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Effect of Diet on Colonic-Programmed Cell Death: Molecular Mechanism of Action

Effect of Diet on Colonic-Programmed Cell Death: Molecular Mechanism of Action

R S Chapkin, Y Fan, J R Lupton

Toxicol Lett. 2000 Mar 15;112-113:411-4.

PMID: 10720760

Abstract:

Colon cancer evolves from a progressive inhibition of apoptosis and is influenced strongly by diet. Among dietary factors, butyrate (derived from fermentable fibers) may have utility as a chemopreventive agent because of its ability to promote apoptosis. Because CD95 (APO-1/Fas) transduces signals resulting in apoptosis, we tested the hypothesis that butyrate-dependent colonocyte apoptosis is mediated by this death receptor. Treatment of immortalized mouse colon cells with Fas agonistic antibody induced cell death, indicating that Fas in colonocytes is functional. Antagonism of Fas signaling using a soluble Fas:Fc chimera blocked butyrate induction of apoptosis. Therefore, Fas receptor dependent signal transduction is required for butyrate induction of apoptosis in colonic cells.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4248718	Fas/Fc Chimera from mouse			Price

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