Modulation of nuclear proto-oncogene expression and cellular growth in myeloid leukemic cells by human interferon alpha
To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stim...
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| Autor*in: |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1988 |
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| Umfang: |
6 Ill. 8 |
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| Reproduktion: |
Wiley InterScience Backfile Collection 1832-2000 |
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| Übergeordnetes Werk: |
in: Journal of Cellular Physiology - New York, NY [u.a.] : Wiley-Liss, 135(1988) vom: Feb., Seite 324-331 |
| Übergeordnetes Werk: |
volume:135 ; year:1988 ; month:02 ; pages:324-331 ; extent:8 |
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NLEJ160795494 |
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| 520 | |a To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. | ||
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(DE-627)NLEJ160795494 DE-627 ger DE-627 rakwb eng Modulation of nuclear proto-oncogene expression and cellular growth in myeloid leukemic cells by human interferon alpha 1988 6 Ill. 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. Wiley InterScience Backfile Collection 1832-2000 Marshall, Adele H. oth Alper, Deborah oth Hiscott, John oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 135(1988) vom: Feb., Seite 324-331 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:135 year:1988 month:02 pages:324-331 extent:8 http://dx.doi.org/10.1002/jcp.1041350221 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 135 1988 2 324-331 8 |
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(DE-627)NLEJ160795494 DE-627 ger DE-627 rakwb eng Modulation of nuclear proto-oncogene expression and cellular growth in myeloid leukemic cells by human interferon alpha 1988 6 Ill. 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. Wiley InterScience Backfile Collection 1832-2000 Marshall, Adele H. oth Alper, Deborah oth Hiscott, John oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 135(1988) vom: Feb., Seite 324-331 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:135 year:1988 month:02 pages:324-331 extent:8 http://dx.doi.org/10.1002/jcp.1041350221 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 135 1988 2 324-331 8 |
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(DE-627)NLEJ160795494 DE-627 ger DE-627 rakwb eng Modulation of nuclear proto-oncogene expression and cellular growth in myeloid leukemic cells by human interferon alpha 1988 6 Ill. 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. Wiley InterScience Backfile Collection 1832-2000 Marshall, Adele H. oth Alper, Deborah oth Hiscott, John oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 135(1988) vom: Feb., Seite 324-331 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:135 year:1988 month:02 pages:324-331 extent:8 http://dx.doi.org/10.1002/jcp.1041350221 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 135 1988 2 324-331 8 |
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(DE-627)NLEJ160795494 DE-627 ger DE-627 rakwb eng Modulation of nuclear proto-oncogene expression and cellular growth in myeloid leukemic cells by human interferon alpha 1988 6 Ill. 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. Wiley InterScience Backfile Collection 1832-2000 Marshall, Adele H. oth Alper, Deborah oth Hiscott, John oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 135(1988) vom: Feb., Seite 324-331 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:135 year:1988 month:02 pages:324-331 extent:8 http://dx.doi.org/10.1002/jcp.1041350221 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 135 1988 2 324-331 8 |
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(DE-627)NLEJ160795494 DE-627 ger DE-627 rakwb eng Modulation of nuclear proto-oncogene expression and cellular growth in myeloid leukemic cells by human interferon alpha 1988 6 Ill. 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. Wiley InterScience Backfile Collection 1832-2000 Marshall, Adele H. oth Alper, Deborah oth Hiscott, John oth in Journal of Cellular Physiology New York, NY [u.a.] : Wiley-Liss 135(1988) vom: Feb., Seite 324-331 (DE-627)NLEJ15907097X (DE-600)1478143-8 0021-9541 nnns volume:135 year:1988 month:02 pages:324-331 extent:8 http://dx.doi.org/10.1002/jcp.1041350221 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-WIS GBV_NL_ARTICLE AR 135 1988 2 324-331 8 |
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Modulation of nuclear proto-oncogene expression and cellular growth in myeloid leukemic cells by human interferon alpha |
| abstract |
To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. |
| abstractGer |
To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. |
| abstract_unstemmed |
To address the mechanisms that regulate expression of specific growth-related nuclear proto-oncogenes, the transcript levels of the c-fos, c-myc, (2′5′)-oligoadenylate synthetase, IFN-α1, and IFN-β1 genes have been measured in the human leukemic cell lines KG-1, U937, and HL-60 following growth stimulation by serum, induction of differentiation by tumor-promoting agents, and/or treatment of cells with exogenously supplied alpha interferon (rIFN-α2). Production of fos and myc RNA was measured by S1 mapping, using fos DNA probes which identified either primary unspliced transcripts or steady-state-spliced mRNA levels, and using a myc probe which spanned the two major c-myc start sites, P1 and P2. Pretreatment of a quiescent KG-1 cell population with IFN for 18 hours before serum addition decreased the stimulation of both fos and myc RNA production. In HL-60 and U937 cells, IFN pretreatment had no inhibitory effect on serum-induced fos or myc transcription; however, in U937, rIFN-α2 treatment alone stimulated fos mRNA 11-fold. Expression of 2′5′ oligoadenylate synthetase was induced in IFN-treated cultures but not in cells stimulated with serum alone. No serum-induced IFN-α1 or IFN-β1 gene expression was observed in KG-1 or U937 cells. These results demonstrate that exogenous rIFN-α2 treatment of quiescent KG-1 cells can antagonize the effect of growth factors by altering expression of nuclear proto-oncogenes, but in general growth inhibition is not obligatorily coupled to inhibition of proto-oncogene transcription. |
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Modulation of nuclear proto-oncogene expression and cellular growth in myeloid leukemic cells by human interferon alpha |
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Marshall, Adele H. Alper, Deborah Hiscott, John |
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