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http://purl.uniprot.org/citations/26493679http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26493679http://www.w3.org/2000/01/rdf-schema#comment"

Background and purpose

The rise in intracellular Ca(2+) stimulates the expression of the transcription factor c-Fos. Depending on the mode of entry of Ca(2+) into the cytosol, distinct signal transducers and transcription factors are required. Here, we have analysed the signalling pathway connecting a Ca(2+) influx via activation of transient receptor potential melastatin-3 (TRPM3) channels with enhanced c-Fos expression.

Experimental approach

Transcription of c-Fos promoter/reporter genes that were integrated into the chromatin via lentiviral gene transfer was analysed in HEK293 cells overexpressing TRPM3. The transcriptional activation potential of c-Fos was measured using a GAL4-c-Fos fusion protein.

Key results

The signalling pathway connecting TRPM3 stimulation with enhanced c-Fos expression requires the activation of MAP kinases. On the transcriptional level, three Ca(2+) -responsive elements, the cAMP-response element and the binding sites for the serum response factor (SRF) and AP-1, are essential for the TRPM3-mediated stimulation of the c-Fos promoter. Ternary complex factors are additionally involved in connecting TRPM3 stimulation with the up-regulation of c-Fos expression. Stimulation of TRPM3 channels also increases the transcriptional activation potential of c-Fos.

Conclusions and implications

Signalling molecules involved in connecting TRPM3 with the c-Fos gene are MAP kinases and the transcription factors CREB, SRF, AP-1 and ternary complex factors. As c-Fos constitutes, together with other basic region leucine zipper transcription factors, the AP-1 transcription factor complex, the results of this study explain TRPM3-induced activation of AP-1 and connects TRPM3 with the biological functions regulated by AP-1."xsd:string
http://purl.uniprot.org/citations/26493679http://purl.org/dc/terms/identifier"doi:10.1111/bph.13372"xsd:string
http://purl.uniprot.org/citations/26493679http://purl.uniprot.org/core/author"Thiel G."xsd:string
http://purl.uniprot.org/citations/26493679http://purl.uniprot.org/core/author"Rossler O.G."xsd:string
http://purl.uniprot.org/citations/26493679http://purl.uniprot.org/core/author"Rubil S."xsd:string
http://purl.uniprot.org/citations/26493679http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26493679http://purl.uniprot.org/core/name"Br J Pharmacol"xsd:string
http://purl.uniprot.org/citations/26493679http://purl.uniprot.org/core/pages"305-318"xsd:string
http://purl.uniprot.org/citations/26493679http://purl.uniprot.org/core/title"CREB, AP-1, ternary complex factors and MAP kinases connect transient receptor potential melastatin-3 (TRPM3) channel stimulation with increased c-Fos expression."xsd:string
http://purl.uniprot.org/citations/26493679http://purl.uniprot.org/core/volume"173"xsd:string
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