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Bax inhibitor peptide P5
Discontinued ProductBax inhibitor peptide P5 (Cat. No. 1786) has been withdrawn from sale for commercial reasons.
Biological Activity for Bax inhibitor peptide P5
Sold under license
Technical Data for Bax inhibitor peptide P5
|Storage||Desiccate at -20°C|
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.
Product Datasheets for Bax inhibitor peptide P5
References for Bax inhibitor peptide P5
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
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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
1 Citation for Bax inhibitor peptide P5
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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Literature in this Area
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.
Programmed Cell Death Poster
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.