Regulation of tyrosine hydroxylase gene expression by the m1 muscarinic acetylcholine receptor in rat pheochromocytoma cells

Chen, Yang; Best, Joseph A; Nagamoto, Kumi; Tank, A. William

doi:10.1016/0169-328x(96)00030-7

Cited by 14 publications

(32 citation statements)

References 32 publications

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“…Plasmids TH(− 272/+27)‐CAT and TH(mAP1)‐CAT were constructed as previously described (Best et al . 1995; Chen et al . 1996).…”

Section: Methodsmentioning

confidence: 99%

“…Cells were transiently transfected with 10 µg of TH‐reporter gene construct using the liposome‐mediated transfection procedure described previously (Chen et al . 1996; Nagamoto‐Combs et al .…”

Section: Methodsmentioning

confidence: 99%

“…Transfection efficiencies were monitored as described in our previous publications (Best et al . 1995; Chen et al . 1996; Nagamoto‐Combs et al .…”

Section: Methodsmentioning

confidence: 99%

“…1991; Hiremagalur et al . 1993; Hiremagalur and Sabban 1995), muscarinic acetylcholine receptors (Chen et al . 1996; Piech‐Dumas et al .…”

mentioning

confidence: 99%

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Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma  PC18 cells

Sun¹,

Tank²

2002

Journal of Neurochemistry

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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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“…Plasmids TH(− 272/+27)‐CAT and TH(mAP1)‐CAT were constructed as previously described (Best et al . 1995; Chen et al . 1996).…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma  PC18 cells

Sun¹,

Tank²

2002

Journal of Neurochemistry

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“…Transfection efficiencies were monitored by transfecting companion dishes (in triplicate) with 5 μg of plasmid DNA containing the structural CAT gene driven by the RSV promoter (pRSV‐CAT), as described in our previous publications (Best et al . 1995; Chen et al . 1996; Nagamoto‐Combs et al .…”

Section: Th Gene Promoter Assaysmentioning

confidence: 99%

c‐Fos is essential for the response of the tyrosine hydroxylase gene to depolarization or phorbol ester

Sun¹,

Tank²

2003

Journal of Neurochemistry

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Tyrosine hydroxylase (TH) gene transcription rate increases in response to numerous pharmacological and physiological stimuli. The AP1 site within the TH gene proximal promoter is thought to play an important role in mediating many of these responses; however, it is unclear which AP1 factors are required. To investigate whether c-Fos is essential for the response of the TH gene to different stimuli, c-Fos-deficient PC12 cell lines were produced utilizing an antisense RNA strategy. In these cell lines, stimulus-induced increases in c-Fos protein levels were dramatically attenuated, while c-Jun and CREB levels remained unchanged. TH gene transcription rate increased from four-to eight-fold in control cells after treatment with either 50 mM KCl or TPA. These responses were dramatically decreased in the c-Fos-deficient cell lines. In contrast, c-Fos down-regulation had little effect on the response of the TH gene to forskolin. Stimulation of TH gene promoter activity, which was observed in control cell lines treated with either 50 mM KCl or TPA was also dramatically inhibited in the c-Fos-deficient cells. These results suggest that c-Fos induction is essential for maximal stimulation of the TH gene in response to either depolarization or PKC activation in PC12 cells.

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Katecholamine

Kopf¹,

Schulz²,

Lehnert³

2001

Klinische Endokrinologie Und Stoffwechsel

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Regulation of tyrosine hydroxylase gene expression by the m1 muscarinic acetylcholine receptor in rat pheochromocytoma cells

Cited by 14 publications

References 32 publications

Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma  PC18 cells

Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma  PC18 cells

c‐Fos is essential for the response of the tyrosine hydroxylase gene to depolarization or phorbol ester

Katecholamine

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Regulation of tyrosine hydroxylase gene expression by the m1 muscarinic acetylcholine receptor in rat pheochromocytoma cells

Cited by 14 publications

References 32 publications

Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma PC18 cells

Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma PC18 cells

c‐Fos is essential for the response of the tyrosine hydroxylase gene to depolarization or phorbol ester

Katecholamine

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Product

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About

Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma  PC18 cells

Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma  PC18 cells