Immunological quantitation of phospholipid/Ca2+-dependent protein kinase of human mammary carcinoma cells: inverse relationship to estrogen receptors

Détails

ID Serval
serval:BIB_75FE69B93A81
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Immunological quantitation of phospholipid/Ca2+-dependent protein kinase of human mammary carcinoma cells: inverse relationship to estrogen receptors
Périodique
International Journal of Cancer
Auteur(s)
Borner  C., Wyss  R., Regazzi  R., Eppenberger  U., Fabbro  D.
ISSN
0020-7136 (Print)
Statut éditorial
Publié
Date de publication
09/1987
Volume
40
Numéro
3
Pages
344-8
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Sep 15
Résumé
The amounts of phospholipid- and Ca2+-dependent protein kinase (PKC) of various human mammary tumor cells containing (ER+) or lacking (ER-) estrogen receptors were estimated by quantitative immunoblotting. According to several criteria the polyclonal anti-PKC antibody raised in rabbits against porcine brain PKC specifically recognizes an 80-kDa polypeptide on immunoblots. This 80-kDa PKC presumably represents the autophosphorylated form of the holoenzyme. Immunological quantitation of PKC revealed that the levels of immunodetectable PKC varied widely among the various human mammary carcinoma cell lines but closely matched the amounts determined by enzyme activity and phorbol ester binding in the respective cell line. The largest amounts of immunodetectable PKC were found in the ER- human mammary tumor cells (0.5 to 1.5 micrograms PKC/mg of cytosolic protein). These data indicate that ER- human mammary carcinoma cell lines express significantly higher levels of PKC than their estrogen-receptor-containing counterparts.
Mots-clé
Breast Neoplasms/*analysis Carcinoma/*analysis Cell Line Female Humans Immune Sera/immunology Phosphorylation Protein Kinase C/*analysis/immunology/isolation & purification Receptors, Estrogen/*analysis
Pubmed
Web of science
Création de la notice
24/01/2008 15:29
Dernière modification de la notice
03/03/2018 18:24
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