28 décembre 2012

Cytotoxicity of BAX

The cytotoxicity of paclitaxel, vincristine, and doxorubicin was significantly enhanced in BAX transfectants compared with control clones, whereas the cytotoxicity profile of carboplatin, etoposide, and hydroxyurea was unchanged. The inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk) successfully blocked this protease activity and prevented FAS-induced death but not BAX-induced death.
Posté par tnfalpha à 03:06 - Commentaires [0] - Permalien [#]

28 décembre 2012

Associations of BAX with chemical compounds

Coexpression of BAD and NOXA killed wild-type but not Bax, Bak doubly deficient cells or Puma deficient cells with Bim knockdown, indicating that activator BH3-only molecules function downstream of inactivator BH3-only molecules to activate BAX-BAK. These results suggest that glutathione-dependent BAX activation in cells with normal CFTR represents an early step in oxidative stress-induced apoptosis of these cells. The expression of BCL-2 and BAX, which would occur downstream from p53, was not changed by irradiation and Trolox... [Lire la suite]
Posté par tnfalpha à 03:06 - Commentaires [0] - Permalien [#]
28 décembre 2012

BAX treatment

Interestingly, LDFRT treatment in both cell lines with or without Paclitaxel down-regulated nuclear factor kappa B activity and BCL-2 protein expression and simultaneously up-regulated BAX protein. Recent genetic studies with fibroblasts derived from mutant mouse embryos indicate that a class of the BCL-2 family proapoptotic proteins (designated BH-123 or multidomain proteins) such as BAX and BAK constitutes an essential component of the core apoptosis machinery in animal cells. No germ line BAX mutations were found.
Posté par tnfalpha à 03:05 - Commentaires [0] - Permalien [#]