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Submit ReviewOriginally reported to be a cell-permeable synthetic peptide inhibitor of Bax that blocks apoptosis. Also available: Bax inhibitor peptide V5 (Cat. No. 1785) and Negative control (Cat. No. 1787).
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M. Wt | 616.77 |
Formula | C27H48N6O8S |
Sequence | PMLKE |
Storage | Desiccate at -20°C |
CAS Number | 579492-83-4 |
Smiles | [H]N1CCC[C@H]1C(=O)N[C@@H](CCSC)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CCC(O)=O)C(O)=O |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Sawada et al (2003) Cytoprotective membrane-permeable peptides designed from the Bax-binding domain of Ku70. Nat.Cell.Biol. 5 352 PMID: 12652309
Keywords: Bax inhibitor peptide P5, Bax inhibitor peptide P5 supplier, inhibitors, inhibits, Bax-mediated, apoptosis, Bcl-XL, Mcl-1, Bcl-2, Family, Bax, inhibitor, peptideP5, 1786, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for Bax inhibitor peptide P5 include:
Sanchez-Niño et al (2010) BASP1 promotes apoptosis in diabetic nephropathy. J Am Soc Nephrol 21 610 PMID: 20110383
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.