Role of the cyclic AMP response element in rat fibronectin gene expression

Sun, Miao; Suri, Parmjeet K.; Liu, Shu-Ling; Abraham, Ann; Cook, Nanette; Milos, Patrice M.; Zern, Mark Α.

doi:10.1002/hep.1840170519

Cited by 10 publications

(6 citation statements)

References 43 publications

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“…Although CRE is not the cis-element for Taxinducibility of the FN gene, it may be important in the basal expression of the FN gene because CRE deletion significantly decreased the basal activity of the reporter gene. This is well consistent with the previous study that CRE is indispensable for the constitutive expression of the FN gene (31).…”

Section: Discussionsupporting

confidence: 94%

Transactivation of Fibronectin Promoter by HTLV-I Tax through NF-κB Pathway

Lee

Park

et al. 2000

Biochemical and Biophysical Research Communications

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Section: Discussionsupporting

confidence: 94%

Transactivation of Fibronectin Promoter by HTLV-I Tax through NF-κB Pathway

Lee

Park

et al. 2000

Biochemical and Biophysical Research Communications

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“…the presence of an important regulatory element for the basal activity within the sequence from Ϫ166 to Ϫ123. In support of these results, a previous study reported that the sequence between Ϫ164 and Ϫ90 is important for the basal expression of the rat FN gene and this activity is mediated by CRE at Ϫ160 [Miao et al, 1993]. Further deletion to Ϫ69 decreased the basal promoter activity by 90% relative to that of pGL2F1900 ( Fig.…”

Section: Identification Of the Pma-responsive Region In The Fn Promotersupporting

confidence: 77%

“…Regulatory elements and transcription factors responsible for the regulation of the FN gene expression by the cyclic AMP pathway and several factors have been described . Cyclic AMP-responsive elements (CRE) at position Ϫ160 and Ϫ170 of the rat and human FN promoter, respectively, have been shown to mediate the basal and cAMP-induced expression of the FN gene [Bowlus et al, 1991;Miao et al, 1993]. Among many CRE-binding proteins described, ATF-2 binds to the CRE of the human FN gene and cooperates with NF-1 and CP1 that bind to an adjacent CCAAT element for the transcription of the FN gene in hepatocytes [Srebrow et al, 1993;Alonso et al, 1996].…”

mentioning

confidence: 99%

Transcriptional regulation of fibronectin gene by phorbol myristate acetate in hepatoma cells: A negative role for NF-?B

et al. 2000

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The transcriptional regulation of the fibronectin (FN) gene in hepatoma cells by phorbol myristate acetate (PMA) was investigated. PMA increased the synthesis and mRNA levels of FN and its promoter activity in Hep3B hepatoma cells. The PMA-induced activation of FN expression was blocked by a protein kinase C (PKC) inhibitor and did not require a new protein synthesis. Deletion analysis revealed that the sequence between positions -69 and +136 of the FN gene was responsible for the PMA induction. Two PMA-inducible nuclear protein complexes were found to bind to a putative NF-kappaB site at -41 and were identified as a p65/p50 heterodimer and a p50/50 homodimer of NF-kappaB family. Mutations in the -41 NF-kappaB site, however, did not block the PMA induction of the FN promoter but rather enhanced it. Overexpression of p65 increased the FN promoter activity. While overexpression of p50 alone did not affect the promoter activity, it decreased the p65-induced activation of the FN promoter. Mutations in the -41 NF-kappaB site attenuated the p50-mediated suppression of the p65 transactivation of the FN promoter. Deletion of the sequence between +1 and +136 decreased the basal and PMA-induced activities of the FN promoter. This study shows that PMA induces the transcription of the FN gene in hepatoma cells via the PKC pathway. The DNA sequence between +1 and +136 is responsible, at least in part, for the PMA-induced activation of the FN gene, while the -41 NF-kappaB binding site plays as a negative regulatory element for it. In addition, this study is the first to show a role for NF-kappaB p65 in the transcriptional activation of the FN gene.

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“…*P < 0.05 keloid ®broblasts (Sible et al 1996). Evaluation of transcriptional regulatory elements of the FN gene in rat skin ®broblasts by mutational studies resulted in mutagenesis of the sequence between )164 and )90 which exhibits homology to the consensus binding site for CRE (Miao et al 1993). On the other hand, in adenovirus E1-transformed rat cells, the nuclear factor G10BP binding to the G10 stretch from positions )239 to )230 and two GC boxes consisting of the G10 stretch with one internal C residue insertion from positions )105 to )95 and )54 to )44, showed the strongest repressive activity (Nakamura et al 1992).…”

Section: Discussionmentioning

confidence: 99%