Overexpression of c-Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma PC18 cells
The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription facto...
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| Autor*in: |
Sun, Baoyong [verfasserIn] Tank, A. William [verfasserIn] |
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E-Artikel |
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Oxford, UK: Blackwell Science Ltd ; 2002 |
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Online-Ressource |
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2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 80(2002), 2, Seite 0 |
| Übergeordnetes Werk: |
volume:80 ; year:2002 ; number:2 ; pages:0 |
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| DOI / URN: |
10.1046/j.0022-3042.2001.00692.x |
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| 520 | |a The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. | ||
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10.1046/j.0022-3042.2001.00692.x doi (DE-627)NLEJ243139594 DE-627 ger DE-627 rakwb Sun, Baoyong verfasserin aut Overexpression of c-Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma
PC18 cells Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| activating protein-1 (AP1) site Tank, A. William verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00692.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 2 0 |
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10.1046/j.0022-3042.2001.00692.x doi (DE-627)NLEJ243139594 DE-627 ger DE-627 rakwb Sun, Baoyong verfasserin aut Overexpression of c-Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma
PC18 cells Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| activating protein-1 (AP1) site Tank, A. William verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00692.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 2 0 |
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10.1046/j.0022-3042.2001.00692.x doi (DE-627)NLEJ243139594 DE-627 ger DE-627 rakwb Sun, Baoyong verfasserin aut Overexpression of c-Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma
PC18 cells Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| activating protein-1 (AP1) site Tank, A. William verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00692.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 2 0 |
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10.1046/j.0022-3042.2001.00692.x doi (DE-627)NLEJ243139594 DE-627 ger DE-627 rakwb Sun, Baoyong verfasserin aut Overexpression of c-Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma
PC18 cells Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| activating protein-1 (AP1) site Tank, A. William verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00692.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 2 0 |
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10.1046/j.0022-3042.2001.00692.x doi (DE-627)NLEJ243139594 DE-627 ger DE-627 rakwb Sun, Baoyong verfasserin aut Overexpression of c-Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma
PC18 cells Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| activating protein-1 (AP1) site Tank, A. William verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00692.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 2 0 |
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Overexpression of c-Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma
PC18 cells |
| abstract |
The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. |
| abstractGer |
The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. |
| abstract_unstemmed |
The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site. |
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Overexpression of c-Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma
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| doi_str |
10.1046/j.0022-3042.2001.00692.x |
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PC18 cells</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2002</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c-Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c-Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system. We demonstrate that induction of c-Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run-on assays. This stimulation is closely associated quantitatively with the induction of c-Fos and does not apparently require phosphorylation of c-Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c-Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c-Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2002</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2002||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">activating protein-1 (AP1) site</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tank, A. William</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Journal of neurochemistry</subfield><subfield code="d">Oxford : Wiley-Blackwell, 1956</subfield><subfield code="g">80(2002), 2, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243927584</subfield><subfield code="w">(DE-600)2020528-4</subfield><subfield code="x">1471-4159</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:80</subfield><subfield code="g">year:2002</subfield><subfield code="g">number:2</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1046/j.0022-3042.2001.00692.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">80</subfield><subfield code="j">2002</subfield><subfield code="e">2</subfield><subfield code="h">0</subfield></datafield></record></collection>
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