17β-Estradiol Abrogates Apoptosis Inhibiting PKCδ, JNK, and p66Shc Activation in C2C12 Cells

Author:

La Colla Anabela1,Boland Ricardo1,Vasconsuelo Andrea1

Affiliation:

1. INBIOSUR-CONICET; 8000 Bahía Blanca Argentina

Funder

Agencia Nacional de Promoción Científica y Tecnológica

Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET)

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference50 articles.

1. Chronic PMA treatment of Jurkat T lymphocytes results in decreased protein tyrosine phosphorylation and inhibition of CD3- but not Ti-dependent antibody-triggered Ca2+ signaling;Ahnadi;J Leukoc Biol,2000

2. Oxidative stress stimulates apoptosis and activates NF-kappab in osteoblastic cells via a pkcbeta/p66shc signaling cascade: Counter regulation by estrogens or androgens;Almeida;Mol Endocrinol,2010

3. The role of the mitochondrial permeability transition in cell death;Armstrong;Mitochondrion,2006

4. Upregulation of PKC δ- and downregulation of PKC α-mrna and protein by a phorbol ester in human T84 cells;Assert;FEBS Lett,1996

5. Tyrosine phosphorylation of protein kinase c delta is essential for its apoptotic effect in response to etoposide;Blass;Mol Cell Biol,2001

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