Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics
Kerr JF, AH Wyllie, AR Currie. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer 1972; 26:239-57.
The genetics of programmed cell death in the nematode Caenorhabditis elegans
Horvitz HR, S Shaham, MO Hengartner. The genetics of programmed cell death in the nematode Caenorhabditis elegans. Cold Spring Harb Symp Quant Biol 1994; 59:p.377-85.
BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax
Yin XM, ZN Oltvai, SJ Korsmeyer. BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax [see comments]. Nature 1994; 369:321-3.
Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
Luo X, et al. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors. Cell 1998; 94:481-90.
Caspase Cleaved BID Targets Mitochondria and Is Required for Cytochrome c Release, while BCL-XL Prevents This Release but Not Tumor Necrosis Factor-R1/Fas Death
Gross A, et al. Caspase Cleaved BID Targets Mitochondria and Is Required for Cytochrome c Release, while BCL-XL Prevents This Release but Not Tumor Necrosis Factor-R1/Fas Death. J Biol Chem 1999; 274:1156-63.
published erratum appears in Nature 1993 Oct 7; 365(6446):568
Ogasawara, J et al. Lethal effect of the anti-Fas antibody in mice [published erratum appears in Nature 1993 Oct 7; 365(6446):568]. Nature 1993; 364:806-9.
Tumor necrosis factor is a terminal mediator in galactosamine/endotoxin-induced hepatitis in mice
Tiegs GM, Wolter, A Wendel. Tumor necrosis factor is a terminal mediator in galactosamine/endotoxin-induced hepatitis in mice. Biochem Pharmacol 1989; 38:627-31.
Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection
Pfeffer K et al. Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection. Cell 1993; 73:457-67.
Activation of caspase 3 (CPP32)-like proteases is essential for TNF- Alpha-induced hepatic parenchymal cell apoptosis and neutrophil-mediated necrosis in a murine endotoxin shock model
Jaeschke H et al. Activation of caspase 3 (CPP32)-like proteases is essential for TNF-alpha-induced hepatic parenchymal cell apoptosis and neutrophil-mediated necrosis in a murine endotoxin shock model. J Immunol 1998; 160:3480-6.