CREB is activated by UVC through a p38/HOG-1-dependent protein kinase

M. Iordanov, K. Bender, T. Ade, W. Schmid, C. Sachsenmaier, K. Engel, M. Gaestel, H. J. Rahmsdorf, P. Herrlich

Research output: Contribution to journalArticle

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Abstract

Changes in environmental conditions such as the addition of growth factors or irradiation of cells in culture first affect immediate response genes. We have shown previously that short wavelength UV irradiation (UVC) elicits massive activation of several growth factor receptor-dependent pathways. At the level of the immediate response gene c-fos, these pathways activate the transcription factor complex serum response factor (SRF)-p62(TCF) which mediates part of the UV-induced transcriptional response. These studies have, however, suggested that more that one pathway is required for full UV responsiveness of c-fos. Using appropriate promoter mutations and dominant-negative cAMP response element (CRE)-binding protein (CREB), we now find that UVC-induced transcriptional activation depends also on the CRE at position -60 of the c-fos promoter and on the functionality of a CREB. Upon W irradiation, CREB and ATF-1 are phosphorylated at serines 133 and 63, respectively, preceded by and dependent on activation of p38/RK/HOG-1 and of a p38/RK/HOG-1-dependent p108 CREB kinase. Although p90(RSK1)and MAPKAP kinase 2 are also activated by UV, p90(RSK1) does not, at least not decisively, participate in this signalling pathway to CREB and ATF-1 as it is not p38/RK/HOG-1 dependent, and CREB is a poor substrate for MAPKAP kinase 2 in vitro. On the basis of resistance to the growth factor receptor inhibitor suramin and of several types of cross-refractoriness experiments, the UVC-induced CREB/ATF-1 phosphorylation represents an as yet unrecognized route of UVC-induced signal transduction, independent of suramin-inhibitable growth factor receptors and different from the Erk 1,2-p62(TCF) pathway.

Original languageEnglish (US)
Pages (from-to)1009-1022
Number of pages14
JournalEMBO Journal
Volume16
Issue number5
DOIs
StatePublished - Mar 3 1997

Fingerprint

Activating Transcription Factor 2
Protein Kinases
Growth Factor Receptors
Carrier Proteins
Suramin
Chemical activation
Irradiation
Serum Response Factor
fos Genes
Cyclic AMP Response Element-Binding Protein
Response Elements
Genes
Serine
Transcriptional Activation
Signal Transduction
Intercellular Signaling Peptides and Proteins
Signal transduction
Phosphorylation
Transcription Factors
Cell Culture Techniques

Keywords

  • c-fos
  • CREB
  • MAPKAP kinase 2
  • p108 CREB kinase
  • UV

ASJC Scopus subject areas

  • Genetics
  • Cell Biology

Cite this

Iordanov, M., Bender, K., Ade, T., Schmid, W., Sachsenmaier, C., Engel, K., ... Herrlich, P. (1997). CREB is activated by UVC through a p38/HOG-1-dependent protein kinase. EMBO Journal, 16(5), 1009-1022. https://doi.org/10.1093/emboj/16.5.1009

CREB is activated by UVC through a p38/HOG-1-dependent protein kinase. / Iordanov, M.; Bender, K.; Ade, T.; Schmid, W.; Sachsenmaier, C.; Engel, K.; Gaestel, M.; Rahmsdorf, H. J.; Herrlich, P.

In: EMBO Journal, Vol. 16, No. 5, 03.03.1997, p. 1009-1022.

Research output: Contribution to journalArticle

Iordanov, M, Bender, K, Ade, T, Schmid, W, Sachsenmaier, C, Engel, K, Gaestel, M, Rahmsdorf, HJ & Herrlich, P 1997, 'CREB is activated by UVC through a p38/HOG-1-dependent protein kinase', EMBO Journal, vol. 16, no. 5, pp. 1009-1022. https://doi.org/10.1093/emboj/16.5.1009
Iordanov M, Bender K, Ade T, Schmid W, Sachsenmaier C, Engel K et al. CREB is activated by UVC through a p38/HOG-1-dependent protein kinase. EMBO Journal. 1997 Mar 3;16(5):1009-1022. https://doi.org/10.1093/emboj/16.5.1009
Iordanov, M. ; Bender, K. ; Ade, T. ; Schmid, W. ; Sachsenmaier, C. ; Engel, K. ; Gaestel, M. ; Rahmsdorf, H. J. ; Herrlich, P. / CREB is activated by UVC through a p38/HOG-1-dependent protein kinase. In: EMBO Journal. 1997 ; Vol. 16, No. 5. pp. 1009-1022.
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AU - Sachsenmaier, C.

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