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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Bax inhibitor peptide P5 (BIP P5) is a peptide inhibitor of Bax translocation to mitochondria [1].
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.