Résumé
IGF-1 increased 2-fold protein synthesis in cardiac myocytes. Genistein, whether added during preincubation or with IGF-1 at the start of incubation, significantly inhibited the IGF-1-induced stimulation of protein synthesis, autophosphorylation of the β-subunit of IGF-1 receptor and inhibition of ERK. When added 1 or 6 h after IGF-1, however, genistein was without effect. IGF-1-stimulated protein synthesis was also significantly inhibited by PD-098059, staurosporine, and rapamycin, but not by wortmannin, in cardiac myocytes. Some inhibitors produced a reduction in cell size. Activation of the ERK cascade by IGF-1 may be responsible for some of the features associated with cardiac myocyte hypertrophy.
Langue d'origine | English |
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Pages (de-à) | 193-196 |
Nombre de pages | 4 |
Journal | FEBS Letters |
Volume | 422 |
Numéro de publication | 2 |
DOI | |
Statut de publication | Published - janv. 30 1998 |
Financement
We thank Dr. C.I. Pogson for help with the preparation of the text of this paper. This work was supported in part by Fondo Nacional de Ciencia y Tecnologı́a (FONDECYT) Grants 1950452 (to S.L.) and 2950002 (to R.F.). R.F. is the recipient of a CONICYT fellowship (Chile).
Bailleurs de fonds | Numéro du bailleur de fonds |
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Comisión Nacional de Investigación Científica y Tecnológica | |
Fondo Nacional de Ciencia y Tecnología | 1950452, 2950002 |
ASJC Scopus Subject Areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology