化学性质:
规格 | 5mg 10mg 100mg |
CAS | 579492-83-4 |
别名 |
|
化学名 | (2S)-2-[[(2S)-6-amino-2-[[(2S)-4-methyl-2-[[(2S)-4-methylsulfanyl-2-[[(2S)-pyrrolidine-2-carbonyl]amino]butanoyl]amino]pentanoyl]amino]hexanoyl]amino]pentanedioic acid |
分子式 | C27H48N6O8S |
分子量 | 616.77 |
溶解度 | ≥ 61.7mg/mL in DMSO, ≥ 101 mg/mL in EtOH with ultrasonic, ≥ 94.4 mg/mL in H2O |
储存条件 | Desiccate at -20°C |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
Shipping Condition | Evaluation sample solution : ship with blue ice |
产品描述:
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 P5 is a membrane-permeable peptide inhibitor of Bax translocation to mitochondria. In HeLa cells, BIP P5 protected cells from UVC- and STS-induced apoptosis. In U87-MG glioma cells, MCF-7 breast cancer cells and LNCaP prostate cancer cells, BIP P5 also inhibited apoptosis induced by anti-cancer drugs cisplatin, etoposide and doxorubicin. While BIP P5 did not suppress UVC- or STS-induced apoptosis in Bax-deficient cells (DU145), which suggested BIP P5 only suppressed Bax-mediated apoptosis. The caspase activation and the release of cytochrome c from mitochondria triggered by apoptotic stimuli were also significantly inhibited by BIP P5. BIP P5 inhibited the interaction of Ku70 and endogenous Bax in a dose-dependent way [1].
Reference:
[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.
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