A 5′-flanking region of the bovine tyrosine hydroxylase gene is involved in cell-specific expression, activation of gene transcription by phorbol ester, and transactivation by c-Fos and c-Jun

Goc, Anna; Norman, Sylvia A.; Puchacz, Elzbieta; Stachowiak, Ewa K.; Lukas, Ronald J.; Stachowiak, Michal K.

doi:10.1016/1044-7431(92)90050-c

Cited by 17 publications

(32 citation statements)

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“…The rapid nuclear accumulation of FGF‐2 and FGFR1 in BAMC in response to treatment with AII (Fig. 1) coincides with the transcriptional activation of the TH gene (Goc et al . 1992).…”

Section: Resultsmentioning

confidence: 54%

“…Regulation of the TH promoter is dependent upon both a CREB‐binding cAMP‐responsive element (CRE) and an activating protein‐1 (AP1) site (Goc et al . 1992; Huang et al .…”

mentioning

confidence: 99%

“…1996). However, mutation of the AP1 site only partially reduces the stimulation of the TH promoter (Goc and Stachowiak 1992; Kim et al . 1996; Nagamoto‐Combs et al .…”

mentioning

confidence: 99%

“…1996) and Ca 2 ionophore (Nagamoto‐Combs et al . 1996), and by the PKC‐activating phorbol myristate acetate (PMA; Goc et al . 1992).…”

mentioning

confidence: 99%

“…Up‐regulation of TH mRNA in BAMC by forskolin is not affected by cycloheximide. In contrast, cycloheximide prevents TH mRNA up‐regulation by depolarization, or AII receptors, implicating signaling through inducible or high turnover rate proteins (Goc et al . 1992; Stachowiak et al .…”

mentioning

confidence: 99%

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Integrative nuclear FGFR1 signaling (INFS) pathway mediates activation of the tyrosine hydroxylase gene by angiotensin II, depolarization and protein kinase C

Myers

Fang

et al. 2002

Journal of Neurochemistry

193

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The integrative nuclear FGFR1 signaling (INFS) pathway functions in association with cellular growth, differentiation, and regulation of gene expression, and is activated by diverse extracellular signals. Here we show that stimulation of angiotensin II (AII) receptors, depolarization, or activation protein kinase C (PKC) or adenylate cyclase all lead to nuclear accumulation of fibroblast growth factor 2 (FGF-2) and FGFR1, association of FGFR1 with splicing factor-rich domains, and activation of the tyrosine hydroxylase (TH) gene promoter in bovine adrenal medullary cells (BAMC). The up-regulation of endogenous TH protein or a transfected TH promoter-luciferase construct by AII, veratridine, or PMA (but not by forskolin) is abolished by transfection with a dominant negative FGFR1TK-mutant which localizes to the nucleus and plasma membrane, but not by extracellularly acting FGFR1 antagonists suramin and inositolhexakisphosphate (IP6). Mechanism of TH gene activation by FGF-2 and FGFR1 was further investigated in BAMC and human TE671 cultures. TH promoter was activated by co-transfected HMW FGF-2 (which is exclusively nuclear) but not by cytoplasmic FGF-1 or extracellular FGFs. Promoter transactivation by HMWFGF-2 was accompanied by an up-regulation of FGFR1 specifically in the cell nucleus and was prevented FGFR1(TK-) but not by IP6 or suramin. The TH promoter was also transactivated by co-transfected wild-type FGFR1, which localizes to both to the nucleus and the plasma membrane, and by an exclusively nuclear, soluble FGFR1(SP-/ NLS) mutant with an inserted nuclear localization signal. Activation of the TH promoter by nuclear FGFR1 and FGF-2 was mediated through the cAMP-responsive element (CRE) and was associated with induction of CREB-and CBP/P-300-containing CRE complexes. We propose a new model for gene regulation in which nuclear FGFR1 acts as a mediator of CRE transactivation by AII, cell depolarization, and PKC.

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“…The rapid nuclear accumulation of FGF‐2 and FGFR1 in BAMC in response to treatment with AII (Fig. 1) coincides with the transcriptional activation of the TH gene (Goc et al . 1992).…”

Section: Resultsmentioning

confidence: 54%

“…Regulation of the TH promoter is dependent upon both a CREB‐binding cAMP‐responsive element (CRE) and an activating protein‐1 (AP1) site (Goc et al . 1992; Huang et al .…”

mentioning

confidence: 99%

“…1996). However, mutation of the AP1 site only partially reduces the stimulation of the TH promoter (Goc and Stachowiak 1992; Kim et al . 1996; Nagamoto‐Combs et al .…”

mentioning

confidence: 99%

“…1996) and Ca 2 ionophore (Nagamoto‐Combs et al . 1996), and by the PKC‐activating phorbol myristate acetate (PMA; Goc et al . 1992).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

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