especially High Risk subtypes. Due to its elevated oncogenic activity, c-Fos should be a target for novel therapeutic strategies in OSCC combined or not with other oncogenes involving in signaling transduction pathways.
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Sariban, E., T. Mitchell, J. Griffin, and D. W. Kufe. "Effects of interferon-gamma on proto-oncogene expression during induction of human monocytic differentiation." Journal of Immunology 138, no. 6 (March 15, 1987): 1954–58. http://dx.doi.org/10.4049/jimmunol.138.6.1954.
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Abstract Activation of the proto-oncogenes c-fos, c-fms, and c-sis has been associated with monocytic differentiation. In the present study, we monitored the relationship of c-myc, c-fos, c-fms, and c-sis expression to interferon-gamma (IFN-gamma)-induced monocytic differentiation of human HL-60 promyelocytic leukemia cells. Treatment of HL-60 cells with 500 U/ml IFN-gamma arrested cell proliferation after 3 days. Appearance of the monocytic phenotype was manifested within 24 hr of IFN-gamma exposure by: increased nitroblue tetrazolium reduction; increased cell surface expression of the HLA-DR, Mo1, and MY4 antigens; and induction of transcripts for the second component of complement (C2) and tumor necrosis factor. In contrast, c-myc expression decreased as a later event after 72 hr of IFN-gamma exposure, and c-fos transcripts remained undetectable until 5 days of treatment. Furthermore, c-fms RNA and transcripts for the macrophage marker apolipoprotein E were induced only after 7 days. Finally, expression of the c-sis proto-oncogene at the RNA and protein levels remained undetectable after induction with IFN-gamma. These findings would thus suggest that declines in c-myc RNA, as well as induction of c-fos, c-fms, and c-sis expression, are not requisite events in the commitment of HL-60 cells to IFN-gamma-induced monocytic differentiation. Expression of c-fos and c-fms, however, is associated with acquisition of markers associated with maturation to macrophages.
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Kousvelari, E., C. K. Yeh, P. M. Mertz, and M. Chinchetru. "Regulation of Proto-Oncogenes and Salivary Gland Cell Proliferation." Advances in Dental Research 4, no. 1 (June 1990): 61–68. http://dx.doi.org/10.1177/08959374900040010901.
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The proto-oncogenes c-fos and c-jun express proteins targeted into the nucleus. The fos and jun proteins form a heterodimeric complex that binds to regulatory elements in the promoter region of specific genes to influence their transcription. Through such a mechanism, the fos and jun proteins have been suggested to link extracellular stimuli to short- and long-term functional changes in cells. Recently we have shown that β-adrenergic receptor stimulation of rat parotid acinar cells in vitro or addition of 8-BrcAMP in a rat submandibular cell line (RSMT-A5) increases the expression of the c-fos gene in a time-dependent manner. Maximal responses were found at 60 min. The expression of the c-fos gene did not correlate with DNA synthesis in either cell type, and c-fos transcripts were undetectable in the glands of animals treated for eight days with isoproterenol. The new data presented here extended our observations to c-jun gene expression in both salivary cell types where a similar pattern of expression for this proto-oncogene was seen. Conversely, treatment of rats with isoproterenol for nine days resulted in the appearance of two c-abl mRNAs of unique size, in addition to the known 5.3-kb c-abl transcripts. The data suggest that β-adrenergic receptor stimulation or exposure to 8-BrcAMP induces the early expression of the "nuclear proto-oncogenes" c-fos and c-jun before changes are noted in salivary epithelial cell proliferation. Differences in c-abl mRNA size, occurring later, may be associated with the morphological and biochemical changes known to occur in rat parotid glands after chronic β-adrenoreceptor stimulation.
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Kaufmann, Y., T. Silverman, B. Z. Levi, and K. Ozato. "Induction of c-ets and c-fos gene expression upon antigenic stimulation of a T cell hybridoma with inducible cytolytic capacity." Journal of Experimental Medicine 166, no. 3 (September 1, 1987): 810–15. http://dx.doi.org/10.1084/jem.166.3.810.
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Expression of cellular oncogenes was studied in a T cell hybridoma that undergoes cytolytic activation when stimulated by specific antigen or by anti-Thy-1 antibody. The activation occurs without induction of hybridoma proliferation, providing a model to examine oncogene expression during functional differentiation of lymphocytes. We found that c-fos and c-ets-1 mRNAs were transiently induced at high levels in the hybridoma 30 min and 4 h after stimulation, respectively. c-myc and c-ets-2 oncogenes were constitutively expressed in the hybridoma and their mRNA levels were unaffected during 4 h of stimulation, although c-myc expression was reduced in the later stage of stimulation. Inhibitors of T cell activation, cyclosporin A and anti-LFA-1 antibody, blocked the induction of c-fos and c-ets-1 mRNAs without reducing the levels of c-myc and c-ets-2. The results indicate that the functional activation of the CTL hybridoma is associated with induction of c-fos and c-ets-1 genes.
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Ransone, Lynn J., and Inder M. Verma. "Nuclear Proto-Oncogenes Fos and Jun." Annual Review of Cell Biology 6, no. 1 (November 1990): 539–57. http://dx.doi.org/10.1146/annurev.cb.06.110190.002543.
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Zabulionis, R. B., B. G. Atkinson, J. D. Procunier, and D. B. Walden. "Maize (Zea mays L.) DNA sequences homologous to the oncogenes myb, ras, and src." Genome 30, no. 5 (October 1, 1988): 820–24. http://dx.doi.org/10.1139/g88-132.
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The presence of genes that may govern cell division and differentiation is being investigated in the agronomically important higher plant Zea mays. Heterologous animal oncogene probes (v-myb, v-fos, v-src, and v-Ki-ras) were hybridized to Southern-blotted endonuclease-restricted fragments of maize DNA under conditions that allowed up to 28% mismatch between the probe and genomic sequence. Human, yeast, and Escherichia coli endonuclease restricted DNA served as controls for the hybridization conditions used. The Southern blotted DNAs were hybridized with probes to ribosomal DNA and pBR322 to ensure that the observed hybridization signals were not due to spurious binding or contamination of the oncogene probes. Maize DNA sequences homologous to v-myb, v-src, and v-Ki-ras were detected. No maize sequences homologous to the v-fos probe were detected. The oncogene probes did not detect any homologous sequences in E. coli DNA and all the reported homologous bands in human and yeast DNA were observed. These results illustrate the evolutionary conservation of animal proto-oncogenes within the plant kingdom, and suggest that these sequences may play a role in the replication and differentiation of plant cells.Key words: oncogenes, v-myb, v-fos, v-src, v-Ki-ras, Zea mays.
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Gutman, A., C. Wasylyk, and B. Wasylyk. "Cell-specific regulation of oncogene-responsive sequences of the c-fos promoter." Molecular and Cellular Biology 11, no. 10 (October 1991): 5381–87. http://dx.doi.org/10.1128/mcb.11.10.5381-5387.1991.
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We have identified oncogene-responsive sequences in the human c-fos promoter that mediate induction of transcription by several nonnuclear oncoproteins and the tumor promoter TPA. These sequences are regulated in a cell-specific manner. (i) In NIH 3T3 cells, the CArG box of the c-fos promoter is sufficient to mediate activation by oncogenes. (ii) In contrast, in HeLa cells, additional flanking sequences are also required, including the outer arm of the serum response element and the FAP site. We also show that the serum response factor, which binds to the CArG box, activates transcription in vivo in NIH 3T3 cells but not in HeLa cells. Finally, we present evidence that the intracellular level of the c-Fos protein could be a major determinant of cell-specific regulation of these oncogene-responsive elements of the c-fos promoter.
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Gutman, A., C. Wasylyk, and B. Wasylyk. "Cell-specific regulation of oncogene-responsive sequences of the c-fos promoter." Molecular and Cellular Biology 11, no. 10 (October 1991): 5381–87. http://dx.doi.org/10.1128/mcb.11.10.5381.
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We have identified oncogene-responsive sequences in the human c-fos promoter that mediate induction of transcription by several nonnuclear oncoproteins and the tumor promoter TPA. These sequences are regulated in a cell-specific manner. (i) In NIH 3T3 cells, the CArG box of the c-fos promoter is sufficient to mediate activation by oncogenes. (ii) In contrast, in HeLa cells, additional flanking sequences are also required, including the outer arm of the serum response element and the FAP site. We also show that the serum response factor, which binds to the CArG box, activates transcription in vivo in NIH 3T3 cells but not in HeLa cells. Finally, we present evidence that the intracellular level of the c-Fos protein could be a major determinant of cell-specific regulation of these oncogene-responsive elements of the c-fos promoter.
11
McNerney, R., D. Darling, and A. Johnstone. "Differential control of proto-oncogene c-myc and c-fos expression in lymphocytes and fibroblasts." Biochemical Journal 245, no. 2 (July 15, 1987): 605–8. http://dx.doi.org/10.1042/bj2450605.
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In lymphocytes stimulated with the mitogen phytohaemagglutinin, an inhibitor of the enzyme ADP-ribosyltransferase (ADPRT) completely blocks the proliferative response and the increase in expression of the proto-oncogene c-myc without affecting c-fos significantly. Conversely, in fibroblasts the serum-induced growth is not affected by the ADPRT inhibitor, and both oncogenes are dramatically super-induced. Hence there are differences between lymphocyte and fibroblast early responses to mitogenic stimulation and also between regulation of c-fos and c-myc gene expression.
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McBride, K., L. Robitaille, S. Tremblay, S. Argentin, and M. Nemer. "fos/jun repression of cardiac-specific transcription in quiescent and growth-stimulated myocytes is targeted at a tissue-specific cis element." Molecular and Cellular Biology 13, no. 1 (January 1993): 600–612. http://dx.doi.org/10.1128/mcb.13.1.600-612.1993.
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Unlike that of skeletal muscle cells in which growth and differentiation appear mutually exclusive, growth stimulation of cardiac cells is characterized by transient expression of early response nuclear proto-oncogenes as well as induction of several cardiac-specific markers. This observation led to the speculation that these proto-oncogenes, particularly c-fos and c-jun, might act as positive regulators of cardiac transcription. We have examined the role of c-jun and c-fos in basal and growth-stimulated cardiac transcription, using the cardiac-specific atrial natriuretic factor (ANF) gene as a marker. The results indicate that c-jun and c-fos are negative regulators of ANF transcription. Inducers of jun and fos activity, such as mitogens and growth factors, inhibited endogenous ANF transcripts. In transient cotransfection assays, jun and fos were able to trans-repress the ANF promoter in both quiescent and alpha 1-adrenergic stimulated myocytes. This repression was specific to myocyte cultures and was not observed in nonmuscle cells. Deletion analysis indicated that repression does not require typical AP-1-binding sites (tetradecanoyl phorbol acetate response elements) or serum response elements but is targeted at a cardiac-specific element within the ANF promoter. Various Fos-related proteins, including Fra-1, Fos B, and v-Fos, were able to trans-repress ANF transcription. In addition, C-terminal c-fos mutants which no longer repress transcription of such early growth response genes as c-fos and EGR-1 retained the ability to repress ANF transcription. Repression by c-jun occurs via the N-terminal activation domain and does not require the DNA-binding domain, suggesting that proto-oncogene repression involves interaction with one or more limiting cardiac-specific coactivators.
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McBride, K., L. Robitaille, S. Tremblay, S. Argentin, and M. Nemer. "fos/jun repression of cardiac-specific transcription in quiescent and growth-stimulated myocytes is targeted at a tissue-specific cis element." Molecular and Cellular Biology 13, no. 1 (January 1993): 600–612. http://dx.doi.org/10.1128/mcb.13.1.600.
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Unlike that of skeletal muscle cells in which growth and differentiation appear mutually exclusive, growth stimulation of cardiac cells is characterized by transient expression of early response nuclear proto-oncogenes as well as induction of several cardiac-specific markers. This observation led to the speculation that these proto-oncogenes, particularly c-fos and c-jun, might act as positive regulators of cardiac transcription. We have examined the role of c-jun and c-fos in basal and growth-stimulated cardiac transcription, using the cardiac-specific atrial natriuretic factor (ANF) gene as a marker. The results indicate that c-jun and c-fos are negative regulators of ANF transcription. Inducers of jun and fos activity, such as mitogens and growth factors, inhibited endogenous ANF transcripts. In transient cotransfection assays, jun and fos were able to trans-repress the ANF promoter in both quiescent and alpha 1-adrenergic stimulated myocytes. This repression was specific to myocyte cultures and was not observed in nonmuscle cells. Deletion analysis indicated that repression does not require typical AP-1-binding sites (tetradecanoyl phorbol acetate response elements) or serum response elements but is targeted at a cardiac-specific element within the ANF promoter. Various Fos-related proteins, including Fra-1, Fos B, and v-Fos, were able to trans-repress ANF transcription. In addition, C-terminal c-fos mutants which no longer repress transcription of such early growth response genes as c-fos and EGR-1 retained the ability to repress ANF transcription. Repression by c-jun occurs via the N-terminal activation domain and does not require the DNA-binding domain, suggesting that proto-oncogene repression involves interaction with one or more limiting cardiac-specific coactivators.
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Annunziata, Christina M., Lidia Hernandez, R. Eric Davis, Adriana Zingone, Laurence Lamy, Lloyd T. Lam, Elaine M. Hurt, Arthur L. Shaffer, W. Michael Kuehl, and Louis M. Staudt. "A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression." Blood 117, no. 8 (February 24, 2011): 2396–404. http://dx.doi.org/10.1182/blood-2010-04-278788.
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Abstract Modulating aberrant transcription of oncogenes is a relatively unexplored opportunity in cancer therapeutics. In approximately 10% of multiple myelomas, the initiating oncogenic event is translocation of musculoaponeurotic fibrosarcoma oncogene homolog (MAF), a transcriptional activator of key target genes, including cyclinD2. Our prior work showed that MAF is up-regulated in an additional 30% of multiple myeloma cases. The present study describes a common mechanism inducing MAF transcription in both instances. The second mode of MAF transcription occurred in myelomas with multiple myeloma SET domain (MMSET) translocation. MMSET knockdown decreased MAF transcription and cell viability. A small-molecule screen found an inhibitor of mitogen-activated protein kinase kinase (MEK), which activates extracellular signal-regulated kinase (ERK)-MAP kinases, reduced MAF mRNA in cells representing MMSET or MAF subgroups. ERK activates transcription of FOS, part of the AP-1 transcription factor. By chromatin immunoprecipitation, FOS bound the MAF promoter, and MEK inhibition decreased this interaction. MEK inhibition selectively induced apoptosis in MAF-expressing myelomas, and FOS inactivation was similarly toxic. Reexpression of MAF rescued cells from death induced by MMSET depletion, MEK inhibition, or FOS inactivation. The data presented herein demonstrate that the MEK-ERK pathway regulates MAF transcription, providing molecular rationale for clinical evaluation of MEK inhibitors in MAF-expressing myeloma.
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Haskill, S., C. Johnson, D. Eierman, S. Becker, and K. Warren. "Adherence induces selective mRNA expression of monocyte mediators and proto-oncogenes." Journal of Immunology 140, no. 5 (March 1, 1988): 1690–94. http://dx.doi.org/10.4049/jimmunol.140.5.1690.
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Abstract Adherence is an important regulatory signal for several monokines and the proto-oncogenes c-fms and c-fos in human peripheral blood monocytes. Although there is little if any constitutive expression of the IL-1 beta, TNF-alpha and CSF-1 genes in freshly isolated monocytes, adherence is sufficient to induce high steady-state levels of mRNA for TNF and c-fos and more slowly that of CSF-1. Expression of mRNA for the CSF-1R gene, c-fms, was transiently down-regulated by 4 h. In contrast, the induction of high levels of IL-1 beta mRNA were achieved independent of culture conditions. Although all of these genes could be induced by adherence, actual secretion of the mediators required the exposure to a second signal derived from LPS. Thus adherence rapidly primes monocytes for a variety of inflammatory responses, the magnitude of which depends on the nature of a second "activating" signal. It is likely that some of these products act locally as paracrine or autocrine factors to further regulate the phenotype of the differentiating macrophage.
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Zullo, J. N., and D. V. Faller. "P21 v-ras inhibits induction of c-myc and c-fos expression by platelet-derived growth factor." Molecular and Cellular Biology 8, no. 12 (December 1988): 5080–85. http://dx.doi.org/10.1128/mcb.8.12.5080-5085.1988.
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The viral oncogene v-ras inhibited the platelet-derived growth factor (PDGF)-induced upregulation of c-myc and c-fos proto-oncogene expression in fibroblast monolayers. These v-ras-containing cells proliferated in the absence of c-myc induction and no longer required PDGF to support growth. Fibroblasts expressing v-ras continued to express the same number of functional PDGF receptors on their surface as uninfected cells, yet the usual induction of transcription of the genes c-myc, c-fos, and JE in response to PDGF stimulation did not occur in the presence of newly introduced v-ras or chronic v-ras gene expression, and synthesis of c-myc protein did not occur. This inhibitory effect on growth factor-mediated induction of cellular proto-oncogenes was specific for PDGF in that induction of the c-myc and c-fos genes by certain other factors was not impaired.
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Zullo, J. N., and D. V. Faller. "P21 v-ras inhibits induction of c-myc and c-fos expression by platelet-derived growth factor." Molecular and Cellular Biology 8, no. 12 (December 1988): 5080–85. http://dx.doi.org/10.1128/mcb.8.12.5080.
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The viral oncogene v-ras inhibited the platelet-derived growth factor (PDGF)-induced upregulation of c-myc and c-fos proto-oncogene expression in fibroblast monolayers. These v-ras-containing cells proliferated in the absence of c-myc induction and no longer required PDGF to support growth. Fibroblasts expressing v-ras continued to express the same number of functional PDGF receptors on their surface as uninfected cells, yet the usual induction of transcription of the genes c-myc, c-fos, and JE in response to PDGF stimulation did not occur in the presence of newly introduced v-ras or chronic v-ras gene expression, and synthesis of c-myc protein did not occur. This inhibitory effect on growth factor-mediated induction of cellular proto-oncogenes was specific for PDGF in that induction of the c-myc and c-fos genes by certain other factors was not impaired.
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Mifflin, David, and John J. Robinson. "Proto-oncogene homologous sequences in the sea urchin genome." Bioscience Reports 8, no. 5 (October 1, 1988): 415–19. http://dx.doi.org/10.1007/bf01121638.
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Using probes specific for several oncogenes/proto-oncogenes we have performed gel blot hybridization analyses of genomic DNA isolated from the sea urchin Strongylocentrotus droebachiensis. Probes prepared from v-erbB, v-myc, c-myb and v-fps were found to hybridize with discrete fragments of HindIII digested genomic DNA. In contrast, probes prepared from v-abl, v-fos, v-sis, v-src, and v-mos either hybridized with multiple fragments, indicating non-specific binding, or failed to hybridize at all above background levels. These results clearly demonstrate the presence of proto-oncogene homologous sequences in the sea urchin genome.
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Wu, Bin. "Expression of c-fos and c-jun proto-oncogenes by ovine preimplantation embryos." Zygote 4, no. 3 (August 1996): 211–17. http://dx.doi.org/10.1017/s0967199400003129.
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SummaryThe c-fos and c-jun proto-oncogenes are involved in the regulation of gene expression, cell proliferation, differentiation and tumorigenesis. Embryogenesis, like tumorigenesis, involves dramatic cell growth, cleavage and differentiation processes. Activation of the c-fos and c-jun proto-oncogenes in sheep conceptuses during the period of rapid growth and elongation was examined using reverse transcription and polymerase chain reaction (RT-PCR). The specificity of PCR products was determined by Southern blot hybridisation analysis with a non-radioactive DNA probe. A band corresponding to a 507 bp fragment (predicted amplified c-fos gene cDNA product) was observed in 3 of 9 day-13, 1 of 4 day-14 and 1 of 2 day-16 embryos. Meanwhile, a 400 bp c-jun transcript was aslo detected in 1 or 2 day-12, 3 of 9 day-13 and 2 of 2 day-16 embroyos. These results suggest that mRNA transcripts of c-fos and c-jun proto-oncogenes were specifically expressed during the period of ovine embryonic elongation and may have a possible role in preimplantation embryonic development of sheep.
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Green, N. K., M. D. Gammage, J. A. Franklyn, and M. C. Sheppard. "Regulation by thyroid status of c-myc, c-fos and H-ras mRNAs in the rat myocardium." Journal of Endocrinology 130, no. 2 (August 1991): 239–44. http://dx.doi.org/10.1677/joe.0.1300239.
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ABSTRACT Effects of thyroid status on expression of a variety of myocardial genes, such as those encoding contractile proteins, have been reported, as well as interactions between thyroid hormones and developmental and haemodynamic regulation of contractile protein synthesis. In addition, it is clear that developmental and haemodynamic factors regulate expression of specific proto-oncogenes, including c-myc, c-fos and H-ras, in the myocardium but the effect of thyroid status on such proto-oncogene products, which are proposed to play a critical signal-transducing role in the heart, has been previously unexplored. In order to determine whether changes in thyroid status are associated with changes in expression of these putative intracellular signals, we examined the effect of hypothyroidism and tri-iodothyronine (T3) treatment on myocardial levels of c-myc, c-fos and H-ras mRNAs in the rat. The induction of hypothyroidism was associated with a marked increase in myocardial c-myc, c-fos and H-ras mRNAs, changes reversed by 72 h of T3 replacement. Administration of T3 to euthyroid rats had no significant effect on myocardial c-myc or c-fos mRNAs, but inhibition of H-ras mRNA by T3 was evident. These observations demonstrating influences of thyroid status on expression of specific proto-oncogenes suggest that thyroid hormones, as well as exerting direct effects on expression of functionally important myocardial genes, also interact with the cellular transduction pathways mediated by the products of the c-myc, c-fos and H-ras genes. Journal of Endocrinology (1991) 130, 239–244
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Green, Nicola K., Jayne A. Franklyn, Vasken Ohanian, Anthony M. Heagerty, and Michael D. Gammage. "Transfection of Cardiac Muscle: Effects of Overexpression of c-myc and c-fos Proto-Oncogene Proteins in Primary Cultures of Neonatal Rat Cardiac Myocytes." Clinical Science 92, no. 2 (February 1, 1997): 181–88. http://dx.doi.org/10.1042/cs0920181.
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1. Studies of cells transfected with specific expression vectors allow functions of specific gene products to be investigated. We first established optimum conditions for transfection of neonatal cardiac myocytes in primary culture. Increased proto-oncogene expression has been implicated in the development of cardiac hypertrophy; we therefore wished to examine the effects of overexpression of the c-myc and c-fos proto-oncogenes induced by cell transfection on cell growth. 2. Neonatal rat ventricular myocytes were transfected by electroporation, voltage and capacitance settings were optimized and these conditions were then used to transfect expression vectors encoding MYC and FOS proteins into this cell type. Effects on cell number, DNA synthesis and protein content were determined. 3. Increased expression of c-myc and c-fos in cells transfected with proto-oncogene expression vectors was confirmed by Northern and Western blotting. Increases in cardiac myocyte cell number, DNA synthesis and total cellular protein were observed in cells transfected with either c-myc or c-fos expression vectors compared with cells transfected with non-coding vectors. 4. Overexpression of MYC and FOS proteins results in hyperplastic rather than hypertrophic growth of the neonatal rat heart, providing evidence for a role of these proteins in the control of myocardial growth.
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Klemsz, M. J., L. B. Justement, E. Palmer, and J. C. Cambier. "Induction of c-fos and c-myc expression during B cell activation by IL-4 and immunoglobulin binding ligands." Journal of Immunology 143, no. 3 (August 1, 1989): 1032–39. http://dx.doi.org/10.4049/jimmunol.143.3.1032.
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Abstract The data presented here indicated that both membrane Ig and IL-4 receptors transduce signals across the plasma membrane of quiescent B cells, which results in the induction of c-fos and c-myc proto-oncogene mRNA expression. Monoclonal anti-Ig antibodies with specificity for mu, delta, or kappa chains, regardless of mitogenicity, induced increased c-fos and c-myc mRNA expression with kinetics and magnitude similar to that observed following stimulation of B cells with IL-4. Maximal levels of c-fos mRNA, approximately 30-fold over background, were observed 30 min after stimulation. Maximal levels of c-myc mRNA, approximately 10-fold over background, were observed 60 min after stimulation. Phorbol myristate acetate alone induced expression of these two oncogenes in a similar fashion, suggesting that protein kinase C may be involved in the regulation of their expression following anti-Ig crosslinking. Ionomycin induced only a small increase in c-myc and c-fos message (three- to four-fold), and did not synergize with phorbol myristate acetate, suggesting that the membrane Ig-mediated calcium mobilization may not play a major role in regulation of c-myc or c-fos expression in mouse B cells. In vitro nuclear run-on analyses indicate that c-myc expression is primarily regulated post-transcriptionally, whereas c-fos expression is regulated at the level of transcription. Anti-sense transcription was found to be constitutive for both the c-myc and C-fos loci and was further induced by anti-Ig and IL-4, suggesting an additional mechanism for regulation of these genes. The observation that both anti-Ig and IL-4 regulate the expression of c-fos and c-myc suggests that multiple second messenger generating systems regulate the expression of these oncogenes in normal B cells and that their expression may be necessary, but is not sufficient to drive quiescent B cells into cell cycle.
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Skouv, Jan, Ilona Kryspin-Sørensen, Henrik Frandsen, Eva Selzer Rasmussen, and Jes Forchhammer. "The Reducing Agent Dithiothreitol (DTT) Increases Expression of c-myc and c-fos Proto-oncogenes in Human Cells." Alternatives to Laboratory Animals 23, no. 4 (July 1995): 497–503. http://dx.doi.org/10.1177/026119299502300413.
Full textAbstract:
— The objective of the present study was to assess the possible tumour promoting activity of the food mutagen 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5- b]pyridine ( N-OH-PhIP), by studying its influence on the expression of three genes considered to be of relevance in the tumour promotion step. The genes were two proto-oncogenes, c- fos and c- myc, and the tumour suppressor gene, p53. We observed that the expression of the c- fos and c- myc genes was induced when human bladder epithelial cells were treated with a standard solution of N-OH-PhIP and dithiothreitol (DTT), previously shown to be genotoxic. However, when cells were treated with DTT alone, the expression of c- fos and c- myc was also transiently induced. We therefore conclude that DTT, and not N-OH-PhIP, induced oncogene expression. Induction of both c- fos and c- myc expression by a reducing agent, DTT, which is frequently used in in vitro toxicology studies, is a novel observation that suggests the need for a cautious interpretation of such studies.
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O'Hara, B. M., H. P. Klinger, T. Curran, Y. D. Zhang, and D. G. Blair. "Levels of fos, ets2, and myb proto-oncogene RNAs correlate with segregation of chromosome 11 of normal cells and with suppression of tumorigenicity in human cell hybrids." Molecular and Cellular Biology 7, no. 8 (August 1987): 2941–46. http://dx.doi.org/10.1128/mcb.7.8.2941-2946.1987.
Full textAbstract:
The tumorigenicity in nude mice of human carcinoma-derived D98AH2 (D98) cells is suppressed when cell hybrids are made by fusing these cells with normal human diploid cells. Selection for hybrids that have segregated chromosomes results in the recovery of tumorigenic segregants. These segregants have all lost at least one copy of chromosome 11 of the diploid cell parent. Earlier we found that the parental D98 cells had detectable levels of mRNA specific for 13 of 21 proto-oncogenes examined. To determine if transregulation of proto-oncogenes by genes of the normal cell occurs in such hybrids, the steady-state levels of mRNA specific to 22 proto-oncogenes in the parental cells were compared with those of nontumorigenic D98 X human diploid hybrids as well as with those of their tumorigenic segregants and with the cells of the resulting tumors. The only chromosome consistently segregated in the latter was chromosome 11 of the diploid cell. fos and ets2 RNA levels and the amount of fos protein were consistently elevated in the segregants compared with amounts in the original hybrids. An unexpected finding was the inverse relationship for myb RNA that was barely detected in the parental D98 cells but was at least 10-fold elevated in hybrids that did not have segregated chromosomes compared with those that did. These patterns were evident in RNAs prepared from both subconfluent and confluent cell cultures. The findings suggest that genes of the normal cell parent can affect proto-oncogene expression. Whether the genes affecting fos, ets2, and myb RNA levels are on chromosome 11 and whether these alterations are causally related to the tumorigenic phenotype of the hybrid remain to be determined.
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O'Hara, B. M., H. P. Klinger, T. Curran, Y. D. Zhang, and D. G. Blair. "Levels of fos, ets2, and myb proto-oncogene RNAs correlate with segregation of chromosome 11 of normal cells and with suppression of tumorigenicity in human cell hybrids." Molecular and Cellular Biology 7, no. 8 (August 1987): 2941–46. http://dx.doi.org/10.1128/mcb.7.8.2941.
Full textAbstract:
The tumorigenicity in nude mice of human carcinoma-derived D98AH2 (D98) cells is suppressed when cell hybrids are made by fusing these cells with normal human diploid cells. Selection for hybrids that have segregated chromosomes results in the recovery of tumorigenic segregants. These segregants have all lost at least one copy of chromosome 11 of the diploid cell parent. Earlier we found that the parental D98 cells had detectable levels of mRNA specific for 13 of 21 proto-oncogenes examined. To determine if transregulation of proto-oncogenes by genes of the normal cell occurs in such hybrids, the steady-state levels of mRNA specific to 22 proto-oncogenes in the parental cells were compared with those of nontumorigenic D98 X human diploid hybrids as well as with those of their tumorigenic segregants and with the cells of the resulting tumors. The only chromosome consistently segregated in the latter was chromosome 11 of the diploid cell. fos and ets2 RNA levels and the amount of fos protein were consistently elevated in the segregants compared with amounts in the original hybrids. An unexpected finding was the inverse relationship for myb RNA that was barely detected in the parental D98 cells but was at least 10-fold elevated in hybrids that did not have segregated chromosomes compared with those that did. These patterns were evident in RNAs prepared from both subconfluent and confluent cell cultures. The findings suggest that genes of the normal cell parent can affect proto-oncogene expression. Whether the genes affecting fos, ets2, and myb RNA levels are on chromosome 11 and whether these alterations are causally related to the tumorigenic phenotype of the hybrid remain to be determined.
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Lord, K. A., A. Abdollahi, B. Hoffman-Liebermann, and D. A. Liebermann. "Proto-oncogenes of the fos/jun family of transcription factors are positive regulators of myeloid differentiation." Molecular and Cellular Biology 13, no. 2 (February 1993): 841–51. http://dx.doi.org/10.1128/mcb.13.2.841-851.1993.
Full textAbstract:
The proto-oncogenes c-jun, junB, junD, and c-fos recently have been shown to encode for transcription factors with a leucine zipper that mediates dimerization to constitute active transcription factors; juns were shown to dimerize with each other and with c-fos, whereas fos was shown to dimerize only with juns. After birth, hematopoietic cells of the myeloid lineage, and some other terminally differentiated cell types, express high levels of c-fos. Still, the role of fos/jun transcription factors in normal myelopoiesis or in leukemogenesis has not been established. Recently, c-jun, junB, and junD were identified as myeloid differentiation primary response genes stably expressed following induction of terminal differentiation of myeloblastic leukemia M1 cells. Intriguingly, c-fos, though induced during normal myelopoiesis, was not induced upon M1 differentiation. To gain further insights into the role of fos/jun in normal myelopoiesis and leukemogenicity, M1fos and M1junB cell lines, which constitutively express c-fos and junB, respectively, were established. It was shown that enforced expression of c-fos, and to a lesser extent junB, in M1 cells results in both an increased propensity to differentiate and a reduction in the aggressiveness of the M1 leukemic phenotype. M1fos cells constitutively expressed immediate-early and late genetic markers of differentiated M1 cells. The in vitro differentiation of normal myeloblasts into mature macrophages and granulocytes, as well as the increased propensity of M1fos leukemic myeloblasts to be induced for terminal differentiation, was dramatically impaired with use of c-fos antisense oligomers in the culture media. Taken together, these observations show that the proto-oncogenes which encode for fos/jun transcription factors play important roles in promoting myeloid differentiation. The ability of the M1 leukemic myeloblasts to be induced for terminal differentiation in the absence of apparent fos expression indicates that there is some redundancy among the fos/jun family of transcription factors in promoting myeloid differentiation; however, juns alone cannot completely compensate for the lack of fos. Thus, genetic lesions affecting fos/jun expression may play a role in the development of "preleukemic" myelodysplastic syndromes and their further progression to leukemias.
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Lord, K. A., A. Abdollahi, B. Hoffman-Liebermann, and D. A. Liebermann. "Proto-oncogenes of the fos/jun family of transcription factors are positive regulators of myeloid differentiation." Molecular and Cellular Biology 13, no. 2 (February 1993): 841–51. http://dx.doi.org/10.1128/mcb.13.2.841.
Full textAbstract:
The proto-oncogenes c-jun, junB, junD, and c-fos recently have been shown to encode for transcription factors with a leucine zipper that mediates dimerization to constitute active transcription factors; juns were shown to dimerize with each other and with c-fos, whereas fos was shown to dimerize only with juns. After birth, hematopoietic cells of the myeloid lineage, and some other terminally differentiated cell types, express high levels of c-fos. Still, the role of fos/jun transcription factors in normal myelopoiesis or in leukemogenesis has not been established. Recently, c-jun, junB, and junD were identified as myeloid differentiation primary response genes stably expressed following induction of terminal differentiation of myeloblastic leukemia M1 cells. Intriguingly, c-fos, though induced during normal myelopoiesis, was not induced upon M1 differentiation. To gain further insights into the role of fos/jun in normal myelopoiesis and leukemogenicity, M1fos and M1junB cell lines, which constitutively express c-fos and junB, respectively, were established. It was shown that enforced expression of c-fos, and to a lesser extent junB, in M1 cells results in both an increased propensity to differentiate and a reduction in the aggressiveness of the M1 leukemic phenotype. M1fos cells constitutively expressed immediate-early and late genetic markers of differentiated M1 cells. The in vitro differentiation of normal myeloblasts into mature macrophages and granulocytes, as well as the increased propensity of M1fos leukemic myeloblasts to be induced for terminal differentiation, was dramatically impaired with use of c-fos antisense oligomers in the culture media. Taken together, these observations show that the proto-oncogenes which encode for fos/jun transcription factors play important roles in promoting myeloid differentiation. The ability of the M1 leukemic myeloblasts to be induced for terminal differentiation in the absence of apparent fos expression indicates that there is some redundancy among the fos/jun family of transcription factors in promoting myeloid differentiation; however, juns alone cannot completely compensate for the lack of fos. Thus, genetic lesions affecting fos/jun expression may play a role in the development of "preleukemic" myelodysplastic syndromes and their further progression to leukemias.
28
Kizaka, S., and A. Hakura. "A cell mutant that exhibits temperature-dependent sensitivity to transformation by various oncogenes." Molecular and Cellular Biology 9, no. 12 (December 1989): 5669–75. http://dx.doi.org/10.1128/mcb.9.12.5669-5675.1989.
Full textAbstract:
We previously isolated a Fisher rat fibroblast mutant, B812, that has the unique property of temperature-dependent transformation by various oncogenic retroviruses. At the permissive temperature (35 degrees C), this mutant was sensitive to oncogenic transformation and formed foci on a dish at the same frequency as did the parental fibroblast cell line. When Kirsten murine sarcoma virus (Ki-MSV) was applied to the cells, the frequency of focus formation decreased more than 25-fold at the nonpermissive temperature (39 degrees C), whereas the cells expressed nearly the same level of the ras transcript as well as the ras protein. The temperature-restricted focus formation was fully reversible and was completely suppressed upon fusion with the wild-type parent cell. In addition to ras, the mos, fos, src, and erbB-2 oncogenes transformed this mutant with the same temperature dependence as described above; polyomavirus middle T antigen, adenovirus type 12, and human papillomavirus 16-E67 also transformed, but without temperature dependence. These results suggest that ras, fos, mos, src, and erbB-2 use a common cellular pathway for transforming cells.
29
Kizaka, S., and A. Hakura. "A cell mutant that exhibits temperature-dependent sensitivity to transformation by various oncogenes." Molecular and Cellular Biology 9, no. 12 (December 1989): 5669–75. http://dx.doi.org/10.1128/mcb.9.12.5669.
Full textAbstract:
We previously isolated a Fisher rat fibroblast mutant, B812, that has the unique property of temperature-dependent transformation by various oncogenic retroviruses. At the permissive temperature (35 degrees C), this mutant was sensitive to oncogenic transformation and formed foci on a dish at the same frequency as did the parental fibroblast cell line. When Kirsten murine sarcoma virus (Ki-MSV) was applied to the cells, the frequency of focus formation decreased more than 25-fold at the nonpermissive temperature (39 degrees C), whereas the cells expressed nearly the same level of the ras transcript as well as the ras protein. The temperature-restricted focus formation was fully reversible and was completely suppressed upon fusion with the wild-type parent cell. In addition to ras, the mos, fos, src, and erbB-2 oncogenes transformed this mutant with the same temperature dependence as described above; polyomavirus middle T antigen, adenovirus type 12, and human papillomavirus 16-E67 also transformed, but without temperature dependence. These results suggest that ras, fos, mos, src, and erbB-2 use a common cellular pathway for transforming cells.
30
Staňková, J., and M. Rola-Pleszczynski. "Leukotriene B4 stimulates c-fos and c-jun gene transcription and AP-1 binding activity in human monocytes." Biochemical Journal 282, no. 3 (March 15, 1992): 625–29. http://dx.doi.org/10.1042/bj2820625.
Full textAbstract:
We have examined the effect of leukotriene B4 (LTB4), a potent lipid proinflammatory mediator, on the expression of the proto-oncogenes c-jun and c-fos. In addition, we looked at the modulation of nuclear factors binding specifically to the AP-1 element after LTB4 stimulation. LTB4 increased the expression of the c-fos gene in a time- and concentration-dependent manner. The c-jun mRNA, which is constitutively expressed in human peripheral-blood monocytes at relatively high levels, was also slightly augmented by LTB4, although to a much lower extent than c-fos. The kinetics of expression of the two genes were also slightly different, with c-fos mRNA reaching a peak at 15 min after stimulation and c-jun at 30 min. Both messages rapidly declined thereafter. Stability of the c-fos and c-jun mRNA was not affected by LTB4, as assessed after actinomycin D treatment. Nuclear transcription studies in vitro showed that LTB4 increased the transcription of the c-fos gene 7-fold and the c-jun gene 1.4-fold. Resting monocytes contained nuclear factors binding to the AP-1 element, but stimulation of monocytes with LTB4 induced greater AP-1-binding activity of nuclear proteins. These results indicate that LTB4 may regulate the production of different cytokines by modulating the yield and/or the function of transcription factors such as AP-1-binding proto-oncogene products.
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Muller, M., J. Gauley, and John J. Heikkila. "Hydrogen peroxide induces heat shock protein and proto-oncogene mRNA accumulation in Xenopus laevis A6 kidney epithelial cells." Canadian Journal of Physiology and Pharmacology 82, no. 7 (July 1, 2004): 523–29. http://dx.doi.org/10.1139/y04-059.
Full textAbstract:
In this study, we examined the effect of hydrogen peroxide on the accumulation of various mRNAs encoding heat shock proteins (hsps) and proto-oncogenes in Xenopus A6 kidney epithelial cells. Hydrogen peroxide treatment enhanced the accumulation of hsp90, hsp70, hsp30, c-jun, c-fos, and actin mRNAs with distinct temporal patterns. Although hsp70, c-fos, and c-jun mRNA levels peaked at 1–2 h before declining, hsp30 and hsp90 mRNA levels were maximal at 4–6 h. Other mRNAs, including heat shock cognate hsc70, immunoglobulin binding protein, and ribosomal L8, were unaffected. Treatment of kidney cells with a combination of mild heat shock plus hydrogen peroxide resulted in a synergistic increase in the relative levels of both hsp70 and hsp30 mRNA, but not hsp90, c-fos, c-jun, or actin. This study suggests that analysis of hsp and proto-oncogene mRNA levels may be of value as molecular biomarkers of oxidative stress associated with various disease states and nephrotoxicity in kidney.Key words: Xenopus, kidney, mRNA, heat shock protein, hydrogen peroxide.
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Schneider, M. D., P. A. Payne, H. Ueno, M. B. Perryman, and R. Roberts. "Dissociated expression of c-myc and a fos-related competence gene during cardiac myogenesis." Molecular and Cellular Biology 6, no. 11 (November 1986): 4140–43. http://dx.doi.org/10.1128/mcb.6.11.4140-4143.1986.
Full textAbstract:
Cardiac myocytes irreversibly lose their proliferative capacity soon after birth, and cardiac DNA synthesis becomes uncoupled from mitotic division. Therefore, we examined cardiac muscle for developmental down regulation of inducible proto-oncogenes associated with cell proliferation. c-myc mRNA decreased continuously from day 13 of embryonic development and was dissociated from expression of the fos-related gene r-fos, which decreased precipitously between days 3 and 7 after birth.
33
Schneider, M. D., P. A. Payne, H. Ueno, M. B. Perryman, and R. Roberts. "Dissociated expression of c-myc and a fos-related competence gene during cardiac myogenesis." Molecular and Cellular Biology 6, no. 11 (November 1986): 4140–43. http://dx.doi.org/10.1128/mcb.6.11.4140.
Full textAbstract:
Cardiac myocytes irreversibly lose their proliferative capacity soon after birth, and cardiac DNA synthesis becomes uncoupled from mitotic division. Therefore, we examined cardiac muscle for developmental down regulation of inducible proto-oncogenes associated with cell proliferation. c-myc mRNA decreased continuously from day 13 of embryonic development and was dissociated from expression of the fos-related gene r-fos, which decreased precipitously between days 3 and 7 after birth.
34
Holt, J. T. "Antisense rescue defines specialized and generalized functional domains for c-Fos protein." Molecular and Cellular Biology 13, no. 6 (June 1993): 3821–30. http://dx.doi.org/10.1128/mcb.13.6.3821-3830.1993.
Full textAbstract:
Serum induces the expression of a number of proteins with similar transcriptional properties, including those encoded by the proto-oncogenes c-fos and c-jun. This study employs a novel antisense rescue method to determine whether antisense-resistant genes (constructed by deletion of antisense RNA target sequences) can replace c-fos expression during serum-induced DNA synthesis. Immunoprecipitation studies and nuclease protection assays demonstrated that anti-fos RNA inhibited endogenous c-fos expression but did not inhibit expression of transfected antisense-resistant mutant c-fos genes. The results of nuclear-labelling and cellular-proliferation studies indicated that C terminally truncated Fos mutants, including FBR v-fos, could not rescue endogenous Fos, although full-length and minimally truncated c-fos expression vectors could restore serum-induced DNA synthesis in cells expressing anti-fos RNA. Overexpression of c-Jun protein (Jun) could not restore serum-induced DNA synthesis to cells expressing inducible anti-fos RNA despite equivalent transactivation of an AP-1 target gene. Thus, the antisense rescue method defines a specialized function for c-Fos protein which is distinct from the function(s) of Jun and/or transforming FBR v-Fos proteins.
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Holt, J. T. "Antisense rescue defines specialized and generalized functional domains for c-Fos protein." Molecular and Cellular Biology 13, no. 6 (June 1993): 3821–30. http://dx.doi.org/10.1128/mcb.13.6.3821.
Full textAbstract:
Serum induces the expression of a number of proteins with similar transcriptional properties, including those encoded by the proto-oncogenes c-fos and c-jun. This study employs a novel antisense rescue method to determine whether antisense-resistant genes (constructed by deletion of antisense RNA target sequences) can replace c-fos expression during serum-induced DNA synthesis. Immunoprecipitation studies and nuclease protection assays demonstrated that anti-fos RNA inhibited endogenous c-fos expression but did not inhibit expression of transfected antisense-resistant mutant c-fos genes. The results of nuclear-labelling and cellular-proliferation studies indicated that C terminally truncated Fos mutants, including FBR v-fos, could not rescue endogenous Fos, although full-length and minimally truncated c-fos expression vectors could restore serum-induced DNA synthesis in cells expressing anti-fos RNA. Overexpression of c-Jun protein (Jun) could not restore serum-induced DNA synthesis to cells expressing inducible anti-fos RNA despite equivalent transactivation of an AP-1 target gene. Thus, the antisense rescue method defines a specialized function for c-Fos protein which is distinct from the function(s) of Jun and/or transforming FBR v-Fos proteins.
36
Hamatani, K., K. Yoshida, H. Kondo, H. Toki, K. Okabe, M. Motoi, S. Ikeda, S. Mori, K. Shimaoka, and M. Akiyama. "Histologic typing of non-Hodgkin's lymphomas by in situ hybridization with DNA probes of oncogenes." Blood 74, no. 1 (July 1, 1989): 423–29. http://dx.doi.org/10.1182/blood.v74.1.423.423.
Full textAbstract:
Abstract Expression of six proto-oncogenes (fos, myc, myb, Ki-ras, Ha-ras, and N- ras) in 43 cases of non-Hodgkin's lymphoma was analyzed by means of in situ hybridization. Biotinylated DNA probes of the six oncogenes and those of immunoglobulin H (IgH) gene and T-cell receptor beta (TCR beta) chain gene were used. The results of in situ hybridization performed under blind conditions by IgH gene and TCR beta chain gene probes were compatible with those of typing by cell surface markers. The nuclear protein-related proto-oncogenes, fos, myc, and myb, were expressed in about 70% to 80% of all cases regardless of phenotype, histology, or histologic grade. On the contrary, genes of ras family were expressed in more limited numbers of cases except for the Ki-ras gene, which was more frequently expressed by cases of the T-cell immunophenotype with a high malignancy grade. The results of dot hybridization with RNA extracted from some cases were compatible with those of in situ hybridization, further demonstrating the specificity of in situ hybridization.
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Hamatani, K., K. Yoshida, H. Kondo, H. Toki, K. Okabe, M. Motoi, S. Ikeda, S. Mori, K. Shimaoka, and M. Akiyama. "Histologic typing of non-Hodgkin's lymphomas by in situ hybridization with DNA probes of oncogenes." Blood 74, no. 1 (July 1, 1989): 423–29. http://dx.doi.org/10.1182/blood.v74.1.423.bloodjournal741423.
Full textAbstract:
Expression of six proto-oncogenes (fos, myc, myb, Ki-ras, Ha-ras, and N- ras) in 43 cases of non-Hodgkin's lymphoma was analyzed by means of in situ hybridization. Biotinylated DNA probes of the six oncogenes and those of immunoglobulin H (IgH) gene and T-cell receptor beta (TCR beta) chain gene were used. The results of in situ hybridization performed under blind conditions by IgH gene and TCR beta chain gene probes were compatible with those of typing by cell surface markers. The nuclear protein-related proto-oncogenes, fos, myc, and myb, were expressed in about 70% to 80% of all cases regardless of phenotype, histology, or histologic grade. On the contrary, genes of ras family were expressed in more limited numbers of cases except for the Ki-ras gene, which was more frequently expressed by cases of the T-cell immunophenotype with a high malignancy grade. The results of dot hybridization with RNA extracted from some cases were compatible with those of in situ hybridization, further demonstrating the specificity of in situ hybridization.
38
Di Fiore, P. P., J. Falco, I. Borrello, B. Weissman, and S. A. Aaronson. "The calcium signal for BALB/MK keratinocyte terminal differentiation counteracts epidermal growth factor (EGF) very early in the EGF-induced proliferative pathway." Molecular and Cellular Biology 8, no. 2 (February 1988): 557–63. http://dx.doi.org/10.1128/mcb.8.2.557-563.1988.
Full textAbstract:
BALB/MK mouse epidermal keratinocytes require epidermal growth factor (EGF) for proliferation and terminally differentiate in response to high calcium concentrations. We show that EGF is an extremely potent mitogen, causing BALB/MK cultures to enter the cell cycle in a synchronous manner associated with a greater than 100-fold increase in DNA synthesis. Analysis of the expression of proto-oncogenes which have been reported to be activated during the cascade of events following growth factor stimulation of fibroblasts or lymphoid cells revealed a very rapid but transient 100-fold increase in c-fos RNA but little or no effect on the other proto-oncogenes analyzed. Exposure of EGF-synchronized BALB/MK cells to high levels of calcium was associated with a striking decrease in the early burst of c-fos RNA as well as the subsequent peak of cell DNA synthesis. Since the inhibitory effect of high calcium on c-fos RNA expression was measurable within 30 min, our studies imply that the EGF proliferative and calcium differentiation signals must interact very early in the pathway of EGF-induced proliferation. Our results also establish that c-fos RNA modulation is an important early marker of cell proliferation in epithelial as well as mesenchymal cells.
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Di Fiore, P. P., J. Falco, I. Borrello, B. Weissman, and S. A. Aaronson. "The calcium signal for BALB/MK keratinocyte terminal differentiation counteracts epidermal growth factor (EGF) very early in the EGF-induced proliferative pathway." Molecular and Cellular Biology 8, no. 2 (February 1988): 557–63. http://dx.doi.org/10.1128/mcb.8.2.557.
Full textAbstract:
BALB/MK mouse epidermal keratinocytes require epidermal growth factor (EGF) for proliferation and terminally differentiate in response to high calcium concentrations. We show that EGF is an extremely potent mitogen, causing BALB/MK cultures to enter the cell cycle in a synchronous manner associated with a greater than 100-fold increase in DNA synthesis. Analysis of the expression of proto-oncogenes which have been reported to be activated during the cascade of events following growth factor stimulation of fibroblasts or lymphoid cells revealed a very rapid but transient 100-fold increase in c-fos RNA but little or no effect on the other proto-oncogenes analyzed. Exposure of EGF-synchronized BALB/MK cells to high levels of calcium was associated with a striking decrease in the early burst of c-fos RNA as well as the subsequent peak of cell DNA synthesis. Since the inhibitory effect of high calcium on c-fos RNA expression was measurable within 30 min, our studies imply that the EGF proliferative and calcium differentiation signals must interact very early in the pathway of EGF-induced proliferation. Our results also establish that c-fos RNA modulation is an important early marker of cell proliferation in epithelial as well as mesenchymal cells.
40
Green, N. K., M. D. Gammage, J. A. Franklyn, A. M. Heagerty, and M. C. Sheppard. "Regulation of β myosin heavy chain, c-myc and c-fos proto-oncogenes in thyroid hormone-induced hypertrophy of the rat myocardium." Clinical Science 84, no. 1 (January 1, 1993): 61–67. http://dx.doi.org/10.1042/cs0840061.
Full textAbstract:
1. In order to investigate the molecular mechanisms determining the hypertrophic response of the ventricular myocardium to thyroid hormone administration, changes in left and right ventricular expression of the c-myc, c-fos and H-ras proto-oncogenes in response to treatment with 3,3′,5-tri-iodothyronine were defined. 2. Adult female Wistar rats were treated with daily subcutaneous injections of 3,3′,5-tri-iodothyronine (50 μg) for 1, 3, 7 or 14 days (n = 6 in each treatment group) and the results from 3,3′,5-tri-iodothyronine-treated animals were compared with those obtained from untreated controls (n = 6). Changes in the weight of the left and right ventricles in response to 3,3′,5-tri-iodothyronine treatment were measured; changes in expression of the c-myc, c-fos and H-ras proto-oncogenes were determined in parallel by measurement of specific messenger RNAs by Northern and dot hybridization, as well as changes in expression of β myosin heavy chain messenger RNA. 3. Treatment with 3,3′,5-tri-iodothyronine resulted in increases in both left and right ventricular weights after 3 days, an effect maintained up to 14 days. Despite an increase in left ventricular weight, levels of β myosin heavy chain, c-myc, c-fos and H-ras mRNAs in the left ventricle were unchanged; in contrast, an increase in right ventricular weight was associated with increased expression of β myosin heavy chain, c-myc and c-fos messenger RNAs. 4. These specific ventricular changes in gene expression, in the face of a hypertrophic response of both ventricles to 3,3′,5-tri-iodothyronine, suggest that the cardiac growth response to thyroid hormones reflects the well-documented secondary haemodynamic influences rather than direct gene regulatory actions of 3,3′,5-tri-iodothyronine at the transcriptional level on the genes studied. Changes in right ventricular proto-oncogene and β myosin heavy chain expression may in turn reflect an increase in right ventricular pressure load.
41
McBride, Kevin, and Mona Nemer. "The C-Terminal Domain of c-fos Is Required for Activation of an AP-1 Site Specific forjun-fos Heterodimers." Molecular and Cellular Biology 18, no. 9 (September 1, 1998): 5073–81. http://dx.doi.org/10.1128/mcb.18.9.5073.
Full textAbstract:
ABSTRACT The proto-oncogenes jun and fos are members of the AP-1 family of transcription factors, which activate transcription of target genes via the tetradecanoyl phorbol acetate response element (TRE). Both jun and foscontain activation domains, but their relative contributions to transcriptional activation of different TREs remain unclear. It is not apparent whether the cellular availability of specific AP-1 members is the major determinant for regulation of TREs or whether other factors including the TRE sequence itself contribute to selectivity. We have identified in the promoter of the rat atrial natriuretic factor (ANF) a novel AP-1 site which is unresponsive to jun homodimers and is inducible only in the presence of c-fos. This activation is potentiated by mitogen-activated protein (MAP) kinase. The jun proteins appear to be required solely to tether c-fos to the promoter, and c-fos mutants lacking putative activation domains abrogate transactivation. Unexpectedly, the oncogenic form of c-foswhich diverges most significantly in the carboxy-terminal 50 amino acids is unable to mediate transactivation at this specialized AP-1 site. Mutations within the C terminus of c-fos at serine residues that are phosphorylation targets for growth factors and MAP kinase completely abrogate transactivation and block potentiation by MAP kinase. Using GAL4 fusions, we show that the 90-amino-acid C terminus of c-fos contains autonomous activation domains and that the serine residues are essential for full activity. These results suggest that phosphorylation of the C terminus of c-fos affects its transactivation properties and provide evidence for novel regulatory mechanisms that may contribute to biologic specificities of the AP-1 transcription complex.
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Cleveland, J. L., U. R. Rapp, and W. L. Farrar. "Role of c-myc and other genes in interleukin 2 regulated CT6 T lymphocytes and their malignant variants." Journal of Immunology 138, no. 10 (May 15, 1987): 3495–504. http://dx.doi.org/10.4049/jimmunol.138.10.3495.
Full textAbstract:
Abstract The cloned murine cytotoxic T cell line CT6 solely requires interleukin 2 (IL 2) for viability and cell cycle progression. Treatment of G arrested cultures of CT6 cells with recombinant IL 2 induces the rapid sequential expression of the nuclear proto-oncogenes c-fos, c-myc, and c-myb but does not affect the expression of several cytosolic or membrane-associated proto-oncogenes. A comparison of early genes induced by growth factor treatment of quiescent NIH/3T3 fibroblasts and CT6 cells demonstrated that only c-fos and c-myc induction is shared in the two different lineages. Factor-independent lines derived from CT6 cells show no mitogenic response to IL 2, yet binding of IL 2 with its receptor in the cells was capable of inducing the expression of c-fos and c-myc. In factor-independent cell lines, c-myc was uniformly expressed at high constitutive levels, suggesting that c-myc abrogates growth factor requirements of these cells. The levels of c-myc expression in the factor-independent lines was not due to an autocrine production of IL 2 but may be a consequence of constitutively activated IL 2 receptors.
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Zhan, X., and M. Goldfarb. "Growth factor requirements of oncogene-transformed NIH 3T3 and BALB/c 3T3 cells cultured in defined media." Molecular and Cellular Biology 6, no. 10 (October 1986): 3541–44. http://dx.doi.org/10.1128/mcb.6.10.3541-3544.1986.
Full textAbstract:
We report conditions for the efficient growth of NIH 3T3 and BALB/c 3T3 cells cultured in a defined medium supplemented with either platelet-derived growth factor (PDGF) or pituitary-derived fibroblast growth factor (FGF). The oncogenes v-mos, v-src, v-sis, and c-H-ras Val 12 can induce morphological transformation of these cells and can release them from the mitogen requirement for growth, while the oncogene v-fos cannot abrogate the PDGF-FGF requirement. The radically different behavior of normal and transformed NIH 3T3 cells in PDGF-FGF-free defined medium can form the basis of a sensitive new fibroblast transformation assay.
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Zhan, X., and M. Goldfarb. "Growth factor requirements of oncogene-transformed NIH 3T3 and BALB/c 3T3 cells cultured in defined media." Molecular and Cellular Biology 6, no. 10 (October 1986): 3541–44. http://dx.doi.org/10.1128/mcb.6.10.3541.
Full textAbstract:
We report conditions for the efficient growth of NIH 3T3 and BALB/c 3T3 cells cultured in a defined medium supplemented with either platelet-derived growth factor (PDGF) or pituitary-derived fibroblast growth factor (FGF). The oncogenes v-mos, v-src, v-sis, and c-H-ras Val 12 can induce morphological transformation of these cells and can release them from the mitogen requirement for growth, while the oncogene v-fos cannot abrogate the PDGF-FGF requirement. The radically different behavior of normal and transformed NIH 3T3 cells in PDGF-FGF-free defined medium can form the basis of a sensitive new fibroblast transformation assay.
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Kizaka-Kondoh, S., K. Sato, K. Tamura, H. Nojima, and H. Okayama. "Raf-1 protein kinase is an integral component of the oncogenic signal cascade shared by epidermal growth factor and platelet-derived growth factor." Molecular and Cellular Biology 12, no. 11 (November 1992): 5078–86. http://dx.doi.org/10.1128/mcb.12.11.5078-5086.1992.
Full textAbstract:
Our recent studies with cell mutants indicate that a cascade shared by the epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) signals exists in NRK cells and mediates oncogenic signals induced by many oncogenes (A. Masuda, S. Kizaka-Kondoh, H. Miwatani, Y. Terada, H. Nojima, and H. Okayama, New Biol. 4:489-503, 1992). We have employed the antisense RNA technique to investigate possible involvement of Raf-1 kinase in this signal transduction cascade. NRK cell clones highly reduced in the Raf-1 production are generated by the expression of a c-raf-1 antisense RNA. They have no apparent growth defects and retain proper mitotic responses to growth factors but are refractory to transformation by EGF or PDGF plus transforming growth factor beta, v-erbB, v-fms, v-K-ras, v-mos, v-fos, v-src, simian virus 40 large T, and polyomavirus middle T but not by v-raf or adenovirus E1A. These results not only support our model for the oncogenic signal cascade but also lead to the conclusion that Raf-1 protein kinase is a downstream component of this oncogenic signal cascade shared by EGF and PDGF.
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Kizaka-Kondoh, S., K. Sato, K. Tamura, H. Nojima, and H. Okayama. "Raf-1 protein kinase is an integral component of the oncogenic signal cascade shared by epidermal growth factor and platelet-derived growth factor." Molecular and Cellular Biology 12, no. 11 (November 1992): 5078–86. http://dx.doi.org/10.1128/mcb.12.11.5078.
Full textAbstract:
Our recent studies with cell mutants indicate that a cascade shared by the epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) signals exists in NRK cells and mediates oncogenic signals induced by many oncogenes (A. Masuda, S. Kizaka-Kondoh, H. Miwatani, Y. Terada, H. Nojima, and H. Okayama, New Biol. 4:489-503, 1992). We have employed the antisense RNA technique to investigate possible involvement of Raf-1 kinase in this signal transduction cascade. NRK cell clones highly reduced in the Raf-1 production are generated by the expression of a c-raf-1 antisense RNA. They have no apparent growth defects and retain proper mitotic responses to growth factors but are refractory to transformation by EGF or PDGF plus transforming growth factor beta, v-erbB, v-fms, v-K-ras, v-mos, v-fos, v-src, simian virus 40 large T, and polyomavirus middle T but not by v-raf or adenovirus E1A. These results not only support our model for the oncogenic signal cascade but also lead to the conclusion that Raf-1 protein kinase is a downstream component of this oncogenic signal cascade shared by EGF and PDGF.
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Slootweg, M. C., R. P. de Groot, M. P. M. Herrmann-Erlee, I. Koornneef, W. Kruijer, and Y. M. Kramer. "Growth hormone induces expression of c-jun and jun B oncogenes and employs a protein kinase C signal transduction pathway for the induction of c-fos oncogene expression." Journal of Molecular Endocrinology 6, no. 2 (April 1991): 179–88. http://dx.doi.org/10.1677/jme.0.0060179.
Full textAbstract:
ABSTRACT Although the structure of several members of the GH receptor family has been defined, signal transduction following GH binding to its receptor has not been elucidated. Mouse osteoblasts were used to study the effect of GH on immediate early gene expression and, subsequently, the cellular signal(s) mediating this expression were analysed. GH rapidly and transiently induced the expression of c-jun and jun B in concert with the already reported expression of c-fos. The GH-induced expression of c-fos was completely blocked by the protein kinase inhibitors staurosporine and H7, indicating that the action of GH is mediated by one or several protein kinases. We next analysed the identity of the putative protein kinases in more detail by using a more specific protein kinase inhibitor, namely the ether-lipid 1-O-alkyl-2-O-methylglycerol, understood to be an inhibitor of protein kinase C (PKC). Data obtained from these studies revealed that GH-induced expression of c-fos is mediated by PKC. In addition, we observed a profound increase in formation of the PKC activator diacyglycerol upon addition of GH, a natural activator of PKC. In conclusion, upon binding of GH to mouse osteoblasts, the receptor-mediated cellular signal involves diacyglycerol formation and activation of PKC, leading to the induction of oncogene expression. Finally, the expression of c-fos, c-jun and jun B results in an increased binding of protein complexes to AP-1 binding sites.
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Baranes, D., and E. Razin. "Protein kinase C regulates proliferation of mast cells and the expression of the mRNAs of fos and jun proto-oncogenes during activation by IgE-Ag or calcium ionophore A23187." Blood 78, no. 9 (November 1, 1991): 2354–64. http://dx.doi.org/10.1182/blood.v78.9.2354.2354.
Full textAbstract:
Abstract Short-term stimulation (up to 16 hours) of interleukin-3 (IL-3)- dependent mouse bone marrow-derived mast cells, Abelson transformed mouse liver-derived mast cells, or rat basophilic leukemia cells by either IgE-Ag or calcium ionophore A23187 resulted in inhibition of their proliferation as measured by 3H-thymidine incorporation and MTT (tetrazolium) assays, and in accumulation of the mRNAs of c-fos, c-jun, junB and slightly of junD proto-oncogenes. The involvement of protein kinase C (PKC) in these responses was investigated by using several approaches of enzyme activity regulation. Direct activation of the PKC was achieved by short-term exposure of the cells to the PKC-specific activator phorbol 12-myristate-13-acetate (PMA). Inhibition of PKC activity was obtained by either prolonged treatment of the cells with PMA or by exposure of the cells to the PKC inhibitors H-7 and staurosporine. The results showed the following: (1) Short-term exposure of mast cells to PMA was sufficient to induce inhibition of proliferation. (2) An increase in PKC activity was associated with a decrease in the proliferation of IgE-dinitrophenol (DNP) or calcium ionophore A23187-stimulated cells. (3) A direct correlation was found between the increase in PKC activity and the increase in the level of the mRNAs of the jun proto-oncogenes in cells activated by both stimuli mentioned. (4) While an increase in PKC activity was associated with the upregulation of the level of c-fos mRNA during calcium ionophore A23187 stimulation, it showed the opposite effect on the expression of the mRNA of this proto-oncogene when the cells were triggered by IgE- DNP. Therefore, we concluded that PKC plays various roles in the expression of the mRNA of c-fos in activated mast cells depending on the stimulus involved. In addition, the expression of the mRNA of c-jun and junB proto-onogenes is not coordinately regulated with that of c- fos during immunologic stimulation. This discordancy, which is associated with the increase in PKC activity in mast cells, may play a role in the regulation of the transcription of AP-1-responsive genes, and therefore could be associated with the regulation of proliferation of these cells.
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Baranes, D., and E. Razin. "Protein kinase C regulates proliferation of mast cells and the expression of the mRNAs of fos and jun proto-oncogenes during activation by IgE-Ag or calcium ionophore A23187." Blood 78, no. 9 (November 1, 1991): 2354–64. http://dx.doi.org/10.1182/blood.v78.9.2354.bloodjournal7892354.
Full textAbstract:
Short-term stimulation (up to 16 hours) of interleukin-3 (IL-3)- dependent mouse bone marrow-derived mast cells, Abelson transformed mouse liver-derived mast cells, or rat basophilic leukemia cells by either IgE-Ag or calcium ionophore A23187 resulted in inhibition of their proliferation as measured by 3H-thymidine incorporation and MTT (tetrazolium) assays, and in accumulation of the mRNAs of c-fos, c-jun, junB and slightly of junD proto-oncogenes. The involvement of protein kinase C (PKC) in these responses was investigated by using several approaches of enzyme activity regulation. Direct activation of the PKC was achieved by short-term exposure of the cells to the PKC-specific activator phorbol 12-myristate-13-acetate (PMA). Inhibition of PKC activity was obtained by either prolonged treatment of the cells with PMA or by exposure of the cells to the PKC inhibitors H-7 and staurosporine. The results showed the following: (1) Short-term exposure of mast cells to PMA was sufficient to induce inhibition of proliferation. (2) An increase in PKC activity was associated with a decrease in the proliferation of IgE-dinitrophenol (DNP) or calcium ionophore A23187-stimulated cells. (3) A direct correlation was found between the increase in PKC activity and the increase in the level of the mRNAs of the jun proto-oncogenes in cells activated by both stimuli mentioned. (4) While an increase in PKC activity was associated with the upregulation of the level of c-fos mRNA during calcium ionophore A23187 stimulation, it showed the opposite effect on the expression of the mRNA of this proto-oncogene when the cells were triggered by IgE- DNP. Therefore, we concluded that PKC plays various roles in the expression of the mRNA of c-fos in activated mast cells depending on the stimulus involved. In addition, the expression of the mRNA of c-jun and junB proto-onogenes is not coordinately regulated with that of c- fos during immunologic stimulation. This discordancy, which is associated with the increase in PKC activity in mast cells, may play a role in the regulation of the transcription of AP-1-responsive genes, and therefore could be associated with the regulation of proliferation of these cells.
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Chiu, C. P., and F. Lee. "IL-6 is a differentiation factor for M1 and WEHI-3B myeloid leukemic cells." Journal of Immunology 142, no. 6 (March 15, 1989): 1909–15. http://dx.doi.org/10.4049/jimmunol.142.6.1909.
Full textAbstract:
Abstract IL-6 has multiple biologic activities in different cell systems including both the ability to support cell proliferation and to induce differentiation. We reported previously the isolation and functional expression of a mouse IL-6 (mIL-6) cDNA clone derived from bone marrow stromal cells. In this paper, we show that mIL-6 is a potent inducer of terminal macrophage differentiation for a mouse myeloid leukemic cell line, M1. Addition of mIL-6 to cultures of M1 cells rapidly inhibits their proliferation and induces phagocytic activity and morphologic changes characteristic of mature macrophages. These phenotypic changes are accompanied at the molecular level by a decrease in proto-oncogene c-myc mRNA accumulation and increases in Fc gamma R, proto-oncogenes c-fos and c-fms (CSF-1R) mRNA expression. Furthermore, IL-6 enhances the expression of Fc gamma R and c-fms in differentiation-responsive D+, but not unresponsive D- sublines of mouse myelomonocytic leukemic WEHI-3B cells. Together with our previous observation that IL-6 stimulates colony formation by normal myeloid progenitors, these results strongly suggest an important regulatory role for IL-6 in myeloid cell growth and differentiation.