Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells
Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a parac...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Pasumarthi, Kishore B. S. [verfasserIn] Jin, Yan [verfasserIn] Cattini, Peter A. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 1997 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 68(1997), 3, Seite 0 |
| Übergeordnetes Werk: |
volume:68 ; year:1997 ; number:3 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1046/j.1471-4159.1997.68030898.x |
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| 520 | |a Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. | ||
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10.1046/j.1471-4159.1997.68030898.x doi (DE-627)NLEJ243169442 DE-627 ger DE-627 rakwb Pasumarthi, Kishore B. S. verfasserin aut Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells Oxford, UK Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Fibroblast growth factor-2 gene Jin, Yan verfasserin aut Cattini, Peter A. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 68(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:68 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1997.68030898.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 68 1997 3 0 |
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10.1046/j.1471-4159.1997.68030898.x doi (DE-627)NLEJ243169442 DE-627 ger DE-627 rakwb Pasumarthi, Kishore B. S. verfasserin aut Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells Oxford, UK Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Fibroblast growth factor-2 gene Jin, Yan verfasserin aut Cattini, Peter A. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 68(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:68 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1997.68030898.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 68 1997 3 0 |
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10.1046/j.1471-4159.1997.68030898.x doi (DE-627)NLEJ243169442 DE-627 ger DE-627 rakwb Pasumarthi, Kishore B. S. verfasserin aut Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells Oxford, UK Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Fibroblast growth factor-2 gene Jin, Yan verfasserin aut Cattini, Peter A. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 68(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:68 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1997.68030898.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 68 1997 3 0 |
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10.1046/j.1471-4159.1997.68030898.x doi (DE-627)NLEJ243169442 DE-627 ger DE-627 rakwb Pasumarthi, Kishore B. S. verfasserin aut Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells Oxford, UK Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Fibroblast growth factor-2 gene Jin, Yan verfasserin aut Cattini, Peter A. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 68(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:68 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1997.68030898.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 68 1997 3 0 |
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10.1046/j.1471-4159.1997.68030898.x doi (DE-627)NLEJ243169442 DE-627 ger DE-627 rakwb Pasumarthi, Kishore B. S. verfasserin aut Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells Oxford, UK Blackwell Science Ltd 1997 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Fibroblast growth factor-2 gene Jin, Yan verfasserin aut Cattini, Peter A. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 68(1997), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:68 year:1997 number:3 pages:0 http://dx.doi.org/10.1046/j.1471-4159.1997.68030898.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 68 1997 3 0 |
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Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells Fibroblast growth factor-2 gene |
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Blackwell Science Ltd |
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misc Fibroblast growth factor-2 gene |
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Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells |
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Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells |
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Pasumarthi, Kishore B. S. |
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Journal of neurochemistry |
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Journal of neurochemistry |
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1997 |
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Pasumarthi, Kishore B. S. Jin, Yan Cattini, Peter A. |
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68 |
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Pasumarthi, Kishore B. S. |
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10.1046/j.1471-4159.1997.68030898.x |
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verfasserin |
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cloning of the rat fibroblast growth factor-2 promoter region and its response to mitogenic stimuli in glioma c6 cells |
| title_auth |
Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells |
| abstract |
Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. |
| abstractGer |
Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. |
| abstract_unstemmed |
Abstract: Basic fibroblast growth factor (FGF-2) is abundant in the developing and adult brain and has been linked with the origin and growth of neuronal and glial cells. Glial cells produce high levels of FGF-2, stimulating autocrine growth as well as the survival and function of neurons in a paracrine manner. Abnormal levels of FGF-2 have been linked with Alzheimer's, Huntington's, and Parkinson's diseases. Recent evidence has suggested that a component of the mitogenic response of glial cells is exerted on FGF-2 at the transcriptional level. To assess transcriptional regulation of this potent growth factor, we cloned a 1.4-kb genomic fragment containing the rat FGF-2 promoter region. DNA blotting results indicated that the rat FGF-2 gene exists as a single copy in the genome. The promoter region contains no TATA box but appears to rely instead on multiple GC-rich start sites (P0, P1, and P2) for transcription initiation in rat brain as well as C6 glioma cells. One of these sites (P0) was located within four nucleotides of the reported 5′ end of the rat brain cDNA and constituted part of a consensus Egr-1 binding site (5′-GCGGGGGCG-3′). Transcription from this site could be stimulated in C6 glioma cells in response to phorbol ester treatment. The induction of a “new” site (Pi) with phorbol ester also suggested a mechanism to explain the discrepancy between the reported “starts” for the ovarian versus brain cDNAs. A hybrid luciferase gene directed by rat FGF-2 5′-flanking DNA (−1,058/+54) was expressed in rat glioma C6, heart myoblast H9c2, and human astrocytoma U87-MG cells after gene transfer. The level of transfected FGF-2 promoter activity was higher in glial cells (C6 and U87-MG) compared with nonglial (H9c2) cells. Also, expression of this hybrid FGF-2/luciferase gene was increased in response to phorbol ester or serum treatment of C6 cells. Deletion analysis revealed the presence of both positive and negative regulatory regions that are involved in the transcriptional control of rat FGF-2 gene by mitogenic stimuli. |
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Cloning of the Rat Fibroblast Growth Factor-2 Promoter Region and Its Response to Mitogenic Stimuli in Glioma C6 Cells |
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