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2007-03-01 - Article/Dans un journal avec peer-review - Anglais - 13 page(s)

Gallo Dominique, Jacquemotte Françoise, Cleeren Anny, Laïos Ioanna, Hadiy Samira, Rowlands Martin G., Caille Olivier, Nonclercq Denis , Laurent Guy , Jacquot Yves, Leclercq Guy, "Calmodulin-independent, agonistic properties of a peptide containing the calmodulin binding site of estrogen receptor alpha" in Molecular & Cellular Endocrinology, 268, 1, 37-49

  • Edition : North Holland Publishing Company, Amsterdam (The Netherlands)
  • Codes CREF : Histologie (DI3212), Cancérologie (DI3349)
  • Unités de recherche UMONS : Histologie (M118)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)
Texte intégral :

Abstract(s) :

(Anglais) Calmodulin (CaM) contributes to estrogen receptor a (ER)-mediated transcription. In order to study the underlying mechanisms, we synthesized a peptide including the CaM binding site: ERa17p (P295-T311). This peptide inhibited ER-CaM association, unlike two analogs in which two amino acids required for CaM binding were substituted. Exposure of MCF-7 cells to ERa17p down regulated ER, stimulated ER-dependent transcription and enhanced the proliferation of ER-positive breast cancer cell lines. Interestingly, ERa17p analogs unable to bind to CaM induced similar responses, demonstrating that ERa17p-mediated effects are mainly relevant to mechanisms independent of ER-CaM dissociation. The P295-T511 motif is indeed a platform for multiple post-translational modifications not necessarily CaM-dependent. The additional finding that deletion of the P295-T311 sequence in ER produced a constitutive transcriptional activity revealed that this platform motif has autorepressive functions. With regard to cell function, association of CaM to ER would counteract this autorepression, leading thereby to enhanced ER-mediated transactivation.

Identifiants :
  • PMID : 17316976
  • ISSN : 0303-7207
  • DOI : 10.1016/j.mce.2007.01.012