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Bax is a pro-apoptotic member of Bcl-2 family proteins and plays an important role in mitochondria-dependent apoptosis. Bax stays in the cytosol and transfers into mitochondria after apoptotic stimuli [1].

BIP V5 is a membrane-permeable peptide inhibitor of Bax translocation to mitochondria. In HeLa cells, BIP V5 protected cells from UVC- and STS-induced apoptosis. In U87-MG glioma cells, MCF-7 breast cancer cells and LNCaP prostate cancer cells, BIP V5 also inhibited apoptosis induced by anti-cancer drugs cisplatin, etoposide and doxorubicin. While BIP V5 did not suppress UVC- or STS-induced apoptosis in Bax-deficient cells (DU145), which suggested BIP V5 only suppressed Bax-mediated apoptosis. Also, BIP (V5) inhibited Bax translocation to mitochondria stimulated by UVC irradiation and STS treatment. The caspase activation and the release of cytochrome c from mitochondria triggered by apoptotic stimuli were also significantly inhibited by BIP V5. BIP V5 inhibited the interaction of Ku70 and endogenous Bax in a dose-dependent way [1].

In a mouse model, BIP V5 increased expression of anti-apoptotic proteins XIAP and Bcl-2 by more than 11- and 3-fold and reduced expression of apoptosis-inducing proteins Bax, Bad, and nuclear factor-κ B-p65 by 10, 30, and nearly 50%, respectively. Also, BIP V5 increased glucose-responsive insulin secretion [2].

References:

[1].  Sawada M, Hayes P, Matsuyama S. Cytoprotective membrane-permeable peptides designed from the Bax-binding domain of Ku70. Nat Cell Biol, 2003, 5(4): 352-357.

[2].  Rivas-Carrillo JD, Soto-Gutierrez A, Navarro-Alvarez N, et al. Cell-permeable pentapeptide V5 inhibits apoptosis and enhances insulin secretion, allowing experimental single-donor islet transplantation in mice. Diabetes, 2007, 56(5): 1259-1267.

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