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Biological Activity for Maritoclax
Mcl-1 inhibitor; disrupts Mcl-1-Bim interaction and induces Mcl-1 proteasomal degradation. Exhibits no effect on Bcl-XL-Bim interaction. Selectively induces apoptosis in Mcl-1-dependent K562 leukemia cells. Sensitizes K562 and Raji cells to ABT-737-induced apoptosis.
Technical Data for Maritoclax
|Storage||Store 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.
References for Maritoclax
References are publications that support the biological activity of the product.
Doi et al (2012) Discovery of marinopyrrole A (maritoclax) as a selective Mcl-1 antagonist that overcomes ABT-737 resistance by binding to and targeting Mcl-1 for proteasomal degradation. J.Biol.Chem. 287 10224 PMID: 22311987
Pandey et al (2013) Proteasomal degradation of Mcl-1 by maritoclax induces apoptosis and enhances the efficacy of ABT-737 in melanoma cells. PLoS ONE 8 e78570 PMID: 24223823
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Keywords: Maritoclax, Maritoclax supplier, Mcl-1, inhibitors, inhibits, apoptosis, proapoptotic, leukemia, ABT737, marinopyrroleA, Bcl-2, Family, 5368, Tocris Bioscience
Citations for Maritoclax
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Currently there are no citations for Maritoclax.
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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!
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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.