| Texto completo | |
| Autor(es): |
Colabardini, Ana Cristina
[1]
;
de Castro, Patricia Alves
[1]
;
de Gouvea, Paula Fagundes
[1]
;
Savoldi, Marcela
[1]
;
Malavazi, Iran
[2]
;
Goldman, Maria Helena S.
[3]
;
Goldman, Gustavo Henrique
[1, 4]
Número total de Autores: 7
|
| Afiliação do(s) autor(es): | [1] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Sao Paulo - Brazil
[2] Univ Fed Sao Carlos, Dept Genet & Evolucao, CCBS, BR-13560 Sao Carlos, SP - Brazil
[3] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Sao Paulo - Brazil
[4] Lab Nacl Ciencia & Tecnol Bioetanol CTBE, BR-13083970 Sao Paulo - Brazil
Número total de Afiliações: 4
|
| Tipo de documento: | Artigo de Revisão |
| Fonte: | Molecular Microbiology; v. 78, n. 5, p. 1259-1279, DEC 2010. |
| Citações Web of Science: | 27 |
| Resumo | |
P>Previously, we demonstrated that the Aspergillus nidulans calC2 mutation in protein kinase C pkcA was able to confer tolerance to farnesol (FOH), an isoprenoid that has been shown to inhibit proliferation and induce apoptosis. Here, we investigate in more detail the role played by A. nidulans pkcA in FOH tolerance. We demonstrate that pkcA overexpression during FOH exposure causes increased cell death. FOH is also able to activate several markers of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). Our results suggest an intense cross-talk between PkcA and the UPR during FOH-induced cell death. Furthermore, the overexpression of pkcA increases both mRNA accumulation and metacaspases activity, and there is a genetic interaction between PkcA and the caspase-like protein CasA. Mutant analyses imply that MAP kinases are involved in the signal transduction in response to the effects caused by FOH. (AU) | |